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Mouse intestinal microsomes (MIM) were prepared as described for mouse liver microsomes.
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Immunoblot analysis was used to assess the Cyp3a expression in liver and intestinal microsomes from mouse exposed orally to Nar.
With the loss of hepatic CPR, liver microsomes of LCN mice had no activity in formaldehyde formation, whereas the activities of the intestinal microsomes of LCN mice were comparable to those of WT mice.
Human hepatic and intestinal microsomes were obtained as described previously.
Human hepatic microsomes were obtained from 10 donors, and human intestinal microsomes were obtained from 13 donors.
Human intestinal microsomes (HIM) were purchased from BD Gentest Corp. (Woburn, MA, USA).
In contrast, the glucuronidation activity of intestinal microsomes did not significantly differ with the type of metabolites.
We first demonstrated that only two of the synthesized stilbenoids, NI-ST-05 and NI-12a, were substrates for recombinant UGT enzymes and human hepatic and intestinal microsomes.
Glucuronidation by human hepatic and intestinal microsomes is presented as the line of median value and the error bars represent the range of values.
The involvement of hepatic and intestinal UGTs in the metabolism of both compounds was further confirmed using a panel of human liver and intestinal microsomes, and high individual variation in activity was demonstrated between donors.
Screening experiments for glucuronidation activity were also carried out with human hepatic and intestinal microsomes from 10 and 13 donors, respectively, one pooled liver sample, and commercially available hepatosomes.
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