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Purpose: The aim of the study explores probable toxic effects of vancomycin on kidney and analysis of the probable protective effects of melatonin. Materials and Methods: In this study, rats were randomly divided into 4 groups: the control group; the melatonin (10 mg/kg/day) group; the vancomycin-treated (200 mg/kg) group; and the vancomycin (200 mg/kg) + melatonin (10 mg/kg/day) group. Rats in the treatment group were given two doses of vancomycin a day with an interval of seven consecutive days and melatonin (10 mg/kg/day) once daily for seven consecutive days. The experiment was continued for 15 days. In each group, seven rats were grouped together. 15 days after the experiment, the rats were sacrificed under anesthesia and among all groups. Kidney tissues were collected and processed for further TNF- expression analysis, as well as histological analyses such as hematoxylin and eosin (H&E), Masson's tricrom, and Periodic acid schiff (PAS) staining to assess pathological severity. In addition, a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to evaluate apoptosis. Results: While vancomycin upregulated TNF-α expression, melatonin reduced levels of TNF-α immunoreactivity intensity and clearly improved pathological severity in rat kidneys. Further, melatonin significantly inhibited vancomycin-induced TUNEL-positive cell numbers. Conclusion: Melatonin has protective activity against vancomycin-induced pro-inflammatory and proapoptotic effects in kidneys during organ preservation time and improves kidney function.

Introduction: The aim of the current study was to look into any potential ameliorative benefits of boric acid on liver damage in rats caused by cyclophosphamide (CTX). Materials and Methods: Four groups; control, boric acid, CTX, and boric acid + CTX, were created. Female Wistar albino rats were given daily injections of CTX (75 mg/kg) to create the liver damage model. Cyclophosphamide (75 mg/kg) was administered intraperitoneally, and boron (1.3 g/rat/day) was administered by gavage every day for two weeks in the boric acid+CTX group. The histopathological changes were evaluated in ovarian tissue staining with hematoxylin and eosin, masson tricrom, and periodic acid Schiff. We assessed ovarian tissue enzyme activity as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Results: Images in the boric acid+CTX group had lower histological evaluations than those in the CTX group under the light microscope. According to the findings, boric acid reduced the levels of malondialdehyde (MDA) in the liver tissues. Additionally, boric acid improved the actions of oxidative stress indicators to reduce oxidative stress brought on by CTX and upregulated antioxidant parameters. Conclusion: In conclusion, our study have demonstrated that CTX- induced liver injury can be alleviated by reducing the tissue MDA levels, increasing the liver’s SOD, GSH-Px, and CAT activities. In order to reduce the liver damage caused by CTX, boric acid may be administered as a dietary supplement or functional food.

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