DIETARY CHOLESTYRAMINE REDUCES OCHRATOXIN A-INDUCED NEPHROTOXICITY INTHE RAT BY DECREASING PLASMA-LEVELS AND ENHANCING FECAL EXCRETION OF THE TOXIN

Citation
A. Kerkadi et al., DIETARY CHOLESTYRAMINE REDUCES OCHRATOXIN A-INDUCED NEPHROTOXICITY INTHE RAT BY DECREASING PLASMA-LEVELS AND ENHANCING FECAL EXCRETION OF THE TOXIN, Journal of toxicology and environmental health. Part A, 53(3), 1998, pp. 231-250
Citations number
53
Categorie Soggetti
Toxicology,"Environmental Sciences","Public, Environmental & Occupation Heath
ISSN journal
15287394
Volume
53
Issue
3
Year of publication
1998
Pages
231 - 250
Database
ISI
SICI code
1528-7394(1998)53:3<231:DCROAN>2.0.ZU;2-N
Abstract
Ochratoxin A (OTA) is a mycotoxin that may contaminate animal feed (oa t, barley, and rye) and food (wheat, rice, coffee, beer, pig meat), le ading to major health problems (e.g., nephropathy) in several animal s pecies including humans. Several methods have been tested to reduce th e toxicity of OTA in animals but with limited success. In rats, the ef fect of cholestyramine (CHA), a bile acid-binding resin, was investiga ted on OTA-induced nephrotoxicity and bioavailability. Animals were fe d semisynthetic diets containing two levels of OTA: 7 or 3 ppm. kt eac h level of OTA, the diets were enriched with 0. 1, 1, and 5% of CHA. T he results showed that CHA decreased the concentration of TA in plasma . At 1 and 3 ppm of OTA in the diet, CHA is effective at a level of 0. 1% and 5%, respectively. The excretion of CTA and its metabolites (och ratoxin alpha and hydroxylated ochratoxin A) in bile and urine was als o decreased by addition of 5% CHA in the diet. This was associated wit h an increase of OTA excretion in feces. Enzymuria and renal morpholog y revealed that dietary CHA can decrease OTA-induced nephrotoxicity, p robably by reducing renal exposure to the toxin. In conclusion, CHA ca n reduce OTA concentrations in plasma as well as reducing nephrotoxici ty, which may be attributed to a decrease of bioavailability and/or en terohepatic circulation of the toxin.