Brain microsomal metabolism of phencyclidine in male and female rats

被引:13
作者
Laurenzana, EM [1 ]
Owens, SM [1 ]
机构
[1] UNIV ARKANSAS MED SCI HOSP,COLL MED,DEPT PHARMACOL & TOXICOL,LITTLE ROCK,AR 72202
关键词
phencyclidine; brain metabolism; cytochrome P-450; drug abuse; central nervous system; high performance liquid chromatography;
D O I
10.1016/S0006-8993(97)00203-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
These studies examined the microsomal brain metabolism of phencyclidine (PCP) in male and female Sprague-Dawley rats. Several monohydroxylated metabolites of PCP were detected including cis- and trans-1-(1-phenyl-4-hydroxycyclohexyl)piperidine (c-PPC and t-PPC) and 1-(1-phenylcyclohexyl)-4-hydroxypiperidine (PCHP). The in vitro formation of these metabolites required NADPH and was inhibited by carbon monoxide. c-PPC was formed in the male and female brain microsomes at rates of 7.1 +/- 1.3 and 5.7 +/- 1.1 fmol/min per mg, respectively, while t-PPC was formed at rates of 16.2 +/- 3.3 and 16.5 +/- 4.2 fmol/min per mg. PCHP had the highest formation rate at 50.7 +/- 8.9 and 48.2 +/- 8.8 fmol/min per mg, respectively. Although previous studies with rat liver microsomes find higher levels of PCP metabolism in male rats and the formation of an irreversibly bound metabolite in male rats, the present study of brain metabolism found no sex differences in brain metabolism. The formation of PCP metabolites in male rat livers is at least partially mediated by the male-specific isozyme CYP2C11, and possibly CYP2D1. Nevertheless, the formation of the major brain metabolite, PCHP, was not inhibited by an anti-CYP2C11 or an anti-CYP2D6 antibody. However, PCHP formation was inhibited by drug inhibitors of CYP2D1-mediated metabolism, suggesting the involvement of a CYP2D isoform. These data indicate brain metabolism of PCP is significant, but unlike the liver it is not sexually dimorphic.
引用
收藏
页码:256 / 265
页数:10
相关论文
共 54 条
[1]   RAT-BRAIN CYTOCHROMES P-450 - CATALYTIC, IMMUNOCHEMICAL PROPERTIES AND INDUCIBILITY OF MULTIPLE FORMS [J].
ANANDATHEERTHAVARADA, HK ;
SHANKAR, SK ;
RAVINDRANATH, V .
BRAIN RESEARCH, 1990, 536 (1-2) :339-343
[2]  
BARBEAU A, 1985, LANCET, V2, P1213
[3]   SOME ASPECTS OF METABOLIC ACTIVATION OF CHEMICAL CARCINOGENS IN RELATION TO THEIR ORGAN SPECIFICITY [J].
BARTSCH, H ;
MARGISON, GP ;
MALAVEILLE, C ;
CAMUS, AM ;
BRUN, G ;
MARGISON, JM ;
KOLAR, GF ;
WIESSLER, M .
ARCHIVES OF TOXICOLOGY, 1977, 39 (1-2) :51-63
[4]   RECENT DEVELOPMENTS IN HEPATIC DRUG OXIDATION - IMPLICATIONS FOR CLINICAL PHARMACOKINETICS [J].
BROSEN, K .
CLINICAL PHARMACOKINETICS, 1990, 18 (03) :220-239
[5]  
BUCKPITT AR, 1983, J PHARMACOL EXP THER, V225, P8
[6]   ETHOXYPHENOXAZONES, PENTOXYPHENOXAZONES, AND BENZYLOXYPHENOXAZONES AND HOMOLOGS - A SERIES OF SUBSTRATES TO DISTINGUISH BETWEEN DIFFERENT INDUCED CYTOCHROMES-P-450 [J].
BURKE, MD ;
THOMPSON, S ;
ELCOMBE, CR ;
HALPERT, J ;
HAAPARANTA, T ;
MAYER, RT .
BIOCHEMICAL PHARMACOLOGY, 1985, 34 (18) :3337-3345
[7]   CLINICAL IMPLICATIONS OF THE COMPETITIVE-INHIBITION OF THE DEBRISOQUIN-METABOLIZING ISOZYME BY QUINIDINE [J].
CAPORASO, NE ;
SHAW, GL .
ARCHIVES OF INTERNAL MEDICINE, 1991, 151 (10) :1985-1992
[8]   THE ROLE OF HEPATIC MICROSOMAL-ENZYMES IN THE MODULATION OF PHENCYCLIDINE-INDUCED TOXICITY [J].
CHATURVEDI, AK ;
RAO, NGS ;
BERG, IE .
TOXICOLOGY, 1981, 22 (03) :245-254
[9]   ROLE OF THE AROMATIC GROUP IN THE INHIBITION OF PHENCYCLIDINE BINDING AND DOPAMINE UPTAKE BY PCP ANALOGS [J].
CHAUDIEU, I ;
VIGNON, J ;
CHICHEPORTICHE, M ;
KAMENKA, JM ;
TROUILLER, G ;
CHICHEPORTICHE, R .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1989, 32 (03) :699-705
[10]  
CONE EJ, 1992, J PHARM PHARTM, V34, P197