HOW CAN I-3-C REDUCE CANCER RISK? Biochemists tell us that the biochemical reaction pathway which has the dangerous C-16 estrogen (which they call 16-hydroxyestrone) as an intermediate is mediated by certain enzymes in a group called "mixed function oxidases" (MFO's for short). But if this large and diverse set of MFO enzymes is kept in a state of readiness (the enzymes are sufficiently activated), then in principal, at least, virtually any type of toxic substance (including carcinogens) can be rendered harmless before it crosses the inner lining surface of the lungs or intestinal tract and gets into the bloodstream.(Wattenburg and Loub 1978, Mcdanell et al 1987) Now, if our MFO enzymes are so beneficial to us, and if their activation is so important, how then can we keep them activated and in a state of readiness so that our bodies can cope with any toxic substance in the best possible way? There are natural MFO activating substances which can and will do this. They include I-3-C and a member of the vitamin C group (which consists of at least seven distinct compounds) called ascorbigen.(Dashwood 1988) Actually, Ascorbigen contains I-3-C bound to ascorbic acid, but bound I-3-C cannot have the same effect as unbound I-3-C.(Kutacek 1962, Kutacek et al, 1963) I-3-C can come from the breakdown (possibly by intestinal bacteria) of a parent compound (called glucobrassicin) present in brassica vegetables. I-3-C can also combine with the ascorbic acid form of vitamin C to form another form of vitamin C, ascorbigen. (Or, Ascorbigen can split to yield more I-3-C). But there must be a reason why dietary supplements of both I-3-C and ascorbigen have been observed to produce up to an 80-fold increase in intestinal MFO activity --much more than when either substance was used separately (Graham 1978, Byers and Graham 1984, McDanell et al 1987) Now let us further explore the fascinating question of how the injestion of either Brassica vegetables (or the I-3-C ascorbigen combination as a dietary supplement) can lower the blood level of such a dangerous steroid metabolic breakdown product as C-16. We have previously credited Wattenberg with the observation that it appears that I-3-C is responsible for the decrease in the incidence of the cancers he studied, especially intestinal cancer. (Wattenberg 1978, Wattenberg and Loub 1978, Pantuck et al 1979) Later, McDanell observed that this increased MFO activation occurred in the liver as well as the intestinal tract of experimental mammals that were fed cabbage, and that the increased activation was correlated with increases in I-3-C levels that were found in these organs. (McDanell et al 1987)

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