A comparative evaluation of thiobarbituric acid methods for the determination of malondialdehyde in biological materials

Draper, H. H.; Squires, E. J.; Mahmoodi, H.; Wu, Juyou; Agarwal, Sanjiv; Hadley, M.

doi:10.1016/0891-5849(93)90035-s

Cited by 776 publications

(359 citation statements)

References 23 publications

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“…Thiobarbituric acid reacting substances (TBARS) was measured by methods described earlier (Khaled, 1994). The predominant end product of all lipidperoxidation activity is malondialdehyde (MDA), which reacts with thiobarbituric acid (TBA) by giving a pink colour detectable spectrophotometrically between 532 and 535 nM (Draper et al, 1993). MDA and similar products react with TBA, giving a complex of TBA reacting substances (TBARS).…”

Section: Laboratory Studiesmentioning

confidence: 99%

Antioxidant vitamins E and C as adjunct therapy of severe acute lower-respiratory infection in infants and young children: a randomized controlled trial

Mahalanabis

Başak²,

Paul³

et al. 2006

Eur J Clin Nutr

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Objective: To evaluate the effect of antioxidant Vitamins E and C as adjunct therapy of severe acute lower respiratory infection (ALRI) in children. Design: Randomized double-blind placebo-controlled clinical trial. Setting: A large childrens' hospital serving the urban poor in Kolkata, India. Subjects: Children aged 2-35 months admitted with severe ALRI. Intervention: In total, 174 children were randomly assigned to receive a-tocopherol 200 mg and ascorbic acid 100 mg twice daily or placebo for 5 days. All children received standard treatment for severe ALRI. Outcome measures were: time taken to recover from a very ill status, fever, tachypnoea, and feeding difficulty; and improvement in oxidative stress and immune response indicated by thiobarbituric acid reacting substances (TBARS) and response to skin antigens, respectively. Results: Recovery rate ratios (95% CI) using proportional hazards model were 0.89 (0.64-1.25), 1.01 (0.72-1.41), 0.86 (0.57-1.29), and 1.12 (0.77-1.64) for very ill status, feeding difficulty, fever, and tachypnoea, respectively. TBARS values were high and similar in the two groups at admission, discharge, and at 2 weeks follow-up. Serum a-tocopherol significantly increased in treated group at discharge. Immune response to skin antigens were very poor at admission and after 2 weeks, in both groups. Conclusion: Infants with severe ALRI failed to benefit from two antioxidant nutrients as adjunct therapy. Severe ALRI in infants may cause cell-mediated immune dysfunction. We need a better understanding of oxidative processes in growing infants to help us better design interventions with antioxidant therapy.

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Section: Laboratory Studiesmentioning

confidence: 99%

Antioxidant vitamins E and C as adjunct therapy of severe acute lower-respiratory infection in infants and young children: a randomized controlled trial

Mahalanabis

Başak²,

Paul³

et al. 2006

Eur J Clin Nutr

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“…MDA Determination: The samples were analyzed according to the Draper method (Draper et al 1993) with the following modifications: Tissue samples were homogenized in serine-borate buffer; 0.250 ml of homogenate was added to 0.650 ml of 5% trichloroacetic acid and 0.100 ml of 500 ppm butylated hydroxytoluene in methanol. The sample was heated in a boiling water bath for 30 min, followed by cooling on ice and centrifugation.…”

Section: Animal Studiesmentioning

confidence: 99%

Antioxidant Effect of Taurine Against Lead-Induced Oxidative Stress

Gürer

Özgüneş

Saygın

et al. 2001

Arch. Environ. Contam. Toxicol.

139

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Abstract. Oxidative stress is proposed as a molecular mechanism in lead toxicity, which suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate whether taurine has a beneficial effect both on Chinese hamster ovary (CHO) cells and on Fisher 344 (F344) rats following lead exposure. Therefore, oxidative stress parameters (glutathione, malondialdehyde levels, catalase, and glucose-6-phosphate dehydrogenase [G6PD] activities) of lead-exposed CHO cells and F344 rats were determined following taurine treatment. Taurine was found to be effective in (1) increasing glutathione levels that had been diminished by lead; (2) reducing malondialdehyde levels, an end-product of lipid peroxidation; (3) decreasing catalase and erythrocyte G6PD activity, which had been increased by lead exposure; and (4) improving cell survival of CHO cells. However, taurine had no effect on blood and tissue lead levels when 1.1 g/kg/day taurine was administered to F344 rats for 7 days, following 5 weeks of lead exposure (2,000 ppm lead acetate). As a result, taurine seems to be capable of fortifying cells against lead-induced oxidative attack without decreasing lead levels. Therefore, administration of taurine, accompanied by a chelating agent, might increase its effectiveness in the treatment of lead poisoning.

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“…MDA levels were determined as described by Draper et al (1993) and Esterbauer et al (1991). The GSH numerical values for the different experiments varied due to GSH fluctuations.…”

Section: Gsh and Mda Determinationmentioning

confidence: 99%

Comparison of Pure Nicotine- and Smokeless Tobacco Extract-Induced Toxicities and Oxidative Stress

Yıldız

Liu

Erçal

et al. 1999

Archives of Environmental Contamination and Toxicology

111

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Abstract. The toxicities and oxidative stress-inducing actions of (Ϫ)-nicotine and smokeless tobacco extract (STE), containing equivalent amounts of nicotine, were studied. Toxicities were determined by colony formation assays using Chinese hamster ovary (CHO) cells. Results indicated that nicotine is less toxic than smokeless tobacco extract that contained the same amount of nicotine. The generation of reactive oxygen species, following treatment with smokeless tobacco extract and nicotine, was assessed by measurement of changes in glutathione (GSH) and malondialdehyde (MDA) levels. CHO cells (5 ϫ 10 5 cells/5 ml media) were incubated with 4, 0.8, and 0.08 mg of nicotine and STE containing the same amounts of nicotine. All preparations of smokeless tobacco extract significantly decreased GSH levels and increased MDA generation. However, 0.08 mg of nicotine treatment did not result in a significant change in GSH level, and only 4 mg of nicotine were sufficient to increase MDA generation. Addition of free radical scavenging enzymes, superoxide dismutase (SOD) and catalase (CAT), and an intracellular GSH precursor, N-acetyl-L-cysteine (NAC), replenished the GSH levels in nicotine-treated cells. GSH levels in cells exposed to smokeless tobacco extract containing 4 and 0.8 mg nicotine remained significantly lower than the control with the addition of SOD and CAT. However, co-addition of NAC with smokeless tobacco extract preparations returned the GSH levels to the control level. Lactate dehydrogenase (LDH) activities were measured in the media to establish the membrane damage following exposure to smokeless tobacco extract and nicotine. Treatment of cells with 4 mg nicotine caused a significant increase in LDH activity, which was returned to control level in the presence of the antioxidant enzymes and NAC. Smokeless tobacco extract did not change the LDH activity.

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A comparative evaluation of thiobarbituric acid methods for the determination of malondialdehyde in biological materials

Cited by 776 publications

References 23 publications

Antioxidant vitamins E and C as adjunct therapy of severe acute lower-respiratory infection in infants and young children: a randomized controlled trial

Antioxidant vitamins E and C as adjunct therapy of severe acute lower-respiratory infection in infants and young children: a randomized controlled trial

Antioxidant Effect of Taurine Against Lead-Induced Oxidative Stress

Comparison of Pure Nicotine- and Smokeless Tobacco Extract-Induced Toxicities and Oxidative Stress

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