CYP2D: Brain Enzyme Involved in Induction of Analgesia and Codeine Dependency

Smoking is predisposed by social, environmental and genetic factors including variation in CYP2A6, CYP2D and CYP2B6, which encode nicotine and codeine metabolizing enzymes. In early adolescence, CYP2A6-induced slow nicotine metabolism was related with higher dependence and reduced cigarette consumption. Our commentary has fully extended prior work illustrating that slow nicotine metabolism mediated by CYP2A6, CYP2D and possibly CYP2B6, risk for tobacco addiction during adolescence. Inherited differences in the rate of nicotine and codeine elimination may induce neural responses. Thus smoking signals during early selfdiscipline can provide an understanding of possible mechanism involved for differences in smoking behaviors and response to cessation treatment. The levels and tissue distribution of codeine, codeine-6glucuronide (C6G), norcodeine, morphine and the morphine metabolites like morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) are present in blood, liver and brain. CYP2D6 and CYP2D genotypes in brain have not just laid a passive target role with receptor for drugs, pollutants, pesticides but also acted as active metabolizers.