Modulatory effects of sesame oil and ascorbic acid on abamectin-induced oxidative stress in rat liver and brain tissues

International audienceThe present work was designed to assess the modulatory effects of sesame oil (SO) and ascorbic acid (AA) on abamectin (ABM)-induced oxidative stress and altered gene expression of hepatic cytochrome P450 2E1 (CYP-2E1), p38 MAPK, and caspase-3 and cerebral P-glycoprotein (Abcb1a receptor). Male rats were distributed into five groups (6 rats/group), receiving distilled water, ABM 2 mg/kg bwt 1/5 LD50 orally for 5 days, ABM+AA 100 mg/kg bwt orally, ABM+SO 5 mL/kg bwt orally, or ABM+SO+AA at the aforementioned doses. Nineteen compounds were identified in the SO sample by GC-MS analysis, including tetradecane,2,6,10-trimethyl, octadecane, 1-hexadecanol,2-methyl, and octadecane,6-methyl. Abamectin significantly upregulated the hepatic CYP-2E1 expression with excess generation of oxidative radicals, as evident by the significant depletion of reduced glutathione and elevation of malondialdehyde concentration (p ≤ 0.05) in rat liver and brain tissues. Further, ABM significantly increased TNF-α concentration, the expression of caspase-3 and p38 MAPK in the liver, as well as p-glycoprotein and GABA-A receptor in the brain. These results were in line with the observed histopathological changes. Sesame oil and/or AA supplementation alleviated ABM-induced cell damage by modulating all tested parameters. In conclusion, ABM induces oxidative stress and increases the expression of CYP-2E1, caspase-3, and p38 MAPK in the liver, as well as P-gp and GABA-A receptor in the brain. These effects could be ameliorated by SO and AA, alone and in combination, probably due to their anti-oxidant, anti-apoptotic, and gene-regulating activities