High impact information on p-Chloro-N-methylaniline

• By contrast, treatment with phenobarbital did not affect the hepatic microsomal PG's hydroxylation, although the hydroxylation of benzpyrene and the demethylation of ethylmorphine, benzphetamine, and PCMA were enhanced [1].
• p-Chloro-N-methylaniline demethylase activity in liver and extrahepatic tissues of the human fetus and in chick embryo liver [2].
• We achieved a 50-fold increase in sensitivity of a fluorescence assay for p-chloro-N-methylaniline (p-CNMA) demethylase enabling us to examine the kinetics of the reaction in chick embryo liver and human fetal tissues and its inducibility in chick embryo liver [2].
• N-demethylation of p-chloro-N-methylaniline catalyzed by subcellular fractions from the avocado pear (Persea americana) [3].
• The primary products of the reaction between 4-fluoro-N,N-dimethylaniline-N-oxide (FDANO) or 4-chloro-N,N-dimethylaniline-N-oxide (ClDANO) with cytochrome c, 4-fluoro- and 4-chloro-N,N-dimethylaniline, 4-fluoro- and 4-chloro-N-methylaniline, 2-dimethylamino-5-fluoro-phenol, and 2-dimethylamino-5-chloro-phenol were isolated and identified [4].

Biological context of p-Chloro-N-methylaniline

• 1. N-Hydroxylation of p-chloroaniline (PCA) and p-chloro-N-methylaniline (PCMA) was measured in red-winged blackbird (Agelaius phoeniceus) and rat (Rattus norvegicus) hepatic microsomes [5].
• The effect of prostaglandins (PGs) on the hepatic biotransformation of hexobarbital (Hechi) and p-chloro-N-methylaniline (PCMA) was determined in male rats [6].

Associations of p-Chloro-N-methylaniline with other chemical compounds

• Twelve days of continuous s.c. tumor growth significantly increased hepatic cyclic AMP levels, while levels of cyclic GMP, cytochrome P-450, cytochrome b-5, and p-chloro-N-methylaniline metabolism were significantly decreased [7].

Gene context of p-Chloro-N-methylaniline

• The differences in sensitivity of renal and hepatic AHH and PCNMA activities to the inhibitors may have been due to organ-specific differences in the affinities of the inhibitors for interaction with the active site(s) on cytochrome P-450 [8].

References