AFLATOXIN, LIVER-ENZYMES, AND HEPATITIS-B VIRUS-INFECTION IN GAMBIAN CHILDREN

Citation
Cp. Wild et al., AFLATOXIN, LIVER-ENZYMES, AND HEPATITIS-B VIRUS-INFECTION IN GAMBIAN CHILDREN, Cancer epidemiology, biomarkers & prevention, 2(6), 1993, pp. 555-561
Citations number
41
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
10559965
Volume
2
Issue
6
Year of publication
1993
Pages
555 - 561
Database
ISI
SICI code
1055-9965(1993)2:6<555:ALAHVI>2.0.ZU;2-Q
Abstract
The relative contribution of, and possible mechanism of interaction be tween, aflatoxin and hepatitis B virus (HBV) in the development of pri mary hepatocellular carcinoma can be better investigated now that mark ers of individual exposure to both factors are available. In this stud y, blood samples were collected over a 1-month period from 117 childre n aged 3 to 4 years, resident in Kuntair or Kerr Cherno in the Upper N iumi District of The Gambia. Samples were analyzed for aflatoxin-album in (AF-alb) adducts, markers of HBV infection, liver enzymes [serum al anine aminotransferase (ALT)] as markers of liver damage, and glutathi one S-transferase M1 genotype. All but two children showed detectable serum AF-alb with levels ranging from 2.2 to 250.4 pg aflatoxin B1-lys ine equivalent/mg albumin. There was a significant positive correlatio n between AF-alb and ALT (r = 0.4; P < 0.001). HBV carriers showed mod erately higher levels of AF-alb than noncarriers but the difference wa s not statistically significant and the association between AF-alb and ALT was unchanged when the HBV carriers were excluded from the analys is, suggesting that factors other than HBV infection contributed to th e association. The null glutathione S-transferase Ml genotype was infr equent (17.7%) in this population and was not associated with any diff erence in AF-alb adduct levels compared to glutathione S-transferase M 1-positive individuals. However, the percentage of individuals with th e null genotype varied significantly between ethnic groups with 32.1% in Fula, 8.8% in Mandinka, and 13.3% in Wollof. The association betwee n AF-alb and ALT could be a result of the hepatotoxicity of aflatoxin, but the data are also consistent with the hypothesis that liver damag e resulting from HBV and/or other factors can alter aflatoxin metaboli sm resulting in an increased binding to cellular macromolecules includ ing DNA. This hypothesis merits further investigation in appropriate a nimal models and future field studies in aflatoxin-exposed populations .