LAUSR

Background Industrial and agricultural growths in recent years has resulted in the extreme discharge of arsenic into the environment, making arsenic toxicity a major worldwide concern. Oxidative stress is considered the primary mechanism for arsenic toxicity. Purpose The main objective of this study was to evaluate sulforaphane protective ability against arsenic-induced hepatotoxicity in rats via PI3K/Akt mediated Nrf2 activation. Methods For this purpose, male Wistar rats were divided into six groups of 8 rats each: control, Arsenic (As) (5mg/kg BW), As + SFN (5mg/kg; 20, 40, 80 mg/kg BW) and Vitamin C (As (5mg/kg) +100mg/kg). The animals were gavaged for 28 consecutive days. Liver tissue samples were extracted 24 hours after the last treatment and later analyzed for biochemical, molecular and histological alterations. Results Pretreatment with SFN led to decreased levels of ALAD, Ar accumulation, and brought antioxidant enzymes into normal levels without affecting Arsenic metabolism. This was accompanied by stabilizes the apoptotic markers via PI3K/Akt mediated Nrf2 activation as evidenced by western blotting and PCR techniques. Furthermore, SFN pretreatment shield the histoarchitecture of liver tissue in As treated rats. Conclusion The present study has provided mechanistic insights to the phytotherapeutic potential of SFN against As-induced liver injury by up-regulating Nrf2 gene via PI3K/Akt signalling pathway.