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
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
.