Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

Arsenic and human health effects: A review.

Oxidative stress contributes to the pathophysiology of exposure to heavy metals/metalloid. Beneficial renal effects of some medications, such as chelation therapy depend at least partially on the ability to alleviate oxidative stress. The administration of various natural or synthetic antioxidants has been shown to be of benefit in the prevention and attenuation of metal induced biochemical alterations. These include vitamins, N-acetylcysteine, α-lipoic acid, melatonin, dietary flavonoids and many others. Human studies are limited in this regard. Under certain conditions, surprisingly, the antioxidant supplements may exhibit pro-oxidant properties and even worsen metal induced toxic damage. To date, the evidence is insufficient to recommend antioxidant supplements in subject with exposure to metals. Prospective, controlled clinical trials on safety and effectiveness of different therapeutic antioxidant strategies either individually or in combination with chelating agent are indispensable. The present review focuses on structural, chemical and biological aspects of antioxidants particularly related to their chelating properties.

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Structural, chemical and biological aspects of antioxidants for strategies against metal and metalloid exposure.

Age-related changes in glutathione and glutathione-related enzymes in rat brain

In vivo protective effects of quercetin against sodium fluoride-induced oxidative stress in the hepatic tissue

Emerging role of Centella asiatica in improving age-related neurological antioxidant status

The purpose of this study was to examine the effects of dl-α-lipoic acid (LA) on arsenic (As) induced alteration of glutathione (GSH) level and of the activity of glutathione-related enzymes—glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH)—in rat brain regions (cortex, hypothalamus, striatum, cerebellum and hippocampus). Male Wistar rats of 150±10 g weight were divided into four groups: control and three experimental groups supplemented with arsenic (sodium arsenite) alone (100 ppm mixed in drinking water), lipoic acid alone (70 mg kg−1 body weight), arsenic plus lipoic acid (100 ppm arsenic in drinking water plus 70 mg lipoic acid kg−1 body weight). The arsenic content of brain regions was found to increase with the administration of sodium arsenite. Arsenic exposure elicited a significant decline in glutathione content and in the activity of related enzymes, with the greatest decreases seen in the cortex, striatum, and hippocampus, whereas there were no significant differences between control rats and the group treated with lipoic acid alone. Highly elevated content of the thiobarbituric acid-reactive substance malondialdehyde (MDA) in the brain regions of arsenic-exposed rats reflected extensive lipid peroxidation (LPO) processes. Simultaneous lipoic acid treatment was effective in reducing brain regional arsenic levels and lipid peroxidation and in increasing the glutathione content and the activity of its related enzymes. Lipoic acid, by acting as an alternative sulfhydryl nucleophile to glutathione, prevents its oxidation to glutathione disulfide in detoxifying reactions against reactive oxygen species and consequently increases the activity of glutathione-related enzymes.

Arsenic intoxication-induced reduction of glutathione level and of the activity of related enzymes in rat brain regions: reversal by dl-α-lipoic acid

Combined efficacies of dl-α-lipoic acid and meso 2,3 dimercaptosuccinic acid against arsenic induced toxicity in antioxidant systems of rats

Mitochondria link the energy -- releasing activities of electron transport and proton pumping with the energy conserving process of oxidative phosphorylation to form ATP. A declined mitochondrial performance has been generally observed during aging. In the present investigation, the activities of tricarboxylic acid cycle enzymes such as isocitrate, alpha-ketoglutarate, succinate and malate dehydrogenases and electron transport complexes I-IV were measured in mitochondria isolated from brain regions like cortex, striatum and hippocampus of young and aged rats before and after L-Carnitine supplementation. All the three brain regions of aged rats showed decreased activities of isocitrate, alpha-ketoglutarate and succinate dehydrogenases, complexes I and IV when compared to control young rats. Striatum seems to be the most susceptible region when compared to hippocampus and cortex. L-Carnitine supplementation to aged rats reversed the activities of these enzymes to near normal whereas treatment to young rats did not show any significant alterations. These results confirm that L-Carnitine can alleviate the age-associated decline in the metabolic efficiency of mitochondria in all three brain regions under investigation.

Muthuswamy Anusuya Devi

Papers

Emerging role of Centella asiatica in improving age-related neurological antioxidant status

Arsenic intoxication-induced reduction of glutathione level and of the activity of related enzymes in rat brain regions: reversal by dl-α-lipoic acid

Combined efficacies of dl-α-lipoic acid and meso 2,3 dimercaptosuccinic acid against arsenic induced toxicity in antioxidant systems of rats

Age-dependent alterations in mitochondrial enzymes in cortex, striatum and hippocampus of rat brain -- potential role of L-Carnitine.