THERAPEUTIC SUBSTANCES

Our study designed to study the potential of potassium dichromate (KCrO) 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 (KCrO) 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 KCrO(Cr), fourth group received VC together with KCrOby the same former doses (VC + Cr), and the fifth group received the same oral doses of VC 2 weeks prior to and along with KCrOfor 6 weeks (VC + Cr pro/co treated). The obtained results revealed that KCrOinduced a significant decrease in cholinergic activity, glutathione reductase GR activity, reduced glutathione content GSH and ATP levels. Furthermore, KCrOinduced 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. KCrOincreased caspase-3 and decreased Bcl-2 immuno-labeling. VC supply noticeably ameliorates KCrO-induced changes which were more significantly in VC pro and concurrent supplement rather than VC concurrent supply only. Finally, it is concluded that KCrOoral administration induced oxidative apoptotic changes in rat brain and confirms the usefulness of VC pre and concurrent supply for the amelioration of KCrO-induced events more significantly than VC concurrent supply only.