An experimental model of analgesic-induced renal damage--some effects of p-aminophenol on rat kidney mitochondria.
1. p-Aminophenol, a known nephrotoxin, has been studied as a model for phenacetin-induced renal damage. 2. Respiration, oxidative phosphorylation and ATPase activity were inhibited in mitochondria isolated from the kidneys of treated rats; this could not be reversed by the addition of exogenous loosely bound cofactors and bovine serum albumin to the assay medium. 3. After treatment the mitochondrial levels of sodium and calcium were increased, potassium decreased and magnesium unaltered. 4. Mitochondria isolated from treated rats showed ultrastructural damage. 5. The results are interpreted to indicate that renal tubular cell mitochondrial injury is important in triggering cortical analgesic renal damage.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000700:Analgesics / Q000009:adverse effects*; D000818:Animals; D002412:Cations / Q000378:metabolism; D004195:Disease Models, Animal; D066298:In Vitro Techniques; D007668:Kidney / Q000648:ultrastructure; D007674:Kidney Diseases / Q000139:chemically induced*; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D010636:Phenols / Q000009:adverse effects*; D011506:Proteins / Q000378:metabolism; D051381:Rats
D000700:Analgesics; D002412:Cations; D010636:Phenols; D011506:Proteins; D000251:Adenosine Triphosphatases