Human hepatoma which had been xenografted into nude mice have been estimated for their ability to catalyze glucuronic acid and glucose conjugation of endogenous compounds and p-nitrophenol. The xenobiotic p-nitrophenol was glucuronidated with a comparable rate in microsomes from human hepatoma, human liver and host liver. With regard to glucuronic acid or glucose conjugation of the endogenous compounds of bile acids, bilirubin and steroid hormones, glucosidation of bile acids was the only conjugation mechanism that was not decreased or deficient in microsomes from hepatoma, but showed about a 2-fold increase in reaction rate compared to normal human liver. Human hepatoma and host liver were shown to respond to phenobarbital treatment which led to about a 2-fold increase in UDP-glucuronosyltransferase activity toward bilirubin in hepatoma and in host liver. Compared to normal tissues, alterations in the pattern of glycoside conjugating enzymes were not only observed in microsomes from human hepatoma, but also in microsomes from human adenocarcinoma of the kidney, exhibiting negligible UDP-glucuronosyltransferase activities toward bile acids and steroid hormones. Bile acid glucoside formation was measurable in kidney adenocarcinoma with an activity which was similar to the activity observed in hepatoma. In comparison to normal renal tissue, glucose-conjugating activity toward bile acids decreased about 2-fold in kidney adenocarcinoma.