Sıçan böbrek dokusunda etanolün akut toksisitesi ve borik asitin koruyucu rolü

In this study, the potential protective effect of boric acid in the process of inducing oxidative stress on kidneytissue due to acute alcohol toxicity was evaluated by biochemical and histological examination methods. In the study,250-300 gr. Wistar albino female rats aged 3-4 months, matched in weight, age and weight, were used. 28 female ratswere used, seven animals in each group: control, ethanol, boric acid (BA) and ethanol + BA.Renal tissue samples weretaken for histology and biochemistry. Kidney damage was assessed using hematoxylin and eosin (H&E) staining. At thesame time, total antioxidant level (TAS), total oxidant level (TOS) and oxidative stress index (OSI) were measured toevaluate oxidative stress as biochemical markers. While TOS and OSI levels were significantly lower in the BA groupcompared to the ethanol group (p<0.05), no statistically significant change was observed in the TAS level. In theethanol-treated group, deterioration in tubule morphology occurred as a result of epithelial cells spilling into the lumenin H&E staining. In the boric acid administered group, the structure of the renal cortex was observed to be normal,similar to the control group.In the boric acid+ethanol group, dilatation was observed to be less than in the ethanoladministered group with normal renal tubules. As acute ethanol toxicity increases, lipid peroxidation and oxidativestress increase. BA administration has been observed to reduce acute ethanol toxicity oxidative stress-induced kidneydamage, as demonstrated by both biochemical parameters and histological results.Key words: Boric acid, Acute ethanol consumption, Kidney, Oxidative stress