DATS protects cardiac mitochondrial oxidative stress

What is it about?

DATS reduced the extent of mitochondrial damage and improved the mitochondrial structure and function in As-intoxicated rats. This findings strengthened the cardio-protective nature of DATS. We suggest that the possible mechanism for the observed effects of DATS could be due to its quenching of free radicals, lowering of lipid peroxides, lipids and improving the antioxidantenzyme activities, Ca2+ and ATP and thereby improves the cardiac mitochondrial function in As intoxicated rats.

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Why is it important?

Heart is the major target organ in arsenic toxicity and carcinogenesis. Arsenic toxicity involves oxidative damage that plays a vital role for biochemical alteration. A particular target in the cell is the mitochondria, which accumulates arsenic. As to the mechanism of toxicity, inorganic arsenic has been shown to cause impaired tissue respiration in vivo. It inhibits enzyme activity by reacting with the sulfhydryl groups of proteins. In particular, suppression of nicotinamide adenine dinucleotide-linked substrates (pyruvate, glutamate, and a-ketoglutarate) appears to play a crucial part in the toxicity of As. Pentavalent and trivalent forms of arsenic exert similar effects in the inhibition of mitochondrial respiration and uncoupling of mitochondrial oxidative phosphorylation. The mechanism of this inhibition is not clear: one possibility is that arsenate is reduced by the mitochondria to As (III) and that inhibition occurs through the formation of a complex with the lipoic acid cofactor that is necessary for oxidation of the substrate. The current study has proved that the supplementation of DATS reduced the oxidative mitochondrial toxicity of arsenic and thereby plays a significant protective role against arsenic-induced cardiotoxicity

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