Protective effects of boric acid against glyphosate-induced gastrointestinal toxicity in rats: insights from oxidative stress, inflammatory and histopathological markers

Glyphosate (GLY), a widely used herbicide, has been associated with gastrointestinal toxicity primarily via oxidative stress and inflammation. This study aimed to evaluate the protective role of boric acid (BA) against GLY-induced stomach and intestinal injury in rats. Adult male Sprague-Dawley rats were divided into control, GLY-treated, BA-treated, and GLY+BA co-treated groups. Both GLY (150 mg/kg/day) and BA (100 mg/kg/day) were administered orally for 7 consecutive days. Gastrointestinal tissues were assessed for oxidative stress markers including superoxide dismutase (SOD) and catalase (CAT), as well as gene expression via real-time polymerase chain reaction (PCR). Inflammatory markers tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB) were analyzed by Western blot. Histopathological evaluations were performed using hematoxylin-eosin (H&E) staining, and oxidative DNA damage was assessed by immunohistochemical detection of 8-hydroxy-2'-deoxyguanosine (8-OHdG). GLY exposure significantly increased TNF-α and NF-κB expression while downregulating SOD and CAT levels, leading to mucosal injury and marked histopathological alterations. In the GLY+BA group, histopathological evaluation revealed reduced mucosal damage and substantial preservation of glandular architecture. These results suggest that BA confers protection against GLY-induced gastrointestinal toxicity, likely through its antioxidant and anti-inflammatory properties.