The protective effect of boric acid on aluminum-induced hepatotoxicity and genotoxicity in rats

Abstract

The efficacy of boric acid (BA) was examined on liver marker enzymes in aluminum (Al)-treated rats. Also, a liver micronucleus assay was performed to evaluate the genotoxicity in hepatocytes. With these aims, Sprague-Dawley rats were randomly separated into 10 groups of 5 animals. Aluminum chloride (5 mg/kg body weight (b.w.) AlCl3) and BA (3.25, 13, 36 and 58.5 mg/kg b.w.) alone were administered with injections to the experimental animals. Furthermore, the animals were also treated with Al for 4 consecutive days followed by BA exposure for 10 days. The rats were anesthetized after Al and BA injections and the levels of serum enzymes were determined. Hepatocytes were isolated for counting the number of micronucleated hepatocytes (MNHEPs). After exposure to Al, the enzymatic activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) significantly increased. Furthermore, this metal caused a significant increase in MNHEPs' incidence. In contrast, the applications of BA doses did not cause any adverse effect on the above parameters. Moreover, pretreatments with BA significantly modulated the toxic effects of Al.