Beta Glucuronidase

The formation of glucuronides in the liver is an important mechanism for detoxifying and enhancing excretion of a large number of orally ingested nutrients and their end products, other dietary compounds, and drugs, as well as endogenously synthesized compounds, such as estrogens. In humans many of these glucuronides depending on the structure of the aglycone, are excreted in the bile, and subsequently enter the duodenum. The glucuronides are then subject to bacterial deconjugation primarily in the ileum and colon. As a consequence of this bacterial deconjugation physiologically active, toxic, and carcinogenic compounds are regenerated. In addition to their formation in the intestine these compounds can be reabsorbed into the portal blood system. This results in recycling of these hydrolyzed glucuronides, and this process is referred to as the enterohepatic circulation.

Several studies have shown that intestinal beta-glucuronidase can alter or amplify the biological activity of exogenous and endogenous compounds.

The metabolism of the carcinogen N-hydroxyflourenylacetamide administered parenterally to conventional and germfree rats was studied by Weisburger et al. (60). Germfree rats excreted larger amounts of the glucuronides of N-hydroxyflourenylace-tamide in their feces compared to conventional animals. The cecal and fecal contents of conventional rats contained mostly unconjugated N- hydroxyflourenylacetamide, and its metabolites; in contrast most of these metabolites were glucuronide or sulfate conjugates in germfree animals.

It has been shown that cell-free extracts derived from a number of different bacteria residing in the intestinal tract, including Bacteroides fragilis, Bacteroides vulgatus, Bacteroids thetaiotamicron, Eubacterium eligens, Peptostreptoccus, and Escherichia coli, were capable of increasing the mutagenic activity of bile from rats fed 1-nitropyrene via stomach tube. These extracts had beta-glucuronidose activity. Cell-free extracts of bacteria that were not able to enhance the mutangenicity of the bile did not possess beta-glucuronidose activity (61). These data support the hypothesis that glucuronides of 1-nitropyrene metabolites entering the bile can be hydrolyzed by intestinal bacterial beta-glucuronidase to produce active deconjugated mutagenic products.

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