Add time:07/16/2019         Source:sciencedirect.com

Hydroxylation of 4-chloropropionanilide (cas 2759-54-8) to 4-chlorohydracrylanilide, ω-hydroxylation, and to 4-chlorolactanilide, (ω-1)-hydroxylation, by rabbit liver microsomes were found to be stimulated differently by treatment of rabbits with phenobarbital or 3-methylcholanthrene. ω-Hydroxylation was not stimulated by 3-methylcholanthrene, but increased to nineteen times the normal rate by treatment with phenobarbital. (ω)-1)-Hydroxylation increased in rate by only 70 per cent after treatment with phenobarbital and by 200 per cent after treatment with 3-methylcholanthrene. On storage of microsomes for 18 days ω-hydroxylation decreased by 40 per cent and (ω-1)-hydroxylation remained unchanged. ω-Hydroxylation showed lower affinity for oxygen and higher sensitivity to the inhibiting effect of carbon monoxide than (ω-1)-hydroxylation. Hydroxylation of the acetic acid residue in 4-chloroacetanilide and acetophenone did not uniformly follow ω- or (ω-1)-hydroxylation of 4-chloropropionanilide. Treatment of rabbits with phenobarbital stimulated ω-hydroxylation of acetophenone and did not affect ω-hydroxylation of 4-chloroacetanilide.

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