Oyagbemi, A. A.Omobowale, T. O.Adenuga, E. R.Afolabi, J. M.Adejumobi, O. A.Adedapo, A. A.Yakubu, M. A.2026-05-2520172214-7500ui_art_oyagbemi_effect_2017Toxicology Reports, 4, pp. 521–529https://repository.ui.edu.ng/handle/123456789/14128We investigated the effects of withdrawal from Sodium arsenite (NaAsO2) on the hepatic and antioxidant defense system in male Wistar rats using a before and after texicant design. Rats were orally gavaged daily with varying duses of NaAsO fur a period of 4 weeks. One half of the population was sacrificed and the remaining half had the toxicant withdrawn for anodier ferther 4 weeks. Biochemical and immunohistochemical techniques were used to assess the impact of withdrawal on the erythrocyte and hepatic systems. Exposure of Wistar rats to NaASO, led to a significant (p<0.05) increase in hepatic and erythrocyte markers of oxidative stress (malondialdehyde, thiol contents and hydrogen peroxide generation). Concurrently, there was a significant (p < 0.05) increase in hepatic and erythrocyte antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and superoxide dismutase) following exposure. Withdrawal from NaAsO exposure led to a decline in both erythrocyte and hepatic markers of oxidative stress and together with a significant improvement in antioxidant defense system. Histopathology and immunohistochemistry revealed varying degrees of recovery in hepatocyte ultrastructure alongside increased expression of the pre-survival protein Kinase B (Akt/PKB) after 4 weeks of NAO with drawal. Conclusively, withdrawal from exposure led to a partial recovery from uxidative stress-mediated he patotoxicity and derangements in erythrocyte antioxidant system through Akt/PKB pathway.enLiverErythrophleumArsenic-induced hepatotoxicityOxidative stressAkt/PKB signalingArticle