Investigation of the effects of vitamin b12 in nephrotoxicity due to gentamicin use

There is a 10-25% chance of nephrotoxicity due to the use of aminoglycoside group antibiotics. The lack of a preventive agent that can be routinely used against nephrotoxicity due to aminoglycoside use complicates treatment. In this study, we investigated whether vitamin B12 has protective effects on aminoglycoside-induced nephrotoxicity. For this purpose, vitamin B12 was administered with gentamicin or before gentamicin and it was evaluated which application was more effective. In the study, 42 male Wistar Albino rats aged 10-12 weeks and weighing 280-420 g were used. The animals were randomly divided into 6 groups. The control group was administered 0.1 ml/kg saline throughout the study period, and the gentamicin group was administered 100 mg/kg/day gentamicin by intraperitoneal injection for seven days. Vitamin B12 was administered intraperitoneally at 3 mcg/kg/day for one week in one group and two weeks in the other group. In the gentamicin + vitamin B12 groups, 100 mg/kg/day gentamicin was administered intraperitoneally for 7 days; in the pretreatment vitamin B12 group, vitamin B12 was started one week before gentamicin and administered for two weeks; in the concurrent vitamin B12 group, vitamin B12 was started at the same time with gentamicin and administered for only one week. At the end of the study, urea, creatinine, and calcium levels in serum samples; MDA, SOD, TNF-α, IL-6, IL-1β, KIM-1, and NGAL levels in kidney tissue samples were measured and electron microscopic examination was performed. An increase in serum urea, creatinine and renal tissue MDA levels and a decrease in SOD levels were observed in the gentamicin-treated group compared to the control group. Vitamin B12 treatment administered before gentamicin reversed the increased serum urea and creatinine levels due to gentamicin administration. In both simultaneous treatment and pre-treatment groups, vitamin B12 provided an anti-inflammatory effect by significantly improving gentamicin-induced IL-6 and NGAL levels in the kidney and showed antioxidant activity by reversing gentamicin-induced increased renal MDA levels. Additionally, vitamin B12 administration prevented histopathological damage due to gentamicin toxicity in both groups. In conclusion, vitamin B12, with its antioxidant and anti-inflammatory effects, may be a protective option in the prevention of gentamicin-induced nephrotoxicity.