Tolerance to methadone lethality and microsomal enzyme induction in mice tolerant to and dependent on morphine

Drug Alcohol Depend. 1980 Jan;5(1):27-37. doi: 10.1016/0376-8716(80)90168-4.

Abstract

In an attempt to explain a loss of cross-tolerance between morphine and methadone and an increased tolerance to methadone lethality in morphine-dependent mice administered methadone orally for six days, the possibility that methadone was stimulating its own metabolism was investigated. It was found that methadone did enhance its own metabolism two-fold. This increase in activity correlated with the development of tolerance to the lethal effects of methadone as measured by an elevation of the oral methadone LD50. Furthermore, SKF-525A, a potent microsomal inhibitor, abolished this tolerance. The intracerbroventricular methadone LD50 was not altered by six days administration of oral methadone, suggesting that the tolerance observed was dispositional in nature.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Body Weight / drug effects
  • Drug Tolerance
  • Enzyme Induction / drug effects
  • Humans
  • Inactivation, Metabolic
  • Lethal Dose 50
  • Liver / enzymology
  • Male
  • Methadone / pharmacology*
  • Mice
  • Microsomes, Liver / enzymology
  • Microsomes, Liver / metabolism
  • Morphine / pharmacology*
  • Morphine Dependence / metabolism*
  • Oxidoreductases, N-Demethylating / metabolism
  • Proadifen / pharmacology

Substances

  • Morphine
  • Proadifen
  • Oxidoreductases, N-Demethylating
  • Methadone