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Aflatoxin, liver enzymes, and hepatitis B virus infection in Gambian children
Insights
Aflatoxin exposure in Gambian children is widespread and linked to liver damage (ALT). Hepatitis B virus (HBV) infection did not significantly alter this association, suggesting other factors contribute to liver injury.
Area of Science:
- Environmental Health
- Hepatology
- Toxicology
Background:
- Hepatocellular carcinoma (HCC) development is linked to aflatoxin and hepatitis B virus (HBV) exposure.
- Investigating the interaction between these factors is crucial for understanding HCC etiology.
- Biomarkers for individual exposure are now available to facilitate such investigations.
Purpose of the Study:
- To investigate the relative contribution and interaction of aflatoxin and HBV in liver damage among children.
- To assess the correlation between aflatoxin exposure markers, HBV infection, liver enzymes, and GSTM1 genotype.
Main Methods:
- Blood samples were collected from 117 children aged 3-4 years in The Gambia.
- Analysis included aflatoxin-albumin (AF-alb) adducts, HBV markers, alanine aminotransferase (ALT), and glutathione S-transferase M1 (GSTM1) genotype.
- Statistical correlations were performed to assess relationships between measured factors.
Main Results:
- Nearly all children (115/117) had detectable AF-alb adducts, indicating widespread aflatoxin exposure.
- A significant positive correlation was found between AF-alb levels and ALT (liver damage marker).
- HBV carriers did not show significantly higher AF-alb levels, and the AF-alb/ALT association persisted after excluding HBV carriers.
Conclusions:
- Widespread aflatoxin exposure is prevalent in young Gambian children.
- Aflatoxin exposure is significantly associated with liver damage (ALT), independent of HBV infection status.
- GSTM1 genotype prevalence varied by ethnic group but did not influence AF-alb levels in this cohort.
Abstract:
The relative contribution of, and possible mechanism of interaction between, aflatoxin and hepatitis B virus (HBV) in the development of primary hepatocellular carcinoma can be better investigated now that markers of individual exposure to both factors are available. In this study, blood samples were collected over a 1-month period from 117 children aged 3 to 4 years, resident in Kuntair or Kerr Cherno in the Upper Niumi District of The Gambia. Samples were analyzed for aflatoxin-albumin (AF-alb) adducts, markers of HBV infection, liver enzymes [serum alanine aminotransferase (ALT)] as markers of liver damage, and glutathione 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-lysine equivalent/mg albumin. There was a significant positive correlation between AF-alb and ALT (r = 0.4; P < 0.001). HBV carriers showed moderately higher levels of AF-alb than noncarriers but the difference was not statistically significant and the association between AF-alb and ALT was unchanged when the HBV carriers were excluded from the analysis, suggesting that factors other than HBV infection contributed to the association. The null glutathione S-transferase M1 genotype was infrequent (17.7%) in this population and was not associated with any difference in AF-alb adduct levels compared to glutathione S-transferase M1-positive individuals. However, the percentage of individuals with the null genotype varied significantly between ethnic groups with 32.1% in Fula, 8.8% in Mandinka, and 13.3% in Wollof.(ABSTRACT TRUNCATED AT 250 WORDS)