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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Glucuronidation of diflunisal in liver and kidney microsomes of rat and man.

1. The glucuronidation of diflunisal to its phenolic (DPG) and acyl glucuronide (DAG) was measured in vitro using microsomes prepared from rat (n = 4) and human (n = 6) liver and kidney tissue. UGT activities towards bilirubin, 4-nitrophenol and (-)-morphine were also determined. 2. beta-Glucuronidase activity towards phenolphthalein glucuronide was much lower in microsomes prepared from human liver (45.2 +/- 3.1 Fishman Units/mg protein), human kidney (22.0 +/- 3.3 FU/mg), and rat kidney (25.1 +/- 2.5 FU/mg) as compared with rat liver (118.7 +/- 8.8 FU/mg). 3. The formation rate of DAG significantly increased when saccharo-1,4-lactone, a beta-glucuronidase inhibitor, was added to the rat liver microsomal incubation medium. beta-Glucuronidase inhibition, however, had little effect on the formation rate of DAG in human liver microsomes, and no effect in rat and human kidney microsomes. The formation of DPG was not affected by the microsomal beta-glucuronidase activity. 4. Unlike rat kidney microsomes, which only formed DAG, human kidney microsomes formed both diflunisal glucuronides. Formation of both diflunisal glucuronides in human kidney microsomes (Vmax = 0.97 +/- 0.21 and 0.27 +/- 0.07 nmol/min/mg for formation of DAG and DPG respectively) represented 60-70% of the activity found in liver microsomes (Vmax = 1.58 +/- 0.32 and 0.40 +/- 0.08 nmol/min/mg for formation of DAG and DPG respectively). 5. These results demonstrate that the in vitro glucuronidation rate of diflunisal may be affected by the microsomal beta-glucuronidase activity particularly when using rat liver microsomes. Our results also demonstrate that the human kidney has an important UGT-activity towards diflunisal.[1]

References

  1. Glucuronidation of diflunisal in liver and kidney microsomes of rat and man. Brunelle, F.M., Verbeeck, R.K. Xenobiotica (1996) [Pubmed]
 
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