Anticancer potency of the milk extract of Semecarpus anacardium Linn. nutsagainst aflatoxin B-1 mediated hepatocellular carcinoma bearing Wistar rats with reference to tumour marker enzymes

Citation
B. Premalatha et al., Anticancer potency of the milk extract of Semecarpus anacardium Linn. nutsagainst aflatoxin B-1 mediated hepatocellular carcinoma bearing Wistar rats with reference to tumour marker enzymes, PHYTOTHER R, 13(3), 1999, pp. 183-187
Citations number
44
Categorie Soggetti
Pharmacology & Toxicology
Journal title
PHYTOTHERAPY RESEARCH
ISSN journal
0951418X → ACNP
Volume
13
Issue
3
Year of publication
1999
Pages
183 - 187
Database
ISI
SICI code
0951-418X(199905)13:3<183:APOTME>2.0.ZU;2-S
Abstract
Aflatoxin B-1 is an important consideration in the aetiology of human and a nimal hepatocellular carcinoma. The influence of the drug, Semecarpus anaca rdium Linn. nut extract, on hepatocarcinogenicity of aflatoxin B1 was evalu ated in adult albino male Wistar rats. Aflatoxin B1 was administered intrap eritoneally to induce hepatocellular carcinoma, These cancer bearing animal s were treated with Semecarpus anacardium Linn, nut extract (200 mg/kg body weight/day) in sunflower oil orally for 14 days. The plasma and the liver tumour tissue were investigated biochemically for lactate dehydrogenase, as partate aminotransferase, alanine aminotransferase, alkaline phosphatase an d gamma-glutamyl transpeptidase, The elevation of plasma concentration of t hese enzymes were indicative of the persistent deteriorating effect of afla toxin B1 in cancer bearing animals. Lactate dehydrogenase and aminotransfer ases levels were decreased in liver, whereas alkaline phosphatase and gamma -glutamyl transpeptidase were increased in cancer conditions. These enzyme levels were reversed to near normal control values in drug treated animals. The analysis of marker enzyme activities clearly indicates the antitumour efficacy of Semecarpus anacardium Linn, nut extract on aflatoxin B1 induced hepatocellular carcinoma. Copyright (C) 1999 John Wiley & Sons, Ltd.