Immunohistochemical detection of aflatoxin B1-DNA adducts and hepatitis B virus antigens in hepatocellular carcinoma and nontumorous liver tissue.

Abstract

Monoclonal antibodies recognizing the stable imidazole ring-opened form ofthe major N7-guanine aflatoxin B,-DNA adduct have been used in competitive enzyme-linked immunosorbent assays (ELISA) and indirect immunofluorescence assays to quantitate adduct levels in liver tissue. Methods were developed inAFBI-treatedanimals, then applied to paired tumor and nontumor liver tissues of hepatoceliular carcinoma patients from Taiwan. An avidin-biotin complex staining method wasalso used for ofthe detection ofhepatitis B surface (HBsAg) and X (HBxAg) antigens in liversections. A total of 8 (30%) hepatocellular carcinoma (HCC) samples and 7 (26%) adjacent nontumor liver tissue samples from Taiwan were positive for AFB,-DNA adducts. For HEsAg, 10 (37%) HCC samples and 22 (81%) adjacent nontumorous liver samples were positive, and 9 (33%) HCC samples and U (41%) adjacent nontumor liver sunples were HBxAg positive. No association with AFBI-DNA adducts was observed for HBsAg and HBxAg. These methods should be useful in determining the role of exposure in the induction ofHCC in Taiwan.

Associated Factors in Modulating Aflatoxin B1?Albumin Adduct Level in Three Chinese Populations

“…HBV (sAg, sAb, eAg, eAb, cAb), anti-HDV, anti-HEV, and anti-HGV were determined using commercial enzyme-linked immunoassay kits from Intec Products Inc. ( Detection of AFB 1 -Albumin Adduct Level. To determine the AFB 1 -ALB adduct (AAA) levels in serum samples, a previously described competitive enzyme-linked immunosorbent assay (ELISA) was done at Columbia University, New York, USA (10)(11)(12). AAA level is expressed as femtomoles per milligram of albumin.…”

COOH-terminal deletion of HBx gene is a frequent event in HBV-associated hepatocellular carcinoma

“…Transgenic mice created with the X gene have been reported to develop HCC [8][9][10] . Although the transactivation properties of the X gene and HBxAg overexpressed selectively in human HCC [11,12] , its precise role in human hepatocarcinogenesis is still unclear [1,2] . In some studies, X gene containing substantial but different deletions in the COOH-terminal region was found in many HBV-infected HCC patients [13][14][15][16] .…”