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Protection of crocin dyes on the acute hepatic damage induced by aflatoxin B1 and dimethylnitrosamine in rats. Carcinogenesis [Carcinogenesis] Journal article

TitleProtection of crocin dyes on the acute hepatic damage induced by aflatoxin B1 and dimethylnitrosamine in rats.
Author(s)Lin JK, Wang CJ 
SourceCarcinogenesis 1986 Apr; 7(4):595-9.
MeSHAflatoxin B1
Aflatoxins
Alanine Transaminase
Alkaline Phosphatase
Animals
Aspartate Aminotransferases
Carotenoids
Dimethylnitrosamine
Drug Interactions
Female
L-Lactate Dehydrogenase
Liver
Rats
Rats, Inbred Strains
gamma-Glutamyltransferase
AbstractChemopreventive agents are compounds that inhibit carcinogenesis when administered prior or subsequent to a course of carcinogen administration. The effects of dietary administration of crocin dyes on the hepatic damage induced by aflatoxin B1 (AFB1) and dimethylnitrosamine (DMN) in rats were investigated. Female Sprague-Dawley rats were treated with different dosages of AFB1 (0.9 or 4.5 mg/kg) or DMN (8 or 20 mg/kg) by i.p. administration, and the different degrees of hepatic damage were revealed by the elevations of levels of serum marker enzymes such as aspartate amino-transferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and lactic dehydrogenase. Pre-treatment of the animals with crocin dyes 50 mg/kg daily for three consecutive days, the enzyme elevations were significantly suppressed. This suggested that the crocin dyes possessed chemopreventive effects on the early acute hepatic damage induced by AFB1 or DMN. Feeding experiments demonstrated that crocin dyes at 0.1% in the diet could suppress partially the chronic hepatic damage induced by multiple dosages of AFB1 or DMN, but at a higher concentration of 1% crocin dye failed to do so because of their host toxicity. Crocin dyes are extracted from the fruits of Gardenia jasminoides and consist of carotenoids and geniposides as active principles. The protective mechanisms of crocin dyes may be attributed to their carotenoids which are converted metabolically to retinoids in rats.
Languageeng
Pub Type(s)Journal Article
Research Support, Non-U.S. Gov't
PubMed ID2870820