Microsomal enzyme induction following repeated oral administration of LAAM.
The oral administration of 1-alpha-acetylmethadol (LAAM) in the mouse was shown to cause a significant elevation in the hepatic LAAM N-demethylase activity. Compared to the self-induction phenomena found with methadone and propoxyphene, LAAM was three and two times more potent, respectively, on a molar basis than these two structurally similar narcotic analogs. Moreover, microsomal induction by LAAM resulted in significant elevations of aminopyrine N-demethylase and aniline hydroxylase activities. These effects were also correlated with a dose related decrement of pentobarbital sleeping time. Thus LAAM appears to be a relatively potent inducer of microsomal metabolism.
D000633:Aminopyrine N-Demethylase / Q000096:biosynthesis; D000815:Aniline Hydroxylase / Q000096:biosynthesis; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004285:Dogs; D004790:Enzyme Induction / Q000187:drug effects; D008297:Male; D008691:Methadone / Q000031:analogs & derivatives*; D008692:Methadyl Acetate / Q000494:pharmacology* / Q000633:toxicity; D008780:Methyltransferases / Q000096:biosynthesis; D051379:Mice; D008813:Mice, Inbred ICR; D008862:Microsomes, Liver / Q000201:enzymology*; D009929:Organ Size / Q000187:drug effects; D010424:Pentobarbital / Q000494:pharmacology; D012890:Sleep / Q000187:drug effects; D013997:Time Factors
D000815:Aniline Hydroxylase; D000633:Aminopyrine N-Demethylase; D008780:Methyltransferases; D010424:Pentobarbital; D008692:Methadyl Acetate; D008691:Methadone