+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Field studies of aflatoxin exposure, metabolism and induction of genetic alterations in relation to HBV infection and hepatocellular carcinoma in The Gambia and Thailand



Field studies of aflatoxin exposure, metabolism and induction of genetic alterations in relation to HBV infection and hepatocellular carcinoma in The Gambia and Thailand



Toxicology Letters (Shannon) 64-65(SPEC ISSUE): 455-461



The relative contribution of aflatoxins (AF) and hepatitis B virus (HBV) to the aetiology of liver cancer remains to be determined, as does the mechanism of any interaction between these two factors. Methods to measure individual exposure to AF permit the assessment of this possible interaction in field studies. The measurement of AF covalently bound to albumin in peripheral blood has been particularly useful in this respect. In east and west African countries the majority (75-100%) of individuals has been found positive (> 5 pg AFB1-lysine eq./mg albumin) for the AF-albumin adduct with levels ranging up to 720 pg/mg. Levels of adduct to date have been age- and sex-independent, although marked seasonal variations were seen in The Gambia. Exposure also occurs in utero, with the AF-adduct being found in umbilical cord blood. In a study in The Gambia involving 323 children (age 3-8 years) the AF-albumin adduct levels were examined with respect to HBV infection and ethnic group. Over 95% of all sera contained detectable adduct but children positive for HBV surface antigen (HBsAG) had significantly higher adduct levels than children with markers of past infection or who had never been infected (mean (log) AF-albumin adduct levels 4.41 +/- 0.95, 4.04 +/- 0.99, and 4.05 +/- 1.03 respectively, p = 0.04). In addition, there were highly significant differences in adduct levels between the three major ethnic groups (Wollof 4.41 +/- 0.69: Fula 4.05 +/- 1.1; Mandinka 3.7 +/- 1.14). Wollof children were also more likely to be HBsAg positive than the other two groups. These data suggest that ethnic group and HBV infection can influence AF metabolism and this is being examined in this population with respect to genetic polymorphisms in cytochrome P450 and glutathione-S-transferase enzymes. In addition, these biomarkers are being compared to the nature and frequency of mutations in somatic and tumour cells.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 002383070

Download citation: RISBibTeXText

PMID: 1471197

DOI: 10.1016/0378-4274(92)90219-a


Related references

Hepatitis B and C infection and aflatoxin exposure in hepatocellular carcinoma A case-control study from The Gambia, West Africa. Hepatology 34(4 Pt 2): 666A, 2001

P53 Mutations and aflatoxin B-1 exposure in hepatocellular carcinoma patients from Thailand. International Journal Of Cancer. 53(1): 51-55, 1993

Epigenetic alterations caused by aflatoxin b1: a public health risk in the induction of hepatocellular carcinoma. Translational Research 204: 51-71, 2019

Alterations in lipid metabolism during the development of aflatoxin B1 induced experimental hepatocellular carcinoma. Medical Science Research 27(11): 779-782, 1999

Aflatoxin exposure and cytogenetic alterations in individuals from the Gambia, West Africa. Mutation Research 349(2): 209-217, 1996

Hepatitis B and C virus infection, aflatoxin exposure, and hepatocellular carcinoma in Taiwan. Proceedings of the American Association for Cancer Research Annual Meeting 37: 252, 1996

Aflatoxin B1 exposure, hepatitis B virus infection, and hepatocellular carcinoma in Taiwan. Cancer Epidemiology Biomarkers and Prevention 18(3): 846-853, 2009

Expression of P62 in hepatocellular carcinoma involving hepatitis B virus infection and aflatoxin B1 exposure. Cancer Medicine 6(10): 2357-2369, 2017

p53 mutations, chronic hepatitis B virus infection, and aflatoxin exposure in hepatocellular carcinoma in Taiwan. Cancer Research 57(16): 3471-3477, 1997

Urinary 15-F2t-isoprostane, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan. Carcinogenesis 29(5): 971-976, 2008

Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan. Carcinogenesis 28(5): 995-999, 2007

Challenging Role of Dietary Aflatoxin B1 Exposure and Hepatitis B Infection on Risk of Hepatocellular Carcinoma. Open Access Macedonian Journal of Medical Sciences 3(2): 363-369, 2015

Duck hepatitis B virus infection, aflatoxin exposure and hepatocellular carcinoma in domestic Chinese ducks. Journal of Hepatology 17(Suppl. 1): S17, 1992

Aflatoxin B 1 exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption. European Journal of Cancer 94: 37-46, 2018

Aflatoxin B 1 exposure increases the risk of hepatocellular carcinoma associated with hepatitis C virus infection or alcohol consumption. European Journal of Cancer 94: 37-46, 2018