Research Information System
Biological Diversity and Conservation, vol.15, no.1, pp.107-113, 2022 (Peer-Reviewed Journal)
In this study, the potential protective effect of boric acid in the process of inducing oxidative stress on kidney
tissue 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 rats
were used, seven animals in each group: control, ethanol, boric acid (BA) and ethanol + BA.Renal tissue samples were
taken for histology and biochemistry. Kidney damage was assessed using hematoxylin and eosin (H&E) staining. At the
same time, total antioxidant level (TAS), total oxidant level (TOS) and oxidative stress index (OSI) were measured to
evaluate oxidative stress as biochemical markers. While TOS and OSI levels were significantly lower in the BA group
compared to the ethanol group (p<0.05), no statistically significant change was observed in the TAS level. In the
ethanol-treated group, deterioration in tubule morphology occurred as a result of epithelial cells spilling into the lumen
in 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 ethanol
administered group with normal renal tubules. As acute ethanol toxicity increases, lipid peroxidation and oxidative
stress increase. BA administration has been observed to reduce acute ethanol toxicity oxidative stress-induced kidney
damage, as demonstrated by both biochemical parameters and histological results.
Key words: Boric acid, Acute ethanol consumption, Kidney, Oxidative stress