Ascorbic acid protects male rat brain from oral potassium dichromate-induced oxdative DNA damage and apoptotic changes: the expression patterns of caspase-3, P 53, Bax, and Bcl-2 genes

Abstract

Our study designed to study the potential of potassium dichromate (K₂Cr₂O₇) oral exposure to induce damage in male rat brain and to compare the possible protective role of vitamin C (VC) either pre and/or concurrent supply against (K₂Cr₂O₇) induced changes. Thirty male rats were divided into five groups. First control group received distilled water (C), second received 120 mg/kg b.wt (VC), third received 25 mg/kg b.wt K₂Cr₂O₇ (Cr), fourth group received VC together with K₂Cr₂O₇ by the same former doses (VC + Cr), and the fifth group received the same oral doses of VC 2 weeks prior to and along with K₂Cr₂O₇ for 6 weeks (VC + Cr pro/co treated). The obtained results revealed that K₂Cr₂O₇ induced a significant decrease in cholinergic activity, glutathione reductase GR activity, reduced glutathione content GSH and ATP levels. Furthermore, K₂Cr₂O₇ induced a significant increase in oxidative DNA damage indicated by 8-hydroxy 2′-deoxyguanosine (8OH2′dG) and formation of apoptotic DNA ladders, significant increase in malondialdehyde (MDA), protein carbonyl, and lactate dehydrogenase enzyme. Increased mRNA expression of pro-apoptotic genes, including caspase-3, p53, and Bax, unlike Bcl-2 expression, was decreased. K₂Cr₂O₇ increased caspase-3 and decreased Bcl-2 immuno-labeling. VC supply noticeably ameliorates K₂Cr₂O₇-induced changes which were more significantly in VC pro and concurrent supplement rather than VC concurrent supply only. Finally, it is concluded that K₂Cr₂O₇ oral administration induced oxidative apoptotic changes in rat brain and confirms the usefulness of VC pre and concurrent supply for the amelioration of K₂Cr₂O₇-induced events more significantly than VC concurrent supply only.

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