A -Glucuronides

Fingerlings given single ip injection of 60 pg 2,3,7,8-TCDD/kg BW One week after injection, the bile contained at least 3 TODD metabolites plus the parent compound at least one of the metabolites was a glucuronide conjugate 31... 

The metabolites and metabolic pathway of a new anticonvulsant drug, sodium valproate, in rats were investigated using carbon-14 labeled sodium valproate. Most of the metabolites in urine and bile were a glucuronide conjugate of valproic acid. Free sodium valproate was as little as one-seventh of the total metabolites. In feces, only free sodium valproate was detected, and the possibility of enterohepatic circulation of sodium valproate was presumed. A part of dosed sodium valproate was excreted in expired air in the form of CO2. This degradative reaction took place in liter mitochondria and required CoA and oxygen. It was stimulated by ATP... 

The metabolites of ondansetron have been examined in urine and bile from rat and dog. The major pathways for metabolism of ondansetron are A-demethylation and hydroxylation Scheme 7.7). However, whereas A-de-methylation predominates in dog, this is only a minor metabolic route in rat. Hydroxylation may occur at the 6, 7 or 8 position in the carbazolone ring. Hydroxy metabolites of ondansetron are excreted predominantly as glucuronide or sulphate conjugates. Studies with immobilised glucuronyl-transferase (Heath, S.E., personal communication) have demonstrated that O- and A-glucuronidation of ondansetron metabolites may occur. 

In adult female CFY rats exposed by inhalation (whole-body) to nominal concentrations of 1,000 ppm 1,4-dichlorobenzene, 3 hours a day for 10 days, analysis of metabolites in urine indicated that more than 50% was a sulfate of 2,5-dichlorophenol, and much of the rest was a glucuronide conjugate of... 

Methylation of some form of 6-mercaptopurine in man has been established by the identification of 6-(methylsulphinyl)-8-hydroxypurine (LXV), 6-(methylthio)uric acid (LX), and 6-(methylthio)-8-hydroxy-A -glucuronide (LXVll). The oxidation of 6-(methylthio)purine to 6-(methylthio)-8-hydroxy-purine (LXVl) is mediated much more rapidly by rabbit liver aldehyde oxidase than by xanthine oxidase, and the oxidation is not inhibited by 4-hydroxy-pyrazolo [3, 4-d] pyrimidine [269], which is known to be an effective inhibitor of xanthine oxidase, and consequently, of the oxidation of 6-mercaptopurine [12,268]. 

Metabolism - Following an oral dose of dipyridamole, the average time to peak concentration is approximately 75 minutes. The decline in plasma concentration fits a two-compartment model. The half-life (the initial decline following peak concentration) is approximately 40 minutes. The half-life (the terminal decline in plasma concentration) is approximately 10 hours. Dipyridamole is highly bound to plasma proteins. It is metabolized in the liver where it is conjugated as a glucuronide and excreted with the bile. 

Identification of azo pigment B as a glucuronide of azo pigment A was demonstrated independently by Billing et al. (B12) and Schmid... 

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