Metabolic host factors as modifiers of reactive intermediates possibly involved in human cancer.

Abstract

The current theory of the mechanism of chemical carcinogenesis is that precarcinogens are metabolized by mostly mixed-function oxidases into rteacive intermediates that act as ultimate carcinogens (Miller and Miller, 1966) the liver and in extrahepatic organs (Vainio and Hietanen, 1980). The Wide variation among human individuals in the enzymes involved in metabolic actvation of xenobiotics may be due in part to host factors and to interactins with environmental exposures (Table 1; Farrell et al., 1979; Sotaniemi et al., 1980). These factors include different life styles, genetic differences and the various clinical and subclinical diseases that may alter liver metabolism in man during his relatively long life span (Vesell, 1982). Exposure to cancer-causing foreign compounds appears to beone of the most important environmentalrisk factors whereas the host-response to xenobiotics may modify individual risk for cancer arising from such exposures. Some current evidence for such an hypothesis is rerieved herein.