Abstract
Cephaloglycin (CG) is one of several nephrotoxic drugs in the cephalosporin family of antibiotics. The mechanism of injury produced by these drugs is uncertain. Since CA has been implicated in the damage sustained by the kidney following a variety of insults, the effects of CG on CA accumulation in the cortex (CTX) and cortical mitochondria (MITO) and the relationship of mitochondrial oxygen consumption to tissue CA content were studied. The CA content of whole renal CTX and renal cortical MITO was measured two hours after a toxic dose of CG (200mg/kg IV) in control (CTRL) and experimental (EXPT) rabbits. Mitochondrial oxygen consumption supported by succinate in the presence of ADP or CA was measured from the same preparations. Data are expressed as nanomoles/mg protein and as meansĀ±SD, n=6-10, *p<.05 or better compared to CTRL.
CG leads to early accumulation of CA in the renal CTX and cortical MITO. There is a parallel decline in mitochondrial respiratory function. These results suggest that CA may play an important role in the proximal tubular necrosis and mitochondrial dysfunction caused by CG.
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Browning, M., Lorentz, W. 1581 EARLY EFFECTS OF A NEPHROTOXIC CEPHALOSPORIN ON RENAL CORTICAL AND MITOCHONDRIAL CALCIUM (CA) CONTENT AND MITOCHONDRIAL FUNCTION. Pediatr Res 19, 374 (1985). https://doi.org/10.1203/00006450-198504000-01605
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DOI: https://doi.org/10.1203/00006450-198504000-01605