Abstract
The human large intestine is host to a diverse range of bacteria with numbers reaching 10 11 /ml of faecal material. This population plays a significant role in colonic metabolism and health. Undigested dietary substrates and endogenous residues are metabolised by the gut flora. Some of the products of this metabolism have been associated with carcinogenic processes such as tumour promotion (ammonia, secondary bile acids), mutagenesis (fecapenaenes) and carcinogenesis ( N -nitroso compounds). Bacterial enzymes involved with carcinogen formation include g -glucuronidase, g -glycosidase, azoreductase, nitroreductase, nitrate reductase, the conversion of pre-carcinogen 2 amino-3-methyl-7H-imidazo[4,5-f]quinoline (IQ) to 7-hydroxy-2-amino-3,6-dihydro-3-methyl-7H-imidazo[4,5-f]quinoline-7-one (7OHIQ). Protective effects of gut bacterial metabolism include carcinogen binding, detoxification of methylmercury and formation of lignans and isoflavones. Diet is known to play a role in gut microflora metabolism and cancer development. Studies have shown that gut bacterial enzymes are affected by diet and bacterial metabolism of dietary protein releases toxic products including ammonia, phenols and cresols. The interrelationships between diet, gut microflora metabolism and effects on the host are complicated however they may be important in the understanding of epidemiological associations between exogenous factors and colorectal cancer risk.