Fucoidan supplementation modulates hepato-renal oxidative stress and DNA damage induced by aflatoxin B1 intoxication in rats

Aflatoxins are a common food contaminant of global concern. Aflatoxin B-1 (AFB(1)) intoxication is associated with serious health hazards. Recently, fucoidan (FUC) has gained much attention from pharmaceutical industry due to its promising therapeutic effects. The impacts of FUC on AFB(1)-induced liver and kidney injures have not been sufficiently addressed. This research was conducted to evaluate the ameliorative effect of FUC in AFB1-induced hepatorenal toxicity model in rats over 14 days. Five groups were assigned; control, FUC (200 mg/kg/day, orally). AFB(1)(50 mu g/kg, i.p.), and AFB(1) plus a low or high dose of FUC. AFB(1) induced marked hepatorenal injury elucidated by substantial alterations in biochemical tests and histological pictures. The oxidative distress instigated by AFB(1) enhanced production of malondialdehyde (MDA) and nitric oxide (NO) along with reduction in the reduced-glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities. DNA damage in the liver and kidney tissues has been demonstrated by overexpression of proliferating cell nuclear antigen (PCNA). Unambiguously, FUC consumption alleviates the AFB(1) induced mitochondria] dysfunction, oxidative harm, and apoptosis. These ameliorated effects are proposed to be attributed to fucoidan's antioxidant and anti-apoptotic activities. Our results recommend FUC supplementation to food because it exerts both preventive and therapeutic effects against AFB(1)-induced toxicity. (C) 2020 Elsevier B.V. All rights reserved.

Automated summary

This study evaluated the ameliorative effect of fucoidan on AFB(1)-induced hepatorenal toxicity in rats. The results suggest that fucoidan alleviates cell damage and oxidative stress induced by AFB(1), possibly due to its antioxidant and anti-apoptotic activities.