Gallic acid protects against Aflatoxin B1 -induced oxidative and inflammatory stress damage in rats kidneys and liver.

Abstract

The adverse effect of Aflatoxin B1 (AFB1 ) exposure in both humans and rodents has been widely reported. The beneficial health effects of gallic acid (GA) against AFB1 -induced toxicity in vitro have been published. Here, we present in vivo findings on AFB1 and GA on hepatorenal function in rats, exposed to AFB1 (75µg/kg body weight) only or co-treated with GA (20 or 40mg/kg) for 28 successive days. AFB1 significantly increased pro-inflammatory biomarkers and suppressed IL-10 levels in rats' liver and kidney. AFB1 caused increased (p<.05) oxidative stress by decreasing antioxidant enzymes levels and increasing levels of reactive oxygen and nitrogen species. Furthermore, reduction (p<.05) in cellular glutathione (GSH) levels and increased (p<.05) hepatorenal markers of toxicity were detected in rats treated with AFB1 . These observed alterations were, however, reversed in GA co-treated rats. GA ameliorated AFB1 -induced hepatorenal dysfunction by decreasing oxidative stress and inflammation in rats. PRACTICAL APPLICATIONS: GA can chemoprotect against the damaging effects of toxins contaminating food. GA is widely distributed in plants and in use in industries as antioxidant, immune-regulator, and natural defense agent against infections when consumed. Here, we disclosed that GA ameliorates AFB1 -induced hepatorenal dysfunction by suppressing oxidative stress, inflammation, and enhanced apoptosis, thus improving hepatorenal functions in rats exposed to AFB1.