In vivo and in vitro changes in renal function caused by ochratoxin A in the rat.
Ochratoxin A has been suggested to be an important, environmentally prominent nephrotoxin. Possible involvement in both human and animal disease states has been indicated. This study was designed to examine under controlled laboratory conditions, the nephrotoxic potential of ochratoxin A in the rat. Daily administration of ochratoxin A in doses of 0.75 and 2.0 mg/kg caused persistent urinary hypoosmolality coupled with excessive glucose and protein excretion. In addition the renal slice transport of several organic compounds also was altered. Renal slice tissue electrolytes and water were unaffected by ochratoxin A pretreatment. Direct addition of ochratoxin A to fresh renal cortex slices also depressed transport of some organic compounds. Although rats pretreated with ochratoxin A lost large amounts of body weight, the weight loss alone did not account totally for the changes in renal function. These data indicate that ochratoxin A has the capability of producing alterations in renal function suggestive of nephrotoxicity. However, the pattern of response is different than that observed with citrinin.
D000613:Aminobutyrates / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005508:Food Deprivation; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D007672:Kidney Cortex / Q000378:metabolism; D009793:Ochratoxins / Q000633:toxicity*; D000644:Quaternary Ammonium Compounds / Q000378:metabolism; D051381:Rats; D013997:Time Factors; D010130:p-Aminohippuric Acid / Q000378:metabolism
D000613:Aminobutyrates; D001786:Blood Glucose; D009793:Ochratoxins; D000644:Quaternary Ammonium Compounds; D010130:p-Aminohippuric Acid