Cadmium, analgesics, and the chronic progressive nephrosis in the female Sprague-Dawley rat.
Female Sprague-Dawley rats received phenacetin or aspirin at average daily doses of 135 and 27 mg/kg respectively in the diet and either demineralized water (DMW) or a 100 ppm cadmium (Cd) solution as their drinking water for 12 months. This dose of Cd produced borderline tubular toxicity, as measured by the excretion of IV-injected human beta 2-microglobulin. The kidney accumulation of Cd just reached the critical level of 200 ppm in all groups at the end of the study. The various treatments did not significantly affect growth, creatinine clearance, urine osmolality and the urinary excretion of beta-N-acetyl-D-glucosaminidase and aminoacids. No interaction resulted from the concomitant administration of analgesics and Cd. Both aspirin subgroups (receiving DMW or Cd) showed an attenuation of the age-related decline of the renal function as revealed by a lower urinary excretion of albumin and total protein. The accentuation of the mesangial matrix seen upon aging was also partly inhibited in the aspirin rats.
D000118:Acetylglucosaminidase / Q000652:urine; D000700:Analgesics / Q000633:toxicity*; D000818:Animals; D001241:Aspirin / Q000633:toxicity; D002104:Cadmium / Q000633:toxicity*; D002908:Chronic Disease; D005260:Female; D007668:Kidney / Q000187:drug effects; D009401:Nephrosis / Q000139:chemically induced*; D010615:Phenacetin / Q000633:toxicity; D051381:Rats; D011919:Rats, Inbred Strains
D000700:Analgesics; D002104:Cadmium; D000118:Acetylglucosaminidase; D010615:Phenacetin; D001241:Aspirin