Oxidative Stress and Renal Dysfunction in Lincomycin-Induced Nephrotoxicity: Evaluating the Therapeutic Potential of Activated Charcoal
DOI:
https://doi.org/10.63593/JIMR.2788-7022.2025.08.001Keywords:
nephrotoxicity, lincomycin, activated charcoal, oxidative stress, renal dysfunction, antioxidant therapyAbstract
Background: The kidneys play a vital role in homeostasis and metabolic waste elimination, but they are highly susceptible to toxic insults due to their role in drug metabolism. Lincomycin, a lincosamide antibiotic, has been implicated in nephrotoxicity through oxidative stress-mediated mechanisms, leading to renal dysfunction. Activated charcoal, a widely used adsorbent, has shown potential in mitigating renal damage by adsorbing toxins and modulating oxidative stress. However, its efficacy in lincomycin-induced nephrotoxicity remains poorly understood. Aim: This study investigates the protective potential of activated charcoal against lincomycin-induced nephrotoxicity by assessing oxidative stress markers, renal function indices, and histopathological changes. Methodology: Twenty-five (25) Wistar rats were divided into five groups (n=5). Group I (Control) received normal saline, while Group II received lincomycin (200 mg/kg). Groups III, IV, and V were co-administered lincomycin with varying percentages of activated charcoal (25%, 50%, and 75%). Kidney function markers (creatinine, urea), oxidative stress indices (Superoxide Dismutase [SOD], Malondialdehyde [MDA]), and histopathological changes were evaluated. Results: Lincomycin administration significantly reduced creatinine (0.59±0.07 mg/dl) and urea (19.85±2.11 mg/dl) compared to controls (0.85±0.04 mg/dl, 25.78±1.19 mg/dl; P<0.05). Oxidative stress was evident in the lincomycin group, with a decrease in SOD (14.25±1.81 U/mg protein) and an increase in MDA. Activated charcoal co-administration mitigated these effects, improving kidney function and oxidative stress parameters. Conclusion: Activated charcoal offers protective effects against lincomycin-induced nephrotoxicity by reducing oxidative stress and preserving renal function. Its potential as an adjunct therapy in mitigating antibiotic-induced kidney damage warrants further investigation.