The Protective Effect of Boric Acid Against High Fructose-Induced Liver and Kidney Damage in Rats

This study aimed to determine the protective role of boric acid (BA) in high fructose (HF)-induced liver and kidney toxicity in a young rat model. High-fructose consumption causes serious damage to liver and kidney tissue in healthy individuals and contributes to the emergence of various metabolic diseases. Thirty-two healthy female Wistar albino rats (250–300 g weight and 3–4 months) were randomly distributed into four equal groups (n = 8): control, high fructose % 20 (HF), boric acid 20 mg/kg (BA), and HF + BA. High fructose was freshly prepared and administered to the rats as 20 g of d-fructose dissolved in 100 mL of tap water daily for a duration of 30 days. Boric acid (20 mg/kg) was administered through gastric gavage throughout the 30-day study period. At the end of study, blood, liver, and kidney were collected from rats. The results indicated that high fructose induced increased glucose, total cholesterol, triglyceride, and urea levels in rat serum. Boric acid administration significantly decreased glucose, total cholesterol, triglyceride, and urea levels in HF + BA groups. The results indicated that high fructose-induced oxidative stress by increasing the level of MDA and by decreasing GSH levels, and CAT activity in the liver and kidney of rats. However, oral BA administration significantly decreased MDA levels and increased GSH levels, and CAT activity (p < 0.05). Furthermore, BA significantly reduced high fructose-induced histopathological and Immunohistochemistry alteration in the liver and kidney tissues. In conclusion, BA may prevent the oxidative imbalance and histopathological and immunohistochemical damage caused by high fructose in liver and kidney tissues in rats.