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At least 595 records · Page 33Linked to original sources
PubMed1981

Metabolic study of 7-methylbenzo[a]pyrene with rat liver microsomes: separation by reversed-phase and normal-phase high performance liquid chromatography and characterization of metabolites.

The 7-methylbenzo[a]pyrene (7-MBaP) was incubated with liver microsomes of rats pretreated with polychlorinated biphenyls (Aroclor 1254) (PCBs). Metabolites of 7-MBaP were isolated by both reversed-phase and normal-phage high performance liquid chromatography (HPLC) and were characterized by nuclear magnetic resonance, UV-visible and mass spectral analyses. The predominant metabolite of 7-MBaP was found to be 3-hydroxy-7-methylbenzo[a]pyrene (3-hydroxy-7-MBaP). Other identified metabolites include 7-MBaP 4,5-, 7,8-, and 9,10-trans-dihydrodiols, 7-hydroxymethyl-BaP, 7-hydroxymethyl-BaP trans-9,10-dihydrodiol, 9-hydroxy-7-MBaP, 3-hydroxy-7-hydroxymethyl-BaP, 7-MBaP 1,6- and 3,6- quinones, and a hydroquinone which is also formed by further metabolism of the 3-hydroxy-7-MBaP. Comparative metabolic studies of 7-MBaP and BaP indicated that, relative to that of BaP, the methyl substituent of 7-MBaP slightly increases the formation of 3-hydroxy-7-MBaP and decreases the metabolism at other regions of the 7-MBaP molecule. The finding that a 7,8-dihydrodiol is a metabolite indicates that, like BaP, 7-MBaP may also be activated to the potentially reactive 7,8-dihydrodiol 9,10-epoxides although their formations are significantly reduced.

Animals↗
PubMed1982

Formation of mutagenic metabolites from benzo(a)pyrene and 2-aminoanthracene by the s-9 fraction from the liver of the Northern pike (Esox lucius): inducibility with 3-methylcholanthrene and correlation with benzo[a]pyrene monooxygenase activity.

The mutagenicity of benzo[a]pyrene and 2-aminoanthracene in the Ames test using the S-9 fraction from the liver of the Northern pike (Esox lucius) was tested. S-9 fractions were prepared both from fish injected intraperitoneally with 3-methylcholanthrene and from control animals. In addition benzo[a]pyrene monooxygenase activity was assayed in the same S-9 fractions used in the Ames test. S-9 fractions from the liver of the Northern pike were found to convert benzo[a]pyrene and 2-aminoanthracene to mutagenic metabolites. The number of revertants obtained was increased 2--4-fold in the case of 2-aminoanthracene and 3--14-fold in the case of benzo[a]pyrene by pretreatment of the pike with a single intraperitoneal injection of 3-methylcholanthrene. This injection also caused a 2--6-fold increase in the benzo[a]pyrene monooxygenase activity of the S-9 fractions used. These increases in mutagenicity and activity of the S-9 fractions used. these increases in mutagenicity and activity occur mainly during the first 4--12 days after the injection, but further small increases are observed for as long as 60 days. A strong positive correlation was found between the benzo[a]pyrene monooxygenase activity of the S-9 fractions used and their ability to give rise to revertants in the Ames test using 2-aminoanthracene or benzo[a]pyrene. This indicates that the major determining factor in the production of reactive metabolites which attack DNA in this in vitro system is the activity of the phase I cytochrome P-450 system.

Animals↗
PubMed1982

Differences in murine procarcinogen activation enzymes are not accompanied by parallel differences in procarcinogen-induced sister-chromatid exchange.

C57Bl/6 and DBA/2 mice, strains in which there is marked induction of hepatic monooxygenase activity by phenobarbital, were tested for in vivo sister-chromatid exchange (SCE) formation in response to cyclophosphamide, an agent metabolized by this inducible enzyme system. Baseline SCE frequencies were between 4 and 6 SCEs/cell in regenerating liver and bone marrow of both strains of mice. Administration of cyclophosphamide (5mg/kg) led to an increase of nearly 8 SCEs/cell in both tissues of C57Bl/6 mice and an increase of more than 10 SCEs/cell in DBA/2 mice. Prior exposure to phenobarbital induced p-chloromethylaniline demethylase activity in regenerating liver of both mouse strains approx. 6-fold, but the changes in measured SCE frequencies were not significantly different from those obtained in the absence of enzyme induction. These results, together with our previous observation that induction by 3-methylcholanthrene of benzo[a]pyrene hydroxylase activity in the same mouse strains was not accompanied by a comparable change in benzo[a]pyrene-induced SCE formation, reinforce the impression that simple assays of differences in mixed function oxidase activities may not necessarily be good predictors of hereditary differences in the response to genetic damage by procarcinogens which are presumed to be metabolized by these enzymes.

Animals↗
PubMed1982

Hepatic microsomes from freshwater fish--II. Reduction of benzo(a)pyrene metabolism by the fish anesthetics quinaldine sulfate and tricaine.

1. A single in vivo exposure of brook trout (Salvelinus fontinalis) to a 30.0 mg/l solution of quinaldine sulfate or a 112.5 mg/l solution of tricaine for 5 min significantly reduced the in vitro hydroxylation of benzo(a)pyrene. 2. Since quinaldine sulfate and tricaine formed type I and II binding spectra, respectively, with brook trout hepatic cytochrome P-450, these chemicals probably reduced benzo(a)pyrene hydroxylase enzyme activity by altering the form(s) of cytochrome P-450 responsible for this activity. 3. Hepatic microsomal cytochrome P-450 from brook trout treated with tricaine for 5 min and then placed into fresh water for 24 hr had returned to control levels. 4. Caution should be exercised in the use of quinaldine sulfate or tricaine to anesthetize fish prior to analysis of hepatic microsomal mixed function oxidases.

Aminobenzoates↗
PubMed1980

The effect of long term treatment with disulfiram on content of cytochrome P-450 and on benzo(a)pyrene monooxygenase activity in microsomes isolated from the rat small intestinal mucosa.

Disulfiram (DS) was administered perorally once a day to rats for 30 days to investigate the effects on cytochrome P-450 content and benzo(a)pyrene (BP) monooxygenase activity in microsomes isolated from the small intestinal mucosa. 50 mg or 100 mg DS/kg body weight caused a dose-related increase in BP monooxygenase activity, whereas the content of cytochrome P-450 was increased at the higher dose only. Similar absorption characteristics of cytochrome P-450 and turnover rates for BP on the basis o f cytochrome P-450 was observed among the different microsomal preparations. The addition of DS or diethyldithiocarbamate (DDTC) to incubates of intestinal microsomes inhibited BP monooxygenase activity. Microsomes isolated from DS-treated rats were however less sensitive to in vitro inhibition by DS.

Animals↗
PubMed1983

Comparative properties of purified cytochrome P-448 from beta-naphthoflavone treated rats and rainbow trout.

1. Cytochrome P-448 from beta-naphthoflavone treated rainbow trout (Salmo gairdnerii) liver was purified and compared to purified P-448 from beta-naphthoflavone treated rats (Rattus rattus) and purified P-450 from phenobarbital induced rats. 2. The two P-448 forms had similar spectral properties, substrate specificity, sensitivity to inhibitors and regioselectivity in the metabolism of benzo(a)pyrene and testosterone. 3. Rat and trout P-448 differed in apparent monomeric mol. wt (Mr) by at least 2000 daltons, and did not share identical antigenic determinants. Both rat and trout P-448 were shown to be quite different from rat P-450 using all of the above criteria for distinguishing multiple forms.

Animals↗