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

• Published in: Journal of food biochemistry Vol. 44; no. 8
• Main Authors: Owumi, Solomon, Najophe, Eseroghene S., Farombi, Ebenezer O., Oyelere, Adegboyega K.
• Format: Journal Article
• Language: English
• Published: 01-08-2020
• Subjects: Aflatoxin B1; gallic acid; hepatorenal toxicity; inflammatory markers; oxidative stress; rats
• ISSN: 0145-8884; 1745-4514
• DOI: 10.1111/jfbc.13316

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 (75 µg/kg body weight) only or co‐treated with GA (20 or 40 mg/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.
The adverse effect of Aflatoxin B1 (AFB1) and the beneficial 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 only or co‐treated with GA for 28 successive days. AFB1 significantly increased pro‐inflammatory biomarkers, suppressed IL‐10 levels, and increased oxidative stress in rats’ liver and kidney. GA co‐treatment ameliorated AFB1‐induced hepatorenal dysfunction by decreasing oxidative stress and inflammation.