In the 1980s, the above point served as the major reason for the development of centrilobular necrosis after administration of compounds which require metabolic activation. Centilobular localization of the P450s was demonstrated as an alternative to, say, alcohol dehydrogenase located in the periportal region. Does the current branch of biochemical toxicologists, while knowing about multiple molecular forms of hepatic CYP, follow those old dogmas? 

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