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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Apoptosis, Cell Division, Cells, Cultured, Gentamicins, Glomerular Mesangium, Rats, Rats, Wistar, Reactive Oxygen Species, Time Factors.
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Does gentamicin treatment induce simultaneous mesangial proliferation and apoptosis in rats? Context: Gentamicin (G)-induced acute renal failure is characterized by an impairment of glomerular function without apparent changes in glomerular structure. However, G stimulates reactive oxygen species (ROS)-mediated mesangial cell proliferation in vitro. We studied whether G promotes mesangial cell apoptosis in vitro, and if apoptosis and proliferation in parallel may occur in glomerular cells in vivo after a renal damage induced by G treatment. For in vivo studies, rats were treated with G (100 mg/kg body weight/day) for 6 days, and functional and histologic studies were performed. For in vitro studies, mesangial cell proliferation and apoptosis were evaluated after 24, 48, and 72 hours of 10(-5) mol/L G incubation. After G injections, the number of nuclei per glomerulus did not change, whereas proliferating and apoptotic cell numbers increased. G increases DNA synthesis and cell number in cultured mesangial cells, and increases markedly the apoptotic cell number. ROS scavengers superoxide dismutase and catalase reduce G-induced mesangial cell apoptosis, whereas the incubation with the ROS donor system xanthine plus xanthine oxidase increases apoptosis to levels similar to G. G-induced cellular proliferation and apoptosis either in vitro or in vivo is associated to an early increase in the pro-apoptotic protein Bax and a delayed increase in the survival protein Bcl-2.
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G simultaneously induces proliferation and apoptosis of mesangial cells in vitro and glomerular mesangial cells in vivo. ROS may mediate G-induced mesangial apoptosis in vitro. The equilibrium proliferation/apoptosis may maintain mesangial cell number within normal limits after a G-induced glomerular insult. Final Decision: yes