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Microsomal systems

Koshkaryan AO, Aslanyan GT, Mirzoyan MA, et al. 1989. [Impact of isomers and the major metabolite of endosulfan on the state of liver microsomal systems]. Gig Sanit 3 93-94. (Russian)... [Pg.302]

This pathway (the microsomal system ) elongates saturated and unsaturated fatty acyl-CoAs (from Cjg upward) by two carbons, using malonyl-CoA as acetyl donor and NADPH as reductant, and is catalyzed by the microsomal fatty acid elongase system of enzymes (Figure 21-5). Elongation of stearyl-CoA in brain increases rapidly during myehnation in order to provide C22 and C24 fatty acids for sphingoEpids. [Pg.177]

The search for an alternative reactive metabolite for the polycyclic hydrocarbon carcinogens was soon successful. Also in 1973, Borgen et al. (54) reported that, in the presence of a microsomal system from hamster liver, trans 7,8-dihydro-7,8-dihydroxybenzola]-pyrene (a metabolite of benzo[aJpyrene) was bound to DNA in vitro some ten times more extensively than was benzo[a]pyrene itself. [Pg.19]

Studies on the comparative abilities (13) of B[a]P metabolites to bind to DNA in microsomal systems showed that the 7,8-dihydrodiol was the most efficient. This led to the proposal (69) that dihydrodiol epoxides were the ultimate carcinogenic metabolites. Chemical synthesis of all possible isomers (70.71) has allowed complete structural identification of the adducts (72-74). [Pg.200]

Lipid-soluble xenobiotics are commonly biotra ns formed by oxidation in the drug-metabolizing microsomal system (DMMS). For each description below, choose the component of the microsomal mixed-function oxidase system with which it is most closely associated ... [Pg.39]

MAO is a flavoprotein enzyme that is found on the outer membrane of mitochondria. It oxidatively deami nates short-chain monoamines only, and it is not part of the DM MS. ATP is involved in the transfer of reducing equivalents through the mitochondrial respiratory chain, not the microsomal system. [Pg.55]

Goldberg, R. F., Epstein, C.)., Anfinsen, C. B., Acceleration of reactivation of reduced bovine pancreatic ribonuclease by a microsomal system from rat liver, /. Biol. Chem. 238 (1963), p. 628-635... [Pg.104]

Blood protein binding of IQ was found in rats dosed intragastrally with the labelled compound. The same adducts, though in much higher yields, were found when purified rat serum albumin was exposed either to /V-hydroxy-IQ or incubated with parent IQ in the presence of a microsomal system. A tripeptide was isolated which contained lV-(cystein-S -yl)TQ-,S-oxide (sulfinamide) that easily liberated IQ on acidification. Pretreatment of albumin with p-chloromercuri ben zoale reduced covalent binding drastically61. The authors concluded that the reactant most likely to yield this structure is 2-nitroso-3-methylimidazo[4,5-/]quinoline, which is probably formed by autoxidation of /V-hydroxy-IQ. [Pg.1034]

Mueller and Miller (33) and Brodie et al. (34) were the first to show that enzymes in the microsomal fraction of rat liver could effectively oxidize xenobiotics. Comparable enzymes (aryl hydrocarbon monooxygenases) were later reported in the hepatic tissues of fresh water and marine fish by Creaven et al. (35) and Buhler and Rasmusson (36). Reconstituted hepatic microsomal systems require cytochrome P-450 for monooxygenase activity in both mammals (37) and fish (38,39). Bend et al. [Pg.64]

A series of substituted diaryselenides were examined in three lipid peroxidation model systems isolated rat liver microsomes treated with Fe(II)/(ADP)/ascorbate and isolated rat hepatocytes treated with two different initiators of oxidation. In rat hepatocytes, all of the tellurides performed more effectively than the selenides. Particularly for the rat liver microsome system, the substituent effects on lipid peroxidation were consistent with what would be expected Electron-donating groups give more active compounds, while electron-withdrawing groups give poorer antioxidants. The same trends were seen for substituted diaryItellurides in inhibition of linoleic acid peroxidation in a two-phase model, where the dimethylamino... [Pg.139]

DMT elevates pulse rate and blood pressure. In one study, heart rate elevated from around 70 beats per minute at baseline to 100 beats per minute at the highest dose (0.4 mg/kg, IV). Neurophysiological effects Harmane produces excitation in the nucleus accumbens in nanomolar concentrations, but depression in micromolar concentrations (Ergene and Schoener 1993). Harmine and B. caapi extract decrease the acoustic startle, which is reversed to some degree by DMT (Freedland and Mansbach 1999). j3-carbolines may have antioxidant effects through inhibiting oxidative enzymes in the microsomal system (Tse et al. 1991). [Pg.369]

Cytochrome P-450 has been characterized in four stable states [Fe, Fe " RH, Fe RH, (O2—Fe ) RH (metastable)] during its oxygenase reaction cycle. In the complete native system a flavoprotein and a redoxin (putidaredoxin) act as electron donors but also as effectors that complement the cytochrome. In the more complex microsomal system the sequence and intermediates are less well defined the electron-transfer chain contains two flavoproteins and one cytochrome, whose interactions with cytochrome P-450 are still the subject of great controversy. [Pg.252]

No studies were located indicating that any populations are unusually susceptible to heptachlor or heptachlor epoxide. There is a possibility that very young children may exhibit particular susceptibility to hepatic effects because of the immaturity of the hepatic microsomal system. Heptachlor is bioactivated to produce heptachlor epoxide which is more toxic than heptachlor. Preadolescent children have a greater rate of glutathione turnover, and they are expected to be more susceptible to heptachlor epoxide-induced toxicity. Their susceptibility would probably depend upon their ability to detoxify heptachlor epoxide. Individuals who show reduced liver function for other... [Pg.65]

The balance between renal clearance and metabohsm is readily predicted by physicochemical properties [36]. Rate of metabolism and formation of metabolic products can be screened for, using Ever microsomal systems and mass spectrometry. The... [Pg.137]

DMMS—drug-metabolizing microsomal system DNA—deoxyribonucleic acid dopa/DOPA/Dopa—(3,4-dlhydroxyphenylalanine)... [Pg.275]

Natarajan AT, Tates AD, Van Buul PP, Mei-jers M, and De Vogel N. (1976) Cytogenetic effects of mutagens/carcinogens after activation in a microsomal system in vitro 1. Induction of chromosome aberrations and sister chromatid exchanges by diethylnitrosamine... [Pg.195]

Antioxidant activity was also tested in a liver microsome system. In this study, mice were treated by oral intubation (2 times/wk) with 0.2 ml olive oil alone or containing CLA (0.1 ml), linoleic acid (0.1 ml), or dl-a-tocopherol (lOmg). Four weeks after the first treatment, liver microsomes were prepared and subsequently subjected to oxidative stress using a non-enzymatic iron-dependent lipid peroxidation system. Microsomal lipid peroxidation was measured as thiobarbituric acid-reactive substance (TBARS) production using malondialdehyde as the standard. It was found that pretreatment of mice with CLA or dl-a-tocopherol significantly decreased TBARS formation in mouse liver microsomes (p < 0.05) (Sword, J. T. and M. W. Pariza, University of Wisconsin, unpublished data). [Pg.269]

Tipranavir is a newer PI for treating patients with resistance to other PI agents. Bioavailability is poor but is increased when taken with a high-fat meal. The drug is metabolized by the liver microsomal system. Tipranavir must be taken in combination with ritonavir to achieve effective serum levels. It is contraindicated in patients with hepatic insufficiency. Tipranavir contains a sulfonamide moiety and should not be administered to patients with known sulfa allergy. [Pg.1082]

The reduction of nitro groups may also be catalyzed by microsomal reductases and gut bacterial enzymes. The reduction passes through several stages to yield the fully reduced primary amine, as illustrated for nitrobenzene (Fig. 4.39). The intermediates are nitrosobenzene and phenylhydroxylamine, which are also reduced in the microsomal system. These intermediates, which may also be produced by the oxidation of aromatic amines (Fig. 4.21), are involved in the toxicity of nitrobenzene to red blood cells after oral administration to rats. The importance of the gut bacterial reductases in this process is illustrated by the drastic reduction in nitrobenzene toxicity in animals devoid of gut bacteria, or when nitrobenzene is given by the intraperitoneal route. [Pg.97]

Acrylonitrile is mutagenic, especially after bioactivation by a microsomal system. Since formation of DNA adducts with acrylonitrile in vitro is strongly increased by formation of its epoxide, it is very likely that the genotoxicity of acrylonitrile is mediated primarily by this metabolite. The epoxide, therefore, may be implicated in the carcinogenicity of acrylonitrile. [Pg.89]

Acrylonitrile is mutagenic in vitro, in Salmonella systems, bioactivation (to cyanoethylene oxide) is required, but in Escherichia coli and in rodent systems, bioactivation by an added microsomal system is not required. The results of genotoxicity experiments in vivo have in most cases been negative, although acrylonitrile is mutagenic in Drosophila. [Pg.91]

A volatile alkylating metabolite was formed in a mouse-liver microsomal system. The primary metabolite formed in vitro by mixed function oxidases is 2-bromoethylene oxide, which rearranges to 2-bromoacetaldehyde. [Pg.925]

Vinylidene fluoride is taken up rapidly via the pulmonary route in rats, but at equilibrium the mean concentration (by volume) in rats was only 23% of that in the gaseous phase. Metabolism proceeded very slowly and was saturable at exposure concentrations of about 260 mg/m Its maximum rate was 1% that of vinyl chloride and less than 20% that of vinyl fluoride there has been a report of an increase in the urinary excretion of fluoride in exposed rats. No alkylating intermediate was demonstrated after passage through a mouse-liver microsomal system. However, vinylidene fluoride inhibits mixed-function oxidase activity in vitro and, like similar halogenated compounds that are transformed to reactive metabolites, it alters rat intermediary metabolism, leading to acetone exhalation (lARC, 1986). [Pg.1552]

Ozgova S, Hermanek J, Gut I. 2003. Different antioxidant effects of polyphenols on lipid peroxidation and hydroxyl radicals in the NADPH-, Fe-ascorbate- and Fe-microsomal systems. Biochem Pharmacol 66 1127-1237. [Pg.212]

Because vigabatrin is not protein bound, nor is it metabolized by the hepatic microsomal system, it would not expect clinically significant interactions with other drugs. However, vigabatrin was shown to decrease levels by 20-30% in clinical trials. No mechanism of action could account for the decreased level [73, 84], A study found that vigabatrin causes a statistically significant increase in plasma clearance of carba-mazepine [85]. [Pg.343]


See other pages where Microsomal systems is mentioned: [Pg.351]    [Pg.126]    [Pg.627]    [Pg.284]    [Pg.233]    [Pg.298]    [Pg.202]    [Pg.331]    [Pg.590]    [Pg.267]    [Pg.353]    [Pg.377]    [Pg.147]    [Pg.590]    [Pg.215]    [Pg.1639]    [Pg.237]    [Pg.387]    [Pg.338]    [Pg.109]    [Pg.206]   
See also in sourсe #XX -- [ Pg.256 ]




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Drug-metabolizing enzyme system hepatic microsomal, effects

Drug-metabolizing microsomal system

Drug-metabolizing microsomal system DMMS)

Liver microsomes human experimental systems

Microsomal

Microsomal MFO system

Microsomal elongase system

Microsomal enzyme system

Microsomal ethanol oxidizing system

Microsomal ethanol oxidizing system MEOS)

Microsomal ethanol-oxidising system

Microsomal ethanol-oxidising system MEOS)

Microsomal hydroxylation system

Microsomal microsomes

Microsomal mixed-function oxidase system

Microsomal oxidations system

Microsomal system, amino acid incorporation

Microsomes

Microsomes cytochrome P-450 reductase system

Mixed function oxidase system microsomal metabolism

Sorghum microsomal enzyme system

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