An Estrous

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Role of vitamin e and selenium in anestrous andconceptionPublished on: 03/16/2010Rating:

Author : Dr Rajendran Duraisamy

role ofvitamine and selenium in anestrous and conception

"Fertility is a luxurious event

For this, endometrium should be protected by antioxidant

Antioxidant can be given as nutrient

VitaminE and Selenium can be given for this event

Let fed this nutrients in this moment"

With this quote let me start as competent

1. Introduction

Anoestrus-major causes of economic losses in both the large and small ruminants in

India.

Causes of functional infertility included cystic and inactive ovaries withanoestrus

Anoestrus is one of the major causes of economic losses in both the large and smallruminants in India. It is a major problem in the tropics and subtropics, where inadequate nutrition, highambient temperature, high parasite burdens and disease exacerbate the problem. Low body weightand poor body condition, compounded with lactation stress, can further extend the postpartumanoestrous period. Vandeplassche (1982). The causes of functional infertility included cystic andinactive ovaries with anoestrus, early embryonic mortality with repeat breeding, and prolongedgestation. Anoestrus often reflects a hormonal disturbance and accounted for 47.8% of the cases.Repeat breeding, where cows require three or more services to conceive, accounted for 11.5% ofcases. Singh et al (1981) also found functional infertility to be more common than infertility due toinfectious diseases (76 vs 24%). There is a very important interrelationship between nutrition andproductionperformance of dairy cows and this interrelationship has far reaching effects on thephysiological functioning of the reproductive system which is constantly under the influence of theendocrine system.

Anoestrusis a period of sexual quietude in which the animal fails to exhibit normal oestruscycles and no manifestation of heat (Boyd, 1977). Its effects are greater than most dairy farmersrealize. Not only does it lengthen the postpartum interval (a period from parturition to oestrus) but alsosubstantially reduce the farmer's financial returns from milk or calf sales due to overall reducednumber of pregnancies (calving), and the cost of managing prolonged postpartum anoestrus. It isessential to distinguish physiological from or pathological anoestrus. Cows are regarded asphysiologically anoestrous before puberty, during pregnancy and for a few days (up to 60) followingparturition, whereas, lack of oestrus at 60 days postpartum is termed pathological anoestrus(Lamming,1980) The potential problems that breeders may encounter include cows that gave birth totwin calves had retained placenta, have uterine infection or milk fever. Extensive efforts, world-wide,have been put into research to limit the occurrence of this disorder (anoestrus). However despite allthese efforts postpartum infertility is still a significant problem in dairy herds. Nonetheless fewadvances have been made in reducing the postpartum interval through proper nutrition includingsupplementation of antioxidant namelyvitaminE, Selenium and carotenoids.

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A key factor influencing the productivity per cow is conception rate.

The conception rate observed in Tamilnadu was just 34.53 per cent in cows and 25.52 per

cent in buffaloes

The main goal in a commercial dairy cattle operation is to optimize number of calf producedper cow as economically as possible. A key factor influencing the productivity per cow is conceptionrate, both at first service and during the remainder of the breeding season. The conception rateobserved in Tamilnadu (Table 1) was just 34.53 per cent in cows and 25.52 per cent in buffaloes(Thirunavukkarasu, 2006). No data available regarding conception rate in cattle and buffaloes in India.

Nutrition, before and after calving, has an effect on pregnancy rates. Inadequatenutritionprior to calving, results in cows being thin at calving which delays the onset of estrualactivity post-calving. Cows on an inadequate plane of nutrition after calving can easily delay the firstservice and overall conception rates reduced by 5-10 percent and even more dramatic effects, suchas a 20-40 percent reduction in conception rates have been noted in research trials

Table 1. Published estimates of the incidence of retained placenta indifferent countries. Lavenand Peters (1996)

Soils in many of the important dairy regions of the world are Se-deficient.

Dairy cattle consuming stored forages are often low invitaminE unless supplemented., and

vitamin E deficiencies are frequently observed during the periparturient period, leading to

retain placenta and subsequently Anoestrus

Calving Difficulty, It include retain placenta, a number of studies have shown that increasedcalving difficulty will not only increase the length of time required for the cows to cycle after calving,but decrease the percent of cows conceiving in the first post-partum estrus and often reduce overallconception rate during the breeding season. Two to 30% of cows retain their foetal membranes for 12to 24 hours after a normal delivery. The afterbirth, or foetal membranes, is retained if the cotyledonaryvilli fail to detach from the caruncular crypts. Membranes retained for more than 2 or 3 daysdecompose in the uterus, leading to metritis. A number of reproductive diseases can have a majorimpact on the overall reproductive performance of a cow herd.

The two conditions mentioned above is related with few aspects of stress, immunity andhealth. Antioxidant can have the role to reduce factors affecting estrous cycle and conception rate.

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Soils in many of the important dairy regions of the world are Se-deficient, and feedstuffsgrown on these soils provide inadequate dietary Se. Dairy cattle consuming stored forages areoften low in vitamin E unless supplemented, and vitamin E deficiencies are frequently observedduring the periparturient period leading to retain placenta and subsequently anoestrus.Supplementation of vitamin E and Se is best result of improve overall health, increases conceptionrate and reduces the incidence of anestrous. The main aim of this essay is to explore the newer data

regarding the role of vitamin E and selenium on anestrous and conception.

Table 2. Conception rates observed in different agro-climatic zones ofTamilnadu (Thirunavukkarasu, 2006)

2. HEALTH VS. ANOESTRUS AND CONCEPTION RATE

Often one of the key factors reducing conception rates in a cow herd is health problems.Subclinical uterine infection is major cause of infertility in crossbred cattle and buffaloes in India.Subclinical uterine infection can be reduced or prevented by the increasing animal immune statuseither by vaccination or by increasing general immunity. There is evidence that deficiencies of E andSe can lead to impaired resistance to disease. A number of reproductive diseases can have a majorimpact on the overall reproductive performance of a cow herd casing anoestrus and reduceconception rate.

Many species of bacteria inhabit the vagina, uterus, and cervix of cows. Some are symbionts

that become pathogenic when the animal is stressed; others are immediately pathogenic.

Namboothripad and Raja (1976), Eduvie et al (1984) and El-Azab et al (1988)isolated Staphylococcus aureus, Escherichia coli, Pseudomonas pyocyanea, Corynebacteriumpyogenes, Proteus mirabilis, Streptococcusspp., Pasteurella multocida, Proteus vulgaris,Klebsiellaspp. and several anaerobic microorganisms from the uteri of cows with a history of repeatbreeding, retained placenta and metritis, as well as from the uteri of normal sucklingcows. Mycobacterium tuberculosiswas isolated by Mohanty et al (1980) from a Haryana heifer thatwas a chronic repeat breeder.

Subclinical uterine infection is major cause of infertility in crossbred cattle and buffaloes

in India.

There is evidence that deficiencies of E and Se can lead to impaired resistance to disease.

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Listeria monocytogenesmay also cause abortion in cattle. When the organism infects apregnant cow, it invades the foetal nervous system and forms necrotic foci on the liver, lungs andspleen (Watson, 1979), killing the foetus. Vandeplassche (1982) indicated that, although theorganisms are easily eliminated from the uterus, they may persist in the mammary system. Antibodiesto Listeriaare short-lived, and immunity is thus only temporary and cows can be re-infected.Treatment is often futile, even with antibiotics. However if the animal are sound nutritional background

and good immunity, the rate of infection is less.

Harrison and others (1984) found that supplementing cows with selenium significantlydecreased the incidence of cystic ovarian disease from 47 to 19 per cent, but that the vitamin E statusof the cows had no effect on the incidence ofcystic ovarian disease. In contrast, Jaskowski (1993)found that vitamin E supplementation significantly increased the beneficial effect of seleniumsupplementation on ovarian cysts. Erskine and others (1997) reported that 3000 iu of vitamin E giveneight to 14 days before parturition significantly decreased the incidence of metritis, probably as a sideeffect of the reduction in retained fetal membranes which is usually associated with a significantlyincreased risk of uterine infection. However, Harrison and others (1984) found that supplementingcows with vitamin E in addition to selenium had no further beneficial effect on the incidence ofmetritis, despite a significant reduction in the incidence of retained fetal membranes.

3. IMMUNE STATUS VS. ANOESTRUS AND CONCEPTION RATE

The immune system can be partitioned into two broad categories; specific (or acquired) andnonspecific. Specific or acquired immunity is the basis of vaccination programs. Specific immunityoccurs when animals develop or acquire immunity to a specific pathogen once it is exposed to thepathogen. Antibodies specific to that pathogen are produced and the immune system "memorizes"the antigenic properties of the pathogen so that an immune response can be initiated quickly whenthe host is exposed to the pathogen again. Lymphocytes and macrophages are the cells primarilyinvolved with specific immunity. The nonspecific immune system is designed to protect the body fromall antigens. Vaccination will not influence nonspecific immunity and the nonspecific immune systemdoes not have a "memory." Neutrophils are the cells most involved with nonspecific immunity.

When a pathogen invades the uterus or reproductive tract of a cow, a cascade of eventsoccurs. First, neutrophils from the blood are drawn to the infection site. Neutrophils are the first lineof defense after a pathogen invades the body. The function of neutrophil is to engulf (phagocytize)and then kill bacteria. After a neutrophil engulfs a bacterium, and chemical reaction called arespiratory burst occurs and this produces a high concentration of free radicals. These free radicalshelp kill the bacteria, but if they are not controlled, they also can damage and kill the neutrophil. Thelife span of neutrophils is short; each neutrophil can engulf 5 to 20 bacteria before the cell is killed. Aspart of the inflammatory response, macrophages also are drawn into the infection site. These cellscan kill bacteria directly but more importantly they initiate the acquired immune response. Antibodiesare produced against the bacteria and lymphocytes are drawn to the infection site. The combinedefforts of neutrophils, macrophages, lymphocytes, and antibodies help to eliminate the invadingpathogen and reduce the disease condition of reproductive tract and increase the occurrence ofestrus and there by increases conception rate.VitaminE and se containing glutathione peroxidase

have sparing effects on the requirements for one another relative to intracellular killing of bacteria.The protection afforded cellular membranes by vitamin E may spare the requirement for glutathioneperoxidase by reducing free radicals at the membrane, thereby preventing leakage of free radicalsinto the cytosol and maintaining intracellular killing capacity of the cell. Conversely, glutathioneperoxidase activity in the cytosol may spare the requirement for vitamin E in the membranes.

Feeding approximately 1000 IU/day ofsupplemental vitamin E with adequate selenium -

reducedthe prevalence ofretained fetal membranes

3000 iu of vitamin E given eight to 14 days before parturition significantly decreased the

incidence of metritis

Clinical studies have been conducted to evaluate the effect of supplemental vitamin E onprevalence of retained fetal membranes, intramammary infections, and clinicalmastitis. Feeding

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approximately 1000 IU/day of supplemental vitamin E (usually all-rac--tocopheryl acetate) to drycows when adequate selenium was supplemented reduced the prevalence of retained fetalmembranes in some (Harrison et al., 1984; Miller et al., 1993). When vitamin E was injected (usuallyin combination with selenium) rather than fed, about half the time there was no effect for prevalenceof retained fetal membranes and about half the time there was a positive response (Miller et al.,1993).

Two fairly common diseases, vibriosis and trichomoniasis, will cause lower conception rates.Cows will breed, but then return to heat fairly soon afterwards. Two other diseases that can impactconception rates are red-nose (IBR) and bovine viral diarrhea (BVD). A number of diseases will causeabortion to occur and leave the animals infertile. This would include diseases such as leptospirosis,hemopholaus somnus and brucellosis. Presence of immunity against these diseases reduces theincidence of anestrous and increases the conception rate. Feeding of vitamin E and Seleniumincreases non specific immunity and can reduce the occurrence of bacterial and viral diseases thereby increase estrus cycle and conception rate.

3.1IMMUNE RESPONSEONVITAMINE AND SELENIUMSUPPLEMENTATION

Several studies have shown that vitamin E supplementation has a protective effect. Reddy etal. (1987) fed 32 Holstein calves up to 500 iu per day of supplementary vitamin E. They found thatsupplementation increased the blastogenic responses of both T cells and B cells, and that theanamnestic antibody response was highest in calves supplemented with 125 iu vitamin E per day.Hidiroglou et al. (1992) reported that the injection of 2700 iu of vitamin E every three weeks from birthfor 12 weeks significantly increased the production of immunoglobulin (Ig) M; the production of IgG,and IgG2 was also increased, but not significantly. Hogan et al. (1992) reported that injecting 3000 iuof vitamin E subcutaneously, 10 and five days before expected calving, significantly increased theintracellular kill of bacteria by neutrophils at calving. However, neither the phagocytic index nor thepercentage of neutrophils phagocytosing bacteria differed between the vitamin E-injected andplacebo-injected cows. Politis and others (1995) supplemented eight dairy cows with 3000 iu ofvitamin E per cow per day orally, beginning four weeks before and continuing until eight weeks afterparturition, and with 5000 iu intramuscularly one week before the expected date of parturition.

Although they found no evidence for an effect of the vitamin E supplementation on mammarymacrophages, it significantly enhanced the chemotactic responsiveness of blood neutrophils from twoto four weeks after parturition. Not all studies have observed a significant response of the immunesystem to vitamin E supplementation. Cipriano et al. (1982) found that the oral supplementation with1000 iu of vitamin E of calves fed on skimmed milk had no significant effects on their IgGconcentrations and lymphocyte stimulation indices. The lack of significance may have been becausetoo few animals were used, because the differences they reported were large. Mudron et al. (1994)investigated the effect of vitamin E on leucocyte parameters in transported calves. The oraladministration of 20 iu of vitamin E 24 hours before they were loaded had no significant effect onleucocyte migration and serum immunoglobulin concentration. Plasma cortisol concentration wasreduced for 24 hours after the administration of vitamin E, but this reduction had no effect on thecalves' cortisol response to the stress of transport. The mechanism by which vitamin Esupplementation has immune stimulatory effects is not fully understood. One effect may be the

reduction in corticosteroids observed by Reddy et al. (1987), because glucocorticoids areimmunosuppressive compounds and inhibit lymphocyte proliferation directly. Another effect may bedue to a change in arachidonic acid metabolism.VitaminE supplementation has been shown toreduce the production of prostaglandin F2cx and prostaglandin E2 in chicks (Lawrence et al. 1985).Under conditions of stress, changes in the levels of these compounds can adversely affect thefunction of immune cells, particularly the activity and responsiveness of lymphocytes (Hadden 1987).It is most likely, however, that the protective effect of vitamin E is due to stabilisation of leucocytemembranes. Leucocyte membranes are more vulnerable to peroxidative damage than themembranes of body cells because they contain more free fatty acids (Kigoshi and Ito 1973). On thebasis of serum enzyme levels, Reddy et al. (1987) reported that the cell membranes ofunsupplemented calves were more prone to damage.

4 OXIDATIVE DAMAGE OF ENDOMETRIUM ON ANOESTRUS AND CONCEPTION RATE

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During parturition and after heavy milk yield causes stress to the animal. In stresscondition, normal cell processes, environmental insults, and inflammatory responses producecompounds called reactive oxygen species or free radicals. Environmental insults include solarradiation, heavy milk yield , certainmycotoxins, nitrates, and a host of other toxic compounds. When apathogen invades the uterus or reproductive tract of a cow, a cascade of events occurs. Respiratoryburst occurs and this produces a high concentration of free radicals. Themajor free radicals found in

biological systems are superoxide, hydrogen peroxide, hydroxyl radical, and fatty acidradicals. Hydrogen peroxide is found primarily in the cytosol of cells and fatty acid radicals arefound primarily in cell membranes. Superoxide and hydroxyl radicals can be found in both cellcomponents. Because free radicals are extremely toxic to cells, the body has developed asophisticated antioxidant system (Table 1). Superoxide dismutase (an enzyme that contains copperand zinc) converts superoxide to hydrogen peroxide. Hydrogen peroxide is converted to water bythe enzyme Glutathione peroxidase (GSHpx). Those two enzymes effectively control most freeradicals within the cytosol. Superoxide and the hydroxyl radical can migrate into cell membrane wherethey attack fatty acids (especially unsaturated fatty acids) and produce fatty acid radicals (a processcalled initiation). Fatty acid radicals then react with other fatty acids producing a chain

reaction. Vitamin E and to a lesser extent -carotene reacts with fatty acid radicals and stopsthe chain reaction.

Free radicals are highly reactive compounds because they are missing an electron. Freeradicals can react with nucleic acids causing mutations, they can react with enzymes and render theminactive, and they can react with fatty acids in membranes causing membrane instability. Freeradicals can eventually kill cells and damage tissues.

Figure 1. Systems for protection against reactive oxygen metabolites. (Miller et al., 1993)

1) Superoxide is generated during normal metabolism. 2) Exogenous contributors to oxidative stressinclude dietary imbalances, disease, environmental pollutants, and solar radiation 3) Superoxidereduces Fe3+, enabling it to enter into Fenton-type reactions. which produce hydroxyl radical. 4) Theextremely reactive hydroxyl radical attacks macromolecules and initiates peroxidative chain reactions(22). 5) Cytotoxic aldehydes are end products of lipid peroxidation. 6) When tissues are disrupted,aldehyde dehydrogenases are converted to aldehyde oxidases, which generate superoxids. 7)

Superoxide dismutases (Mn, Cu, and Zn) convert superoxide to peroxides. This conversion retardsreduction of Fe3+ to Fez+, which catalyzes formation of .OH 8) Catalase Q andglutathione

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peroxidase (Se)convert peroxides to compounds that do not participate in Fenton-type reactions .Reduction of peroxides is accompanied by oxidation of reduced glutathione. 9) Reduced glutathionecan be regenerated from glutathione disulfide (GSSG) by reducing equivalents from NADPH, which isgenerated by the pentose monophosphate shunt . 10) Glutathione S-transferases conjugateglutathione with peroxy radicals. This pathway may be more active when it is deficient in Se orvitamin E. The resulting destruction of glutathione increases consumption of reducing equivalents,

thus competing with other metabolic pathways that depended on NADPH. 11) Chain-breakingantioxidants interrupt peroxicative chains initiated by reactive oxygen metabolites that escapedenzymatic degradation. 12) Vitamin Eserves as a chain-breaking antioxidant by reacting directlywithfreeradicals . Although vitamin E is consumed when free radicals are quenched . Reducingequivalents are conserved in comparison with glutathione S-transferases serving as chain breakers.13) Vitamin C, in addition to regenerating vitamin E and possibly also glutathione, can actin its ownri&t as a water-soluble antioxidant. 14) Aldehyde dehydrogenases convert aldehydes to less toxicproducts.

Production of free radicals could represent a source of infertility because ovariansteroidogenic tissue (Carlson et al.,1993; Maas, et al.,1993), spermatozoa (Aitken, 1994) andpreimplantation embryos are sensitive to free radical damage. In some studies, administration of betacarotene (Ascarelli, et al., 1985; Bindas, et al., 1984) or vitamin E and selenium (Arechiga, et al.1994;

Segerson, et al. 1977) improved fertility of cattle.

Harrison et al. (1984) suggested that vitamin E and selenium act at the cellular level byregulating the generation of free radicals in the ovaries. Staats and others (1988) showed that vitaminE protected steroidogenic enzymes from oxidative degeneration, and Rapoport et al. (1998) foundthat the concentration of a-tocopherol in ovarian tissue was related to the animals' consumption ofvitamin E during the period of maximal progesterone production. Other work has suggested that thegeneration of free radicals is a potential cause of abnormal embryonic development (Goto et al.,1992), and Barnes and Smith (1975) suggested that vitamin E promoted the release of folliclestimulating hormone (FSH), adrenocorticotrophic hormone (ACTH) and luteinising hormone (LH).There may also be a role for vitamin E in the protection of the pathway from arachidonic acid toprostaglandins, which are closely involved in the regulation of the reproductive system.

4.1 OXIDATIVE STRESS, ANTIOXIDANTS AND THE PERIPARTURIENT DAIRY COW

The periparturient period is especially important for health of dairy cattle. A survey including551 cows and 1305 lactations (Shanks et al., 1981)revealed that over one-half of total health costsresulting from mammary and reproductive problems occurred during the first 30 DIM. In addition tocost of treatment, udder edema (Dentine.

et al., 1983), retained placenta (Joosten et al., 1988), andmastitis(Smith et al., 1984) can reduce milkproduction, market value, and the productive life of the cow and can cause indirect costs that aredifficult to quantify. Delayed first estrus, delayed first breeding, and repeated breeding resulting fromfailure to conceive or from early embryonic death increase days open and prolong calving intervals.Additional expenses include treatment, repeated breeding, and culling of cows for failure to conceive.

Table 3. Antioxidant functions of vitamin E and of mammalian cells.

Component

(location in cell)

Nutrients Involved Function

Alpha-tocopherol

(membranes)

Vitamin E Breaks fatty acid peroxidation chain

reactions

Glutathione peroxidase

(cytosol)

Selenium An enzyme that converts hydrogen

peroxide to water

5 ROLE OFVITAMINE AND SELENIUM

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5.1 VITAMINE ACT AS ANANTIOXIDANT

Vitamin E is the most important lipid-soluble antioxidant and the biologically most active formis d,a-tocopherol (Putnam and Comben, 1987). Vitamin E is an integral component of all lipidmembranes and serves to protecting lipid membranes from attack by ROS (Rice and Kennedy, 1988).Polyunsaturated fatty acids ( PUFA) of membranes are particularly vulnerable to attack by ROS, and

ROS can initiate a chain reaction of lipid destruction that destroys the membrane of the cell. Vitamin Ecan quench peroxidation reactions in membranes and is probably the most important antioxidantlocated in cell membranes (Putnam and Comben, 1987).

Vitamin E and glutathione peroxidase function at two locations within the cell Glutathione peroxidasefunctions in the cytosol of the cell and vitamin E within lipid membranes. An important function of bothsystems is the protection of membrane PUFA. The PUFA are present in all cellular membranes, buttheir concentration varies considerably from tissue to tissue Membrane PUFA are extremelysusceptible to attack from reactive oxygen species, and the higher the concentration of membranePUFA, the more susceptible the cell and tissue to oxidant damage.

An important PUFA in cellular membranes is arachidonic acid ( AA) . Arachidonic acid can be

metabolized to prostaglandins, thromboxanes, and prostacyclin by the enzyme complexcyclooxygenase and to the leukotrienes by the lipoxygenase enzyme complex. vitamin E may functionto control peroxidation of AA or its unstable metabolites. The AA metabolites are important for PMNfunction and the amplification of the inflammatory response following pathogen invasion of tissuesincluding the uterus, which is more prone for infection.

5.2 SELENIUM ACT AS AN ANTIOXIDANT

Beneficial health effects of selenium supplementation in dairy cows (Rayman, 2000; Malbe et al.,1995). It is generally understood that these benefits are achieved through the action of selenium as acomponent of selenoproteins.

The GSH-Px and thioredoxin reductase groups of selenoproteins catalyze reduction of peroxides that

can damage cells and tissues. Being a part of these proteins, selenium has the capacity to affectoxidative processes in the system and is considered an antioxidant nutrient. These antioxidantsprotect cells from oxidative damage from free radicals and peroxides (Rotruck et al., 1973). Theactivity of these enzymes is directly related to the concentration of selenium in the diet. Furthermore,several studies have demonstrated that oxidative stress of the cow contributes to lowering immunityand increases the risk of retained fetal membranes as well asmastitis(Hemmingway, 1999) whichincreases post partum incidence of anestrous and lower conception rate. Higher activity of GSH-Pxhas also been reported in the erythrocytes of cows receiving supplemental selenium compared withnon-supplemented individuals (Ortman and Pehrson, 1999). Selenium therefore has a positiveantioxidant effect in cattle.

Table 4 Interpretation of selenium analyses in cattle

5.3 ANTI-PATHOGENIC ACTIVITIES OF SELENIUM AND VITAMIN E

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Subclinical uterine infection is major cause of infertility in crossbred cattle and buffaloes in India.Subclinical uterine infection can be reduced or prevented by the increasing animal immune statuseither by vaccination or by increasing general immunity. There is evidence that deficiencies of E andSe can lead to impaired resistance to disease Vitamin E supplementation of diets increasedintracellular kill of S. aureusand E. coliby bovine neutrophils but had no effect on phagocytic index(Hogan et al., 1990). The effects of vitamin E and Se supplementation on intracellular kill of bacteria

by neutrophils were not additive. Supplementation with both vitamin E and Se did not result in greaterintracellular kill of bacteria by neutrophils than did supplementation with either one of the nutrientsalone. However, vitamin E and glutathione peroxidase have sparing effects on the requirements forone another relative to intracellular killing of bacteria. The protection afforded cellular membranes byvitamin E may spare the requirement for glutathione peroxidase by reducing free radicals at themembrane, thereby preventing leakage of free radicals into the cytosol and maintaining intracellularkilling capacity of the cell. Conversely, glutathione peroxidase activity in the cytosol may spare therequirement for vitamin E in the membranes.

Clinical studies have been conducted to evaluate the effect of supplemental vitamin E on prevalenceof retained fetal membranes, intramammary infections, and clinical mastitis. Feeding approximately1000 IU/day of supplemental vitamin E (usually all-rac--tocopheryl acetate) to dry cows whenadequate selenium was supplemented reduced the prevalence of retained fetal membranes in some

(Harrison et al., 1984; Miller et al., 1993). When vitamin E was injected (usually in combination withselenium) rather than fed, about half the time there was no effect for prevalence of retained fetalmembranes and about half the time there was a positive response (Miller et al., 1993).

The typical treatment was a single injection of approximately 700 IU of vitamin E and 50 mg ofselenium given about 3 weeks before calving. Relative to the amount of vitamin E normallyconsumed, 700 IU of vitamin E over 21 days is trivial. Most likely, selenium, not vitamin E, wasthe nutrient responsible for the positive effect.

5.4 ACTION OF VITAMIN E AND SELENIUM ON NEUTROPHIL FUNCTION

Neutrophils are the first line of cellular defense against the aggression of invading pathogens. Thus,

their recruitment to the site of pathogen attack will support defense mechanisms that favor reductionof the incidence of disease. The research on vitamin E and immunity in dairy cows has concentratedon neutrophil function. Vitamin E supplementation has consistently improved neutrophil function indairy cows. The results from the two experiments that used fresh cows are noteworthy. Thenonspecific immune system is depressed during the peripartum period and cows are extremelysusceptible to uterine infections at this time. Both studies found that vitamin E supplementationeliminated the depression in neutrophil function associated with parturition and increases over allimmune status.

Table 5. Research results on the effect of vitamin E supplementation on neutrophil

function in dairy cows.

Type of cow Supplementation Response Ref.

Lactating cow, 30days in milk

1000 IU/day of dietary vitaminE during the dry period and

500 IU/day during the first 30

days of lactation

Phagocytosis notaffected

Ability to kill S.

aureus andE.

coli was improved

Hogan etal., 1990

Fresh cow (

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wk pre to 5 wk

postpartum

from 4 wk pre to 8 wk

postpartum + 3000 IU of

vitamin E injected 1 wk

prepartum

chemotaxis

(movement into

infection site) was

improved

al., 1996

Fresh cows (

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Table 6 Incidence of placental retention in dairy cows fed diets contain s.12 ppm of Se with orwithout 1000 IU of supplemental vitamin E during the last 40 d of gestation.

Table 7 Effect of postpartum administration of vitamin E and selenium on reproductivefunction Of lactating dairy cows. (Arechiga, et al., 1998)

Administration of vitamin E and/or selenium can also enhance neutrophil function (Either et al.1994; Ndiweni and Finch 1996, Politis, et al. 1995; Politis, et al. 1996).Perhaps, increased neutrophilactivity promotes removal of microorganisms and supports uterine tissue remodeling and involution.Prepartum treatment with selenium and vitamin E has been reported to hasten uterine involution incows with metritis (Harrison et al. 1986). It is also possible that vitamin E and selenium affect eventsleading to fertilization since treatment with vitamin E and selenium increased fertilization rate in cattle(Segerson et al., 1981) and sheep (Segerson et al., 1977). This effect was ascribed to increasedsperm transport (Segerson et al., 1980; Segerson et al., 1982) and may reflects actions of seleniumon uterine motility (Segerson et al., 1980). Experiments in ewes indicate that selenium status can also

affect embryonic survival (Hartley, 1963). It is not surprising that a single injection of vitamin E andselenium could cause a positive effect on reproductive function several weeks after the injectionbecause administration of these molecules has long-term effects in cattle. Intramuscular injection ofvitamin E caused elevated amounts in serum for at least 28 d (Charmley, et al. 1992), while injectionof selenium increased concentrations of selenium in whole blood and serum for 28 d and increasedwhole blood-glutathione peroxidase activity for at least 84 d (Maas et al., 1993). Injections of vitaminE and selenium 3 and 1.5 wk before calving increased erythrocyte GSH peroxidase in dairy cowsduring the first 12 wk of lactation (Lacetera, et al., 1996).

Effects of selenium, vitamin E or their combination on fertility have been variable, with somestudies reporting of an increase in fertility (Arechiga et al. 1994; Segerson et al., 1977; Segerson etal., 1981) and some reporting no effect (Stowe et al. 1988).Differences between studies in the amountof vitamin E and/or selenium administered, the period of administration, and nutritional status of the

experimental animals with respect to vitamin E and selenium intake could explain some of thesedifferential results.

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Selenium deficiency adversely affectsreproductionin both sexes and all species includinghumans (MacPherson, 1994). The problem is most extensively described in cattle and sheep; andwhile there have been reports of selenium deficiency as a direct cause of abortion, the relatedproblems of increased disease susceptibility and retained placenta make it difficult to view infertility inthe dam in terms of a single factor (Maas,1998). Selenium supply to particular tissues may also beimportant. Conrad (1985) reported that uterine involution was completed eight days sooner in cows

supplemented with selenium and vitamin E. He also found that increasing whole blood selenium wasassociated with higher selenium in the ovary and that GSHPx activity in follicular fluid correlated withplasma GSH-Px. Significant GSH-Px activity was present in luteal tissue as well.

Figure 2. Effect of selenium supplement form on whole blood selenium content of ewes atlambing and newborn lambs (from Kincaid et al., 1999;

abP#0.001).

Egg production is depressed by selenium deficiency in both chickens and turkeys; howeverthe impact on hatchability is more severe in turkeys (Cantor and Scott, 1974; Cantor, 1997). While therole of selenium status in female fertility is more recognized than understood, recent work hasprovided much clearer insight into the well known association between selenium and male fertilitythrough identification of the membrane-bound phospholipid hydroperoxide GSH-Px in the testes.

6.1 EFFECT OF SUPPLEMENTATION OF VITAMIN E AND SELENIUM ON OVA FERTILIZATION

Fertility of ova was greater (P

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Table 8 Means and standard deviations forreproductionand lactation for the lactation prior toand following selenium-vitamin E treatment. (Gwazdauskas et al., 1979)

6.2Effect of supplementation of Vitamin E and Selenium on malereproductionand conception

rate

Vitamin E deficiencies caused testicular degeneration in chickens, rats, hamsters, rabbits, guineapigs, dogs, cats, pigs, and monkeys and resulted in a lower number of germ cells and a reduction insperm production (cited from the Marin-Guzman et al., 1997). Brzezinska- Slebodzinska et al. (1995)suggested that dietary vitamin E may serve as an antioxidant in boar semen. Jones and Mann (1977)demonstrated that peroxidative structural damage to sperm occurred when unsaturated fatty acidswere present in semen; this resulted in a decline in sperm motility, but the addition of tocopherol tothe ejaculate did not protect the sperm from peroxide damage. Because Se and vitamin E can affecttesticular and(or) spermatozoal development and subsequent sperm motility, the deficiency of either

nutrient may affect different aspects of the male reproductive processes and possibly the fertilizationof oocytes in the female. Diets inadequate in Se and vitamin E fed for prolonged periods will affectthe reproductive efficiency of male animal. Testicular tissue has a high priority for Se retention andutilization compared to liver. When low-Se and vitamin E diets were fed, sperm motility declined andthe percentage of abnormal sperm increased. Boars fed low-Se diets produce a higher percentage ofabnormal sperm, mainly by disrupting tail morphology. Boars with a low Se status had fewer spermreaching and penetrating the zona pellucida, and this could affect ovum fertilization rate. Although adiet low in vitamin E can also reduce the percentage of normal sperm, vitamin E seems important forboars, but it may function in a different manner than Se, perhaps through its antioxidant properties onthe sperm.

In sperm, selenium is largely associated with the keratin-like material in the mitochondrial helix in themidpiece of spermatozoa and was previously referred to as the 'mitochondrial capsule selenoprotein'.

Recently it has been determined that GSH-Px-PH is abundantly expressed in spermatogenic cells,but exists as an enzymatically-inactive structural protein in mature sperm where it contributes toformation of the mitochondrial capsule (Ursini et al., 1999). In spermatozoa, GSH-Px-PH thereforereplaces 'sperm capsule selenoprotein' as the link between selenium and fertility. Morphologicaldefects of sperm in selenium-deficient males can be attributed to inadequate GSH-Px synthesis(Khrle et al., 2000).

7. ACTION OF VITAMIN E AND SELENIUM ON OTHER NON-INFECTIOUS DISEASES

There has been much less work to investigate the effect of vitamin E on other diseases, andmost of it has been peripheral to the main investigation. For instance, Miller and others (1993)demonstrated that supplementing primiparous cows with 1000 iu of vitamin E reduced the incidenceof udder oedema when their diet contained at least 0-12 mg of selenium per kg DM, but not whentheir diet contained less than 0-07 mg of selenium per kg DM. Supplementing cows with vitamin E hasbeen shown to have significant effects on the incidence of disease in some studies, but not in others.

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Some of the studies that have observed no effect have supplied vitamin E in insufficient amounts fortoo short a period, or at inappropriate times. Virtually all of the published results are based on NorthAmerican data. The dairy industry in the USA and Canada is significantly different from that in the UKand most of Europe, and a large scale field study of the effect of vitamin E supplementation isrequired in Europe.

8. OPTIMUM LEVEL OF VITAMIN E REQUIREMENT

The NRC (2001) established requirement for dietary vitamin E is 16 -27 IU/kg DMI fornonlactating and lactating cows depend on lactation, equivalent to consumption of 160 and 900 IU/dfor nonlactating and lactating cows, respectively.

Table 9 NRC and commercial recommendation for Vitamin E intake (IU per day) dairy cow

To maintain these blood values, dry cows and heifers fed stored forages during the last 60days of gestation require approximately 1.6 IU of supplemental vitamin E/kg of body weight(approximately 80 IU/ kg of DMI). An additional benefit on calf health may be observed by increasingvitamin E intake by cows and heifers in late gestation. Only minor amounts of vitamin E can pass theplacenta (Van Saun et al., 1989); hence newborn calves rely on colostrum for vitamin E. Increasedintake of vitamin E during the prepartum period significantly elevates vitamin E in colostrum. Forlactating cows, the recommended amount of vitamin E supplemental) was changed to 0.8 IU/kg ofbody weight (approximately 20 IU/kg of DMI) when stored forages are fed. This recommendation isbased on a reduction in retain placenta and other post partum infection, there by improve over allfertility of the animal. The difference between the recommendations for vitamin E for the two classesof cattle is mainly caused by expected differences in intake of vitamin E from basal feedstuffs andperhaps reduced absorption of vitamin E by cows fed conventional dry cow diets.

Based on typical feed intakes and average vitamin E concentrations in feedstuffs, the recom mendedamount of total vitamin E (supplemental plus vitamin provided by feedstuffs) is approximately 2.6IU/ kg of body weight during late gestation and for lactating dairy cows. Of that amount, the basal dietwill provide on average about 1.8 IU/kg of body weight for lactating cows (ranges from about 0.8 forcows fed diets based on severely weathered hay to about 2.8 IU/kg of body weight for cows fed diets

based on pasture) and about 1 IU/kg body weight (ranges from 0.5 to about 2.3 IU/kg of body weight)for dry cows.

Although several factors are known to influence vitamin E requirements, limited data makequantifying the necessary adjustments difficult. The amount of supplemental vitamin E fed may needto be changed during the following situations:

When fresh forage is fed there should be less need for supplemental vitamin E. A diet basedon fresh forage (ca. 50 percent of dietary DM) would require about 67 percent lesssupplemental vitamin E to meet the cows requirements compared with a diet that contained asimilar amount of stored forage. Requirements for supplemental vitamin E is reduced 67percent in the accompanying software when animals are fed pasture.

The amount of supplemental vitamin E probably should be increased when low forage dietsare fed (forages typically have more vitamin E than do concentrates). The requirements listed

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above were generated from studies using diets with 50 to 60 percent forage (lactating cows)and 60 to 80 percent forage (animals in late gestation).

Cows in suboptimal selenium status probably require more vitamin E.

Milk is not a major excretion route for alpha-tocopherol(0.4 to 0.6 g/ml) but colostrum containshigh concentrations of -tocopherol (3 to 6 g/ml). Additional vitamin Emay be useful duringcolostral genesis.

Intake of polyunsaturated fatty acids increases the vitamin E requirement of nonruminants. Asmethods for protecting fats from biohydrogenation in the rumenimprove, additional vitamin Emay be required when protected unsaturated fats are fed.

Additional vitamin E may be useful during periods of immunosuppression (peripartum period).

Large amounts of supplemental vitamin E (1000IU/day) can reduce oxidative flavors in milk.

12 OPTIMUM LEVEL OF SELENIUM REQUIREMENT

In selenium-deficient locales, dietary intakes of .3 mg of selenium/kg of dry matter are necessary tohave some degree of confidence that serum selenium concentrations will be adequate in dairy cattle.A reduction of the legal supplementation allowance to . 1 mg of supplemental selenium/kg of drymatter would have serious negative consequences. Reducing the allowable selenium

supplementation level would result in many herds being inadequately supplemented in seleniumdeficient areas and presumably many more instances of clinical and subclinical selenium deficiency.Productivity losses would be significant in the national dairy herd, much of which is located inselenium-deficient areas.

The level of selenium supplementation in dairy cow diets varies from country to country and is mainlydetermined by the selenium content of feedstuffs, as influenced by soil selenium status. In Canadaand the United States, both organic and inorganic sources of selenium can be supplemented at 0.3mg/kg of DM. In the European Union, inorganic selenium is fed to cows at a recommended level of0.5 mg/kg of DM (Ministry of Agriculture, Fisheries and Food, 2000) and was initially the onlyauthorized form of selenium.

Since selenium was originally known to be toxic, it is imperative that care be taken not to reach toxic

levels during supplementation. Rate of supplementation in most trials does not consider the seleniumconcentration in the other feed ingredients, implying that the final selenium intakes of animals isusually more than current recommended levels. However, little data exist to suggest toxic effects evenwhen selenium was included at levels as high as 50 mg/d for 90 days or 100 mg/day for 28 days indiets of Holstein cows (Ellis et al., 1997).

Givens at al. (2004), as in most studies, observed increasing advantage of selenium inclusion levelson milk selenium concentration with the best results at a rate of 1.14 mg Se/kg as selenium yeast.These results demonstrate that current recommended levels of inclusion should be revisited in orderto set the limits for favorable performance and to avoid toxicity. Since blood selenium concentration isa fairly good variable to measure individual or herd selenium status, Hogan et al. (1993)recommended its use in establishing selenium status. Their recommendation follows that bloodselenium concentration should be at least 0.2 g/ mL, but should not exceed 1 g/mL.

On the other hand, Braun et al. (1991) considered blood selenium levels of 0.08 to 0.3 g/mL asnormal and 0.03 to 0.07 g/mL as inadequate for cattle. To ensure that herd selenium intakes arewithin safe limits, it is imperative that intakes should not exceed the toxic threshold of seleniumsupplementation for dairy cows. Stating the selenium concentration on feed tags and routinelymeasuring concentration level in forages, hay and other feed materials may be one way of ensuringsafe and favorable levels of inclusion and intakes.

10 OTHER UNEXPLORED EFFECTS OF SELENIUM IN DAIRY CATTLE

A further area where selenium seems to play a role, but not yet examined in dairy cattle, is inapoptosis. The ultimate goal of a cell is to perform its function to the best of its ability in the

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maintenance of tissue homeostasis. Apoptosis is the process of deliberate life relinquishment by a cellin an organism. It is also commonly referred to as 'cell suicide.'

In humans, an insufficient amount of apoptosis leads to uncontrolled cell proliferation, such as cancerwhereas excessive apoptosis causes cell loss diseases such as ischemic damage (shortage of bloodsupply to an organism). Data in 1996 indicated that dietary supplementation of 200 g of selenium in

diets resulted in a decreased incidence of human prostate, lung and colorectal cancers (Clark et al.,1996).

The precise role of selenium in modulating cancers is much debated. Some authors are of the opinionthat small molecules of selenium metabolites selectively promote apoptosis in transformed prostateepithelium (Jiang et al., 2004; Ip et al., 2000) while others believe that selenium supplementationprevents DNA damage that could lead to cell transformation by increasing levels of antioxidantselenoproteins (Diwadkar- Navsariwala and Diamond, 2004; Lu and Jiang, 2005).

A recent study with transgenic mouse models showed that selenoprotein deficient mice exhibitedaccelerated development of lesions associated with prostate cancer progression thus suggesting thatselenium may function in cancer prevention by modulating the levels of selenoproteins (Diwadkar-

Navsariwala et al., 2006). Another finding demonstrates that selenoprotein expression and seleniummetabolism are regulated at multiple levels in prostate cells (Rebsch et al., 2006).

Selenium may therefore play a positive role in mediating useful apoptosis necessary for normalfunctioning of cells. Selenium's role in this regard, is however, yet to be established in cattle.

11.CONCLUSION

The periparturient and early lactation periods are critical for the health of dairy cows. Udderedema, milk fever, retained placenta, mastitis, anoestrus and suboptimal reproduction reduce profitsfor dairyproducers. Oxidative stress may contribute to all of these disorders. Antioxidantrequirements of high producing dairy cows may be higher than generally recognized, and intakes ofantioxidants needed to control ROM balance effectively may exceed amounts supplied by average

feeds. For this reason, supplementation with all known nutrients required for antioxidant defense inadequate and balanced amounts would be beneficial. The primary effect of vitamin E supplementationappears to involve the activity and effectiveness of the immune system. Some studies have observedan effect on the lymphocyte system, others have observed an increase in the activity of neutrophils. Inseveral studies there has been a reduction in the incidence of retained fetal membranes after vitaminE supplementation. There is some evidence for a reduction in cystic ovarian disease and metritis.

In the studies in which vitamin E supplementationhad a beneficial effect on fertility, thevitamin E intake of the cows during the dry period has been increased to about 3000 iu per cow perday. Recent research shows that vitamin E and selenium had beneficial effect on reducing theincidence of anestrous, reduces number of services per conception, reduces calvinginterval, increases conception rateand over all fertility of the cattle.

However, more experimentis needed to study on reproductive disorder with supplementalvitamin E and Selenium for treatmentand for further reproductive performance of the animal andto identify optimal amountsof each nutrient Vitamin E and selenium supplementation onthe healthand some aspects of the fertilityof lactating dairy cows. These effects have beenobserved not only in cows which are deficient in vitamin E or selenium, but also in studies in whichsupplemented animals were compared with control cows fed diets containing up to three times thecurrent recommendations for vitamin E intake.

"One calf per annum is dream of farmer

For this, I should come estrus proper"

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"Feed me antioxidant to protect my endometrium

Vitamin E and Se can be given optimum"

"This will increase the conception rate

This quote for my interest"

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