Nexus between Hepatic Enzyme Modulation and Cancer

Order of Publishing in Issue: 
Volume :5
Issue :4
October, 2011
Page No: 
Cinoy Maliakal, Hima Pius, Chris M. Lee and Umesh T. Sankpal
Cancer Research Institute, MD Anderson Cancer Center Orlando Orlando, FL 32827 USA
Florida State University College of Medicine Tallahassee, FL 32306, USA

The risk of developing cancer caused by environmental carcinogens lies in the balance between phase I carcinogen-activating enzymes and phase II detoxifying enzymes. Potentially genotoxic chemicals to which we are exposed to may require metabolic activation to exhibit their mutagenic and carcinogenic effects. Most of the enzyme systems, involved in carcinogen bioactivation, are concentrated in liver, but many extrahepatic organs and tissues have appreciable quantities of such enzymes. Most chemical carcinogens are activated in humans by specific cytochrome P450 (CYP) species, mainly CYP1A1, CYP1A2, CYP2E, and CYP3A. Activation of chemical carcinogens follows various metabolic pathways. The difference could range from only a single oxidation step or several sequential enzymatic steps. Polymorphic differences in carcinogen metabolism may result in difference in carcinogen risk since fast activators and/or slow detoxifiers may have higher steady state tissue concentration of the causative agent than slow activator and/or fast detoxifiers. Cancer prevention through better diet and nutrition has received considerable attention in the past and continues to show promise even today.” It has become increasingly apparent that adopting a diet may allow reduction in cancer incidence worldwide by functioning as inhibitors of tumor initiation, promotion, and progression, which may be mediated by either selective induction or inhibition of the hepatic xenobiotic metabolizing enzymes.

Bioactivation, carcinogens, cytochrome P450, cancer prevention, hepatic enzymes
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