Relationship of ascorbic acid, uric acid, lipid peroxidation and burn size in thermal injury.

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VOL.CPfiIX,No.5

ContentsORIGINAL ARTICLES

Relationship of Ascorbic Acid, Uric Acid, LipidPeroxidation and Burn Size in Thermal Injury

V. R. Bhagwat K. N. PujariM. Subrahmanyam

Oxidant and Antioxidants in Bronchial Asthma

170

t74

Vidyagauri BaligaAnish Desai

Cytodiagnosis of Bronchopulmonary Lesions- A Hospital-based Study

Dushyant Singh Gaur Sandhya KohliLevel of Serum Iron and Serum TIBC in the TubercularCases under Anti{ubercular Drug Treatment withZinc SupplementationD. K. Chattopadhyay D. NagC. R. Maity

COMPARATTVE EVALUATIONComparative Evaluation of Conventional Syringe vs. PenDevice for Self Administration of Follitropin-p Solution

- A Survey Amongst NursesV. B. Sovani

COMPARATTVE STIJDYComparative Assessment of Efficacy, Safety andTolerability of Rosuvastatin and Atorvastatin inAdult Patients with Diabetic Dyslipidemia -The First lndian Study

V. P. Patil

A. S. KhanJ. K. Salve

rn

178

185

217

?30

196

203Post Marketing Surryeillance Study of Esomeprazolein Indian Population

Sumedh Gailovad Girish D. BakhshiP. Pandhi Suresh JainP. C. Negi Dimple ChopraAkramNaikwadi Suhas KhandaveV. H. Kumaraswamy Vinita MoryeSudhir Pawar

Evaluation of a Fixed Dose Combination of DiclofenacSodium & Acetaminophen Injection (Rhumacort Inj.)in Post-surgical Pain

Deepak LangadeGirish BakhshiA. S. Chandanwale

2n

REVIEWSAcute Rheumatic Fever- Indian PerspectiveAsif Hasan H. S. KhanAlvira Shah

Infectious Complications of BCG ImmunotherapyAmal Kumar Bhattacharya

CASE REPORTSE.Coli in Throat Swab of a Patient with Stomatitis

- A Case ReportS. H. Tenpe R. M. PowarV. J. Katkar

Pneumonitis - Atypical Presentation ofMetastatic Chorioca rcinoma

Smiti Nanda Umber AgarwalSangeeta Priyadarshini Nanda Iftishna Sangwan

Metastatic Olfactory Neu roblastom a -A RarityBharat R. Sonwane Sheela L. GaihvadBhaskar M. Sabale

2l

26

Indian Medical Gazette - MAY 200s t70

Relationship of Ascorbic Acid, Uric Acid, LipidPeroxidation and Burn Si2e in Thermal Iniury

V. R. Bhagwtt, Associate Professor & Head, Department of Biochemistry,

Government Medical College, Miraj - 416 410.

M. Subrahmanyam, Professor & Heod, Department of Surgery,

Government Medical College & General Hospital, Sangli - 416 416.

K. N. Pujari, PG. Student, Department of Biochemistry,

Government Medical College, Miraj - 416 410.

Abstract

Thermal injury is a severe form of trauffi&, which notonly destroys the cutaneous barrier but also leads to varioussystemic changes. A prospective study was carried out in53 hospitalized burn patients. Serum level of TBARS, uricacid and ascorbic acid were estimated in the patients alongwith 25 normal healthy controls. The values were analyzedalong with estimates of burn size (% TBSA). There was agood correlation of TBARS (r = 0.629) and uric acid (r :0.724) with the burn size while a poor correlation of ascorbicacid (r : -0.519) with the burn size was observed. These

changes in serum TBARS and uric acid are a reflection ofincreased free radical activity in thermal injury.

Keywords

Ascorbic acid, Burn size, Lipid peroxidation, Thermalinjury, Uric acid

Introduction

Burns is the term most often given to supra-physi o logi cal tem perature effects caused by localizedh eati n g

of tissue. Destruction of skin by heat results in severe localand systemic physiological alterationSr. It is related todamage of proteins and grossly visible changes in the skin.Patients suffer cutaneous exudative losses of fluidcontaining large quantities of proteins, minerals and

micronutrients, which cause acute deficiency states.

Cytological damage occurs as proteins are denatured bysupraphysiological ternperature. There are both immediate

and delayed vascular and cellular inflammatory response at

the injury siter.

Various metabolic and biochemical alterations followthermal injury. These include degradation of adenosine

tri ph o sphate2, s i gni fi cant reducti on i n polyunsaturatd frttyacids in the red cell membrane3, increased free radicalactivit/, and fall in the level of vitamin A and vitamin Crr-These changes are associated with formation of lipidperoxidation product such as malondialdehyde (MDA) as a

consequence of the burn injury and decrease in natural and

endogenous antioxidants.

The present paper reports relationship of lipidperoxidation with non-enzymatic antioxidants such as

ascorbic acid (AA) and uric acid (UA) and severity ofburninjury.

Material and Methods

The study was undertaken in 53 patients with burn injuryadmitted in Burn Ward at General Hospital, Sangli.?S normal

healthy subjects, age and sex matched with patien6, were

included as controls.

The patients were divided into three groups on the basis

Address for correspondence : Dr. V. R. Bhagwat, StaffQrts Type IV, Bldg # 5, Block # 4, Government Medical College, Miraj - 416 410-

L7t

of Vo Total surface ilrea (TBSA) affected by burn injury(burn size). Group I included 30 patients with minor burninjury G25% TBSA), Group II included 18 patients withmoderate burn injury Q6 - 50 Vo TBSA) while last group(m) included 5 patients with severe burn injury (>50Vo

TBSA).

Random blood samples from the patients were collectedimmediately on admission in plain bulbs, and serum was

separated without delay. Lipid peroxidation product MDAwas measured as thiobarbituric acid reactive substances(TBARS) in serum by colorimetric method6, serum AA and

UA were estimated by the colorimetric methodsT. Statisticalanalysis included "t" test and coefficient of correlation.

Results

The results of the biochemical analysis are shown inTable 1. Mean levels of TBARS were significantly elevated(p<0.001) in the patients as compared to the controls.Similarly serum UA levels were also significantly higher (p

<0.001) in all the patients compared to the controls. SerumAA levels were low in the patients, however it was

statistically non significant.

On careful observation of mean values of thebiochemical pilzrmeters, it is seen that there is an increasing

ffend in TBARS and UA values with degree of severity oftherural injury, while AA levels decreased with increasingthe degree of severity of thermal injury. Statistically serumTBARS (r =0.629) and UA (r = 0.734) were directly related

to burn size (Figs. 1 & 2), whereas AA was inverselyrelated (r = -0.519) with burn size (Fig. 3).

Discussion

Thermal injury is associated with the increased activityof free radicals. There is experimental evidence

Indian Medical Gazette - MAY 2005

documenting involvement of superoxide radicals in the

pathogenesis of burn shocks. Increased levels of lipidperoxidation product have been observed in sera of rats

after burn injurye.

MDA measured as TBARS, is a standard index of free

radical mediated lipid peroxidationro. The source of free

radical at the site of thermal injury could be diverse due to

xanthine oxidase activation by tissue ischaemia or it may

be due to compliment the activated neuffophilstl. The tissue

ischaemia gives rise to generation of free radicals, which

cause endothelial damage with increased capillary

Fig. L

Scatter Diagram for Serum TBARS and Estimates ofBurn Size (% TBSA)

C orrelation B etw e en Vo TB S A & TB A RS

E

oEE

q)&EFEl-.o)

C')

r0

9

8

7

6

5

4

3

)

I

0

r = 0 .629141y=0.0435x+4.7588

n"r"I:X[ t'r, o,r.n patients and controts

Groups n % TBSA TBARS(nmol / mI)

UA(mg Vo)

AA(mg 7o)

I 30 L6.9 t 6.3 5.7 + 1.8 6.5 + 2.8 1.05 + 0.13

II 18 42.8 + 6.2 6.3 + 0.7 7.6t1.5 0.99 + 0.1 1

m 5 75.3 + 3.4 8.2 t t.2 '7 .7 + 0.5 0.85 + 0.2,4

NC 25 2.2 + 0.3 4.1 + 1.3 1.20 t 0.40

The values are Mean t SD. P<0.001 cf controls (NC) in all groups except for AA

Fig. 2Scatter Diagram for Serum Uric Acid and Estimates of

Burn Size (% TBSA)

Correlation Between Vo TBSA & Serum Uric Acid

l0

s:38

=()(-)

DEA='q)

ct)

r = 0.733777

I = 0.047x + 5.6204

Indian Medical Gazette - MAY 200s 172

permeability, edema and tissue damage. The local production

of free radicals causes lipid peroxidation. Thus lipidperoxidation plays an important role in the mechanism ofwound response and development of burn syndromer2.

Burn injury leads to release of pro-inflammatorycytokines such as tumour necrosis factorr3. Thesecytokines cause activation of neutrophils leading toincreased superoxide generation, which is responsible forthe oxidative damage to tissuesra. The present results ofsignificantly elevated serum TBARS is a reflection ofdominant free radical activity in thermal injury.

Serum UA levels were higher in burn patients and a

positive correlation (r = 0.734) with Vo TBSA (burn size)

was observed. This could be due to increased activity ofxanthine oxide at tissue level. The pathogenesis of burnedema in the skin of rats is reported as related to increased

activity of histamine, xanthine oxidase and oxygen free

radicals. Histamine and its metabolic derivatives increase

the catalytic activity of xanthine oxidase in plasma and inrats the pulmonary artery endothelial cellsrs.

Thermal injury results in increased breakdown of ATPwith the eventual conversion to hypoxanthine and xanthine2.

These purines would then be converted to uric acid byxanthine oxidase. It is possible that the observed elevated

serum UA could result by above mechanism.

Serum AA levels decreased in patients compared to the

controls. However, this decrease was statistically non-significant. The lower ascorbic acid in the burn patients

could be due to the stress induced by thermal injury.Marginal decrease seen in the patients could be due to results

of thermal injury itself, where tissue as well as bloodascorbic acid is consumed to counteract dominant freeradical activity or it may be due to low ascorbic acid status

of the patients before receiving thermal injury.

Alterations in micronutrients metabolism such as

ascorbic acid may lead to deficient healing of the burnwound. Earlier it was established that acute, significantdepressions in plasma ascorbic acid occurs after severe

burn injuryr6.

The implications of the present results suggest that inthermal injury there is dominant free radical activity whichis the underlined biochemical pathology responsible forvarious cytological and clinical observations. Therapeutic

Fig. 3Scatter Diagram for Serum Ascorbic Acid and Estimates of

Burn Size (% TBSA)

Correlation Between Ascorbic Acid & Vo TBSA

Ba@tl-

q)

cl,.ol-.o()rt)

l-.o)(t)

1.8

r.6

t.4

t.2

I

0.8

0.6

0.4

0.2

0

r = - 0.51865y=-0.003x+1.0714

o3oo

@

173

use of antioxidants such as ascorbic acid, tocopherol maygive the desired benefits to patients for faster and betterrecovery.

References

l. Robson M.C. & Burns B.F. - Treatment of burnvictim. In, Essential Surgical Practice. Cuschieri A.,Giles G.A. & Moosa A.R., 3rd edn. J'ohn Wright Ltd.,England. 555 -57 L, 1995.

2. Woolliscroft J.U., Prasad J.K., Thompson P., TillD.O., Fox I.H. - Metabolic alterations in burnedpatients: Detection of adenosine triphosphatedegradation products and lipid peroxides. Burns.16 :

- 92-96, 1980.

3. Helmkamp G.R. et al - Essential fatty acid deficiencyin red cells after thermal injury: correlation withintravenous fat therapy. Am. J. Clin. Nutn 26 : 1331-

1336, 1973.

4. Nagane N.S., Bhagwat V.R., Subramanium M.Increased free radical activity in burns. Ind. J. Med.Sci. 57 : 7 -l l, 2003.

5. Rai K., Courtemanche A.D. - Vitamin A assay inburned patients. J. Trauma. 15 : 419-424, 197 5.

6. Satoh K. Estimation of lipid peroxide bythiobarbituric acid reactive substances (TBARS). C/in.

Chin. Acta.90 : 37-41, 1978.

7 . Varley H., Gowenlock A.H. and Bell N. - Practicalclinical Biochemistry, Vol 1, 5th edn, WilliamHeinemann Medical Books London. 254 & 946,1981.

Indian Medical Gazette MAY 2005

Saez I.C., Ward P.H., Gunter B ., €t al - Superoxide

radical involvement in the pathogenesis of burn shock.

Cir. Shock. 12 : 229-239, 1984.

Nishigoki f., Hagihora M., Hiramastu M., et al -Effect of thermal injury of lipid peroxide levels of rat.

Biochem. Med. 24 : 185-189, 1980.

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t214, 1997.

Kumar R., Seth R.K., Sekhon M.S. & Bhargava J.S.

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Cetinkale U. , et al - Evalution of lipid peroxidation

and total antioxidant status in plasma of rats followingthermal injury. Burns.23 : ll4-1 16, 1997.

Nayers I., Johnson D. The non-specificinflammatory response to injury. Can. J. Anaeath.

45(9) : 871-879, 1998.

Sayeed M., Neutrophils signaling alteration an

adverse inflammatory response after burn shock.

Medicina (B Aires).58(4) : 386-892, 1998.

Hans P.F., Gerd O.T. et al - Xanthine oxidase and

histamine. Am. J. PathoL L3S : 203-215, 1989.

Levenson S.M., Upjohn H.L., Preston J.A. et al -Effect of thermal burns on wound healing. Ann. Surg.

146 : 37 5, 1957 .

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