Aflatoxin Exposure in Singapore: Blood Aflatoxin Levels in Normal Subjects, Hepatitis B Virus Carriers and Primary Hepatocellular Carcinoma Patients

1994 ◽  
Vol 34 (4) ◽  
pp. 289-298 ◽  
Author(s):  
Tzee Cheng Chao ◽  
Dst Lo ◽  
B Chen Bloodworth ◽  
R Gunasegaram ◽  
T H Koh ◽  
...  

Blood screening conducted on Singaporeans over 1991–1992 showed exposure to predominately aflatoxin B1 and to a lesser extent G1. The extent of exposure to B1 among three groups of residents in Singapore, namely normal subjects (n = 423), hepatitis B virus carriers (n = 302) and primary hepatocellular carcinoma (PHC) patients (n = 58) were extensive as reflected by the positive rates of 15.1, 0.7 and 1.7 per cent respectively. However, the degree of individual exposure to this toxin among the three groups was considered low as shown by the low respective mean blood levels of 5.4 ± 3.2 (range 3.0–17), 7.7 (range 7.5–7.9) and 7.5 picogrammes per ml of blood. It is not immediately clear whether or not such low levels would precipitate an undesirable health effect. The higher positive rate seen in normal subjects as compared with the other groups could be due to differences in dietary intake of aflatoxin B1, differences in metabolic patterns or both. About 70 per cent of PHC patients studied were carriers. The degree of aflatoxin B1 exposure among normal subjects in Singapore was a factor of 22.1 times less than that in Japan, 40.9 times less than that in Indonesia and 51.3 times less than that in the Philippines. Similarly, the extent of exposure among hepatitis B carriers in Singapore was a factor of 8.2 times, 39.6 times and 24.2 times less than those in the other three Asiatic countries respectively. The results reflected stringent Government control over the quality of food stuff imported into this country. As Singapore imports almost all its dietary needs from elsewhere, it can afford to be selective at a cost. Aflatoxin M1, a metabolite of B1, was most commonly encountered in the liver tissues of deceased (n = 154) who died of causes other than sickness or disease in 1992–93, consistent with our blood findings of prevalence of aflatoxin Bl. High performance liquid chromatography (HPLC) with fluorescence detection using one of the aflatoxins G2 or B2 as an internal standard was used for the detection and quantification of aflatoxins. The use of an internal standard structurally and chemically similar to those required to be quantified minimizes errors in quantifications. This is because differences in the quenching of fluorescence between specimen extracts and spiked-standard extracts were internally standardized and compensated for. The presence of an internal standard also helped to locate aflatoxins of interest more accurately. Strict decontamination procedures for cleaning glassware and apparatus were adhered to, to reduce cross-contaminations. Only duplicate-positive results were taken to be positive.

2017 ◽  
Vol 6 (10) ◽  
pp. 2357-2369 ◽  
Author(s):  
Xiao Xiang ◽  
Hong-Gui Qin ◽  
Xue-Mei You ◽  
Yan-Yan Wang ◽  
Lu-Nan Qi ◽  
...  

1983 ◽  
Vol 11 (2) ◽  
pp. 99-104 ◽  
Author(s):  
Whan Kook Chung ◽  
Hee Sik Sun ◽  
Doo Ho Park ◽  
Gerald Y. Minuk ◽  
Jay H. Hoofnagle

1985 ◽  
Vol 151 (4) ◽  
pp. 604-609 ◽  
Author(s):  
W. L. M. Alward ◽  
B. J. McMahon ◽  
D. B. Hall ◽  
W. L. Heyward ◽  
D. P. Francis ◽  
...  

2009 ◽  
Vol 18 (3) ◽  
pp. 846-853 ◽  
Author(s):  
Hui-Chen Wu ◽  
Qiao Wang ◽  
Hwai-I Yang ◽  
Habibul Ahsan ◽  
Wei-Yann Tsai ◽  
...  

1979 ◽  
Vol 24 (4) ◽  
pp. 421-429 ◽  
Author(s):  
A. Goudeau ◽  
Ph. Maupas ◽  
P. Coursaget ◽  
J. Drucker ◽  
J. P. Chiron ◽  
...  

2007 ◽  
Vol 10 (2) ◽  
pp. 15-22 ◽  
Author(s):  
S Metodieva

Molecular Pathogenesis of Hepatocellular CarcinomaThe most important risk factors for the development of human hepatocellular carcinoma (HCC) are chronic infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV), high dietary exposure to hepatic carcinogen aflatoxin B1 and alcohol abuse. Hepatitis B virus exerts its effects through integration of the viral DNA into the hepatocyte genome, or through acting as transcriptional regulator for several cellular proto-oncogenes and tumor-suppressor genes. Hepatitis C virus may affect hepatocytes via the transcriptional regulation activity of the HCV core protein or via the HCV non structural proteins NS5A, NS5B and NS2, interfering with the regulation of cell cycle and apoptosis. Environmental exposure to aflatoxin B1 can cause a specific missense mutation in codon 249 of the p53 tumor-suppressor gene. Habitual alcohol consumption leads to production of reactive oxygen species and peroxidation damage to DNA. The objective of this review is to make you acquainted with the most common risk factors and the most frequent genetic aberrations associated with the development of HCC.


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