抄録
In the previous part of the present studies"), the influennce of eugenol on glucuronidation in the rat was reported.In this part, attempts were made to find similar influences in other glucosidurogenicdrugs, such as phenol, benzyl alcohol, benzoic acid, and aniline. At tlte same time, studies were made on the influence of such drug upon the glucuronic acid pathway inrats subjected to a massive administration of these glucosidurogenic drugs.The following results were obtained.I) Phenol, benzyl alcohol, and aniline orally administered caused a significantincrease in UDP-glucuronyltransferase (GT) activity in rat liver in the same manner aseugenol (Table l).2) The excretion of the ether type of glucuronide in rat urine showed such agreat increase after oral administration of phenol and aniline as eugenol (Table 2).3) In experiments in vitro on phenol, 3.0X 10-3 M of penol exhibited a 505 inhibi-tion of the glucuronidation of a substrate (2.0 x 10 M of 7t-nitrophenol), while 1.1 X 10-4M of eugenol presented the same effect upon this substrate (Fig. l). The inhibition ofGT by phenol was also competitive in nature as in the case of eugenol. The Ki valueof penol, however, was 2.5XlO- M, ox 5 times as large as that of eugenol (Fig. 2).4) None of these glucosidurogenic drugs administered orally to rats exerted anyinfluence on the hepatic or serum /3-glucuronidase activity, the hydrolytic enzyme ofglucuronide (Table 3), or the urinary excretion of t-ascorbic acid and n-glucaric acid, both of which are pathway metabolites of r>-glucuronic acid (Table 4).
