ABSTRACT

CONTENTS 6.1 Acute Toxicity and Carcinogenicity of Aflatoxin to Humans........... 128

6.1.1 Biochemical Activation of Aflatoxins ........................................ 129 6.1.2 Biochemical Activation in the Liver .......................................... 129 6.1.3 Biochemical Activation in the Lung .......................................... 131 6.1.4 Photoactivation.............................................................................. 131

6.2 Molecular Mechanism of Action of Aflatoxins.................................... 132 6.2.1 Relationship between Carcinogenicity, Mutagenicity,

and Acute Toxicity and AF Binding to Cellular Macromolecules ............................................................................ 132

6.2.2 Molecular Aspects of AFB1-DNA Binding .............................. 132 6.2.3 Genetic Consequences of AFB1-DNA Binding........................ 134

6.2.3.1 Mutagenesis .................................................................... 135 6.2.3.2 Immunosuppression...................................................... 135 6.2.3.3 Teratogenicity of Aflatoxin B1 ..................................... 135 6.2.3.4 Relationship between Primary Liver Cancer

and the Specificity of AFB1 in DNA Binding and Mutagenesis ............................................................ 135

6.2.3.5 Synergy between Aflatoxin B1 and Hepatitis Virus in Hepatocellular Carcinoma............................ 136

6.2.4 Prevention of AFB1-Induced Hepatocellular Carcinoma....... 137 6.2.4.1 Monitoring and Detection ............................................ 137 6.2.4.2 Dietary Supplements for Chemoprevention ............. 137

References ........................................................................................................... 138

Aflatoxins (AFs) are products of Aspergillus and Penicillium species. They are highly potent in the induction of acute toxicity in animals and in humans. Approximately 4.5 billion people are exposed to uncontrolled amounts of AFB1 in the third world.