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Background: Nephrotoxicity refers to the toxigenic impact of compounds and medications on kidney function. There are a variety of drug formulations, and some medicines that may affect renal function in multiple ways via nephrotoxins production. Nephrotoxins are substances that are harmful to the kidneys.Purpose: This investigation examines the renoprotective effect of gymnemic acid (GA) on Wistar rats in gentamicin-induced nephrotoxicity by analyzing serum, kidney, and histopathological markers.Study-design/methods: The current study investigated the protective effect of GA at doses of 20, 40, and 60 mg/kg against gentamicin-induced nephrotoxicity in rats. Vitamin E was administered to compare the antioxidant capacity and efficacy of GA. In addition to the treatment groups, 100 mg/kg of gentamicin was administered intraperitoneal for 14 days. At the end of the study protocol, kidney homogenate, blood, and serum were evaluated biochemically. Serum creatinine, blood urea, glomerular filtration rate (GFR), mitochondrial dysfunctions, inflammatory cytokines, and renal oxidative stress were examined to assess gentamicin-induced nephrotoxicity. In addition, the impact of GA on the above-mentioned nephrotoxic markers were evaluated and further confirmed by histological analysis.Results: This study establishes a correlation between antibiotic use, especifically aminoglycosides and acute renal failure. The research demonstrates the nephrotoxic effects of aminoglycosides, inducing mitochondrial ETC-complex dysfunction, and renal tissue inflammation in experimental rats. GA’s antioxidant properties restored renal oxidative stress markers, reducing kidney inflammation and injury. Histopathological analysis revealed a significant reduction in renal injury with GA treatment. Additionally, GA demonstrated greater efficacy than Vitamin E in restoring antioxidant potential and mitochondrial enzymes.Conclusion: Consequently, our findings imply that long-term use of GA may be a suitable therapeutic strategy for reducing aminoglycoside toxicity. The current study suggests GA’s potential in treating gentamicin-induced nephrotoxicity and acute renal failure, meriting further investigation using advanced techniques.

IntroductionThe blood microbiome is still an enigma. The existence of blood microbiota in clinically healthy individuals was proven during the last 50 years. Indirect evidence from radiometric analysis suggested the existence of living microbial forms in erythrocytes. Recently targeted nucleic acid sequencing demonstrated rich microbial biodiversity in the blood of clinically healthy individuals. The morphology and proliferation cycle of blood microbiota in peripheral blood mononuclear cells (PBMC) isolated from freshly drawn and cultured whole blood are obscure.MethodsTo study the life cycle of blood microbiota we focused on light, and electron microscopy analysis. Peripheral blood mononuclear cells isolated from freshly drawn blood and stress-cultured lysed whole blood at 43°C in presence of vitamin K from healthy individuals were studied.ResultsHere, we demonstrated that free circulating microbiota in the PMBC fraction possess a well-defined cell wall and proliferate by budding or through a mechanism similar to the extrusion of progeny bodies. By contrast, stress-cultured lysed whole blood microbiota proliferated as cell-wall deficient microbiota by forming electron-dense or electron-transparent bodies. The electron-dense bodies proliferated by fission or produce in chains Gram-negatively stained progeny cells or enlarged and burst to release progeny cells of 180 – 200 nm size. On the other hand, electron-transparent bodies enlarged and emitted progeny cells through the membrane. A novel proliferation mechanism of blood microbiota called by us “a cell within a cell” was observed. It combines proliferation of progeny cells within a progeny cell which is growing within the “mother” cell.DiscussionThe rich biodiversity of eukaryotic and prokaryotic microbiota identified in blood by next-generation sequencing technologies and our microscopy results suggest different proliferation mechanisms in whole and cultured blood. Our documented evidence and conclusions provide a more comprehensive view of the existence of normal blood microbiota in healthy individuals.