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Phenobarbital with hepatic microsomal

Production of Metabolites from 1,1- Dichloroethane with Hepatic Microsomes from Phenobarbital- Induced Rats... [Pg.9]

Compounds that affect activities of hepatic microsomal enzymes can antagonize the effects of methyl parathion, presumably by decreasing metabolism of methyl parathion to methyl paraoxon or enhancing degradation to relatively nontoxic metabolites. For example, pretreatment with phenobarbital protected rats from methyl parathion s cholinergic effects (Murphy 1980) and reduced inhibition of acetylcholinesterase activity in the rat brain (Tvede et al. 1989). Phenobarbital pretreatment prevented lethality from methyl parathion in mice compared to saline-pretreated controls (Sultatos 1987). Pretreatment of rats with two other pesticides, chlordecone or mirex, also reduced inhibition of brain acetylcholinesterase activity in rats dosed with methyl parathion (2.5 mg/kg intraperitoneally), while pretreatment with the herbicide linuron decreased acetylcholine brain levels below those found with methyl parathion treatment alone (Tvede et al. 1989). [Pg.115]

The hepatic microsomal a-hydroxylase activity for NPYR is inducible in rats by pretreatment with Aroclor, and in hamsters by pretreatment with Aroclor, 3-methylcholanthrene, phenobarbi-tal, and ethanol (10,15,19). In contrast, pretreatment of rats with 3-methylcholanthrene or phenobarbital causes no change or a slight decrease in microsomal NPYR o-hydroxylase activity (19). [Pg.61]

Klingensmith JS, Mehendale HM. 1983b. Hepatic microsomal metabolism of CC14 after pretreatrnent with chlordecone, mirex or phenobarbital in male rats. Drug Metab Dispos 11 (4) 329-334. [Pg.266]

Figure 1. Effect of potential inducing agents on certain hepatic microsomal enzymes of the rainbow trout. Animals were infected intraperitoneally with either phenobarbital (65 mg/kg) 3-methylcholanthrene (20 mg/kg) 2,3-benzanthracene (10 mg/kg) or /3-naphthoflavone (100 mg/kg). The animals were sacrified and hepatic microsome prepared 48 hr after infection. Each bar is the mean SE (n = 3-5) ( ), induced activity (T) significantly different from control (C) activity... Figure 1. Effect of potential inducing agents on certain hepatic microsomal enzymes of the rainbow trout. Animals were infected intraperitoneally with either phenobarbital (65 mg/kg) 3-methylcholanthrene (20 mg/kg) 2,3-benzanthracene (10 mg/kg) or /3-naphthoflavone (100 mg/kg). The animals were sacrified and hepatic microsome prepared 48 hr after infection. Each bar is the mean SE (n = 3-5) ( ), induced activity (T) significantly different from control (C) activity...
Long-term anticonvulsive therapy with diphenylhydantoin or phenobarbital is known to cause osteomalacia by influencing calcium metabolism (24,25). Alteration in the metabolism of vitamin D, presumably secondary to induction of hepatic microsomal enzymes, leads to the calcium and bone abnormalities (26). Patients on anticonvulsive therapy with phenytoin exhibit a decrease in serum 25-hydroxyvitamin D (27). Adequate dietary amounts of vitamin precursors or microsomal enzyme stimulators might prevent these effects of long-term therapy. [Pg.228]

Adaptive Enzyme Theory. The aliesterases are largely found in the microsomes of rat liver cells (44). Recently Hart and Fouts (51,52, 67-69) have presented evidence that in vivo administration of chlordan or chemically related DDT stimulates the activity of hepatic microsomal drug-metabolizing enzymes, as evidenced by proliferation of smooth-surfaced endoplasmic reticulum (SER) which was first noted with phenobarbital. Several reviews of hepatic drug metabolism... [Pg.67]

The effects of 237 in combination with other compounds have been examined. In one study, neither lobeline nor ethyl alcohol were found to be clastogenic in human lymphoblastoid cell cultures. The combination of lobeline with ethyl alcohol, however, produced a marked increase in genetic damage [530]. In another study, the toxicity of 237 in mice was modified by pretreatment with SKF 525-A, phenobarbital, or 3-methylcholanthrene [531]. Pretreatment of mice with SKF 525-A caused a dose-dependent enhancement of lobeline toxicity. Pretreatment with phenobarbital or 3-methylcholanthrene served to decrease the toxicity of 237, suggesting that hepatic microsomal monooxygenases are involved in the detoxification process. [Pg.255]

CAUTION. Phenytoin. (anticonvulsant) and phenobarbital (long-acting barbiturate) can induce hepatic microsomal enzymes and thereby retard the half-life significantly and, therefore, ultimately interfering with the prevalent efficacy of the drug . [Pg.712]

Both alcohol and the barbiturates are CNS depressants, and simple additive CNS depression provides part of the explanation. Acute alcohol ingestion may inhibit the liver enzymes concerned with the metabolism of barbiturates such as phenobarbital and pentobarbital, but chronic exposure to alcohol increases hepatic microsomal enzyme activity and may reduce sedation from barbiturates in patients without liver impairment. - Similarly, chronic exposure to a barbiturate such as phenobarbital may increase alcohol metabolism due to enzyme induction and consequently reduce blood-alcohol levels. ... [Pg.52]

The relationship between alkyl chain length and rates of dealkylation has been explored (9). 3-Methylcholanthrene repressed the dealkylation of DMN, DEN, and dipropylnitrosamine (DPN) by rat hepatic microsomes the degree of repression was inversely proportional to alkyl chain length. Phenobarbital pretreatment resulted in induction of DEN deethylase activity. The effect of 3-methylcholanthrene on DEN deethylase activity in this study contrasted with a previous study, discussed above (3J8). This may indicate multiple forms of DEN deethylase as observed for DMN demethylase. The carbonium ion character of electrophiles generated in these reactions was demonstrated by the isolation of rearranged alcohol in the microsomal metabolism of DPN (366). [Pg.213]

Dicoumarol, warfarin and tromexan (67) have been shown to be metabolised by hepatic microsomal enzymes. These enzymes can be increased by phenobarbital and with the rapid metabolism of the anticoagulant its effect is reduced [451]. In contrast, phenyramidol inhibits the metabolism of coumarin and hence prolongs the duration of the anticoagulant response [445]. In the rat, the major metabolites of these compounds are 7-hydroxylated derivatives (68) [460— 462]. In man, besides the alteration of the ring [463], side-chain hydroxylation also occurs (69) in the rabbit, de-esterification proceeds rapidly (70) (see Figure 3.9). [Pg.127]

Fio. 7. Relationship between changes in hepatic microsomal drug metabolism (aminopyrine demethylase) and microsomal phospholipid content resulting from phenobarbital treatment Rats were injected with phenobarbital (100 mg/kg once daily) at the arrows. The left axis and the s depict demethylation FA = formaldehyde) and the right axis and O s represent phospholipids (mg/g liver). The lack of correlation between the two parameters is particularly noteworthy after discontinuation of phenobarbital. (Orrenius, Ericsson and Emster, J. Cell Biol., 28, 181, 1966.)... [Pg.596]

Oestradiol-17 and estrone are metabolized by hepatic microsomes to a mixture of polar metabolites most of which are hydroxylated (2-, 18-, 16 a-, 16i3-posi-tions) and the rate of the conversion is increased by repeated administration of chlordane or phenobarbital to female rats. Accordingly, the increases in uterine weight caused by the administration of physiological doses of oestradiol-17 P or estrone to immature female rats are abolished by pretreatment with phenobarbital, chlordane, chlorcyclizine, phenylbutazone or DDT. These results appear to confirm older observations that chronic exposure of female animals to chlordane or DDT produces alterations in the estrus cycle and in ovarian and vaginal cytology which are associated with oestrogen deficiency. [Pg.601]

In humans, administration of o,p -DDD [l,l-dichloro-2-(4-chlorophenyl)-2-(2-chlorophenyl) ethane], phenobarbital, diphenylhydantoin, or phenylbutazone causes a marked elevation in the urinary excretion of 6 )5-hydroxycortisol presumably by accelerating the metabolism of glucocorticoids. Accordingly, treatment of animals with phenobarbital stimulates the hydroxylation by hepatic microsomes of corticosterone, deoxycorticosterone, cortisone, and cortisol, whereas 3-methylcholanthrene has negligible effect on the hydroxylation of cortisone or cortisol. The physiological consequences of this induction, however, remain obscure. [Pg.601]

Treatment of rats with phenobarbital or chlordane increases the rate at which exogenous thyroxine is cleared from the plasma by the combined mechanisms of increased biliary excretion, increased hepatocellular binding, and increased deiodi-nation. An enzyme system in hepatic microsomes catalyses the oxidative deiodina-tion of thyroxine and triiodothyronine, is twice as active in smooth-surfaced mem-... [Pg.601]


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