Protective effects of Gallic acid on Glyphosate-induced hepatotoxicity

Abstract

Glyphosate is one of the most widely used herbicides globally. It has been demonstrated that glyphosate exerts hepatotoxic effects by promoting oxidative stress and inflammatory responses. This study investigated the toxic damage caused by glyphosate exposure in rat liver tissue, and the potential of gallic acid to mitigate this damage. The study was conducted under laboratory conditions, using male Wistar albino rats as the experimental model. The rats were divided into four groups of seven: a control group; a group exposed to glyphosate; a group treated with gallic acid; and a group treated with both glyphosate and gallic acid. Glyphosate was administered intraperitoneally at a dose of 50 mg/kg/day for 15 days and gallic acid orally at 100 mg/kg/day. The rats' livers were examined using histopathological methods and the expression of interleukin-6 and B-cell lymphoma-2 was evaluated using immunohistochemistry. Serum levels of total antioxidants and oxidants, as well as malondialdehyde, interleukin-6, aspartate aminotransferase, alanine aminotransferase and bilirubin, were analysed. Glyphosate exposure was found to significantly impact the levels of histopathological damage, total oxidative status, malondialdehyde, interleukin-6, aspartate aminotransferase and bilirubin (P < 0.05). Conversely, the simultaneous administration of gallic acid and glyphosate resulted in a substantial decrease in these parameters compared to glyphosate exposure alone (P < 0.05). No significant differences were observed between the groups in terms of total antioxidant status or alanine aminotransferase levels. These results imply that gallic acid could serve as a protective or supportive therapy against hepatotoxicity resulting from glyphosate exposure.