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Hepatic cytochrome

The principal route of macroHde excretion is by way of the Hver. Effects of macrohdes on hepatic metaboHc enzymes, particularly cytochrome P-450, have been studied in order to identify and reduce potential interference with metaboHsm of other dmgs (21—23,444—447). Several macrohdes are initially... [Pg.108]

Nuclear Receptor Regulation of Hepatic Cytochrome P450 Enzymes... [Pg.427]

Nuclear Receptor Regulation of Hepatic Cytochrome P450 Enzymes. Figure 1 General mechanism for transcriptional activation of CYP genes by xenochemicals that activate their cognate xeno-receptor proteins. In the case of Ah receptor, the receptor s heterodimerization partner is Arnt, whereas in the case of the nuclear receptors CAR, PXR, and PPARa, the heterodimerization partner is RXR. The coactivator and basal transcription factor complexes shown are each comprised of a large number of protein components. [Pg.890]

Few submitted to metabolism variations, in particular to hepatic metabolism Submitted to metabolism variations, in particular via cytochroms... [Pg.1194]

Zhong W, Uss AS, Ferrari E, Lau JY, Hong Z (2000) De novo initiation of RNA synthesis by hepatitis C virus nonstructural protein 5B polymerase. J Virol 74 2017-2022 Zhou S, Yung Chan S, Cher Goh B, Chan E, Duan W, Huang M, McLeod HL (2005) Mechanism-based inhibition of cytochrome P450 3A4 by therapeutic drugs. Clin Pharma-cokinet 44 279-304... [Pg.52]

Evidence suggests that endosulfan can induce microsomal enzyme activity. Increased liver microsomal cytochrome P-450 activity was observed in male and female rats after single and multiple administrations of endosulfan (Siddiqui et al. 1987a Tyagi et al. 1984). Increased enzyme activity was observed in hepatic and extrahepatic tissues. Based on the increase in aminopyrine-A-demethylase and aniline hydroxylase activity, endosulfan has been shown to be a nonspecific inducer of drug metabolism (Agarwal et al. 1978). [Pg.132]

Since endosulfan is a cytochrome P450-dependent monooxygenase inducer, the quantification of specific enzyme activities (e.g., aminopyrine-A -demethylase, aniline hydroxylase) may indicate that exposure to endosulfan has occurred (Agarwal et al. 1978). Because numerous chemicals and drugs found at hazardous waste sites and elsewhere also induce hepatic enzymes, these measurements are nonspecific and are not necessarily an indicator solely of endosulfan exposure. However, these enzyme levels can be useful indicators of exposure, together with the detection of endosulfan isomers or the sulfate metabolite in the tissues or excreta. [Pg.179]

Narayan S, Dani HM, Misra UK. 1984. Effect of intratracheally administered DDT and endosulfan on pulmonary and hepatic respiratory cytochromes. Bull Environ Contam Toxicol 33 193-199. [Pg.307]

Two important examples of reductive metabolism of xenobiotics are the reductive dehalogenation of organohalogen compounds, and the reduction of nitroaromatic compounds. Examples of each are shown in Figure 2.13. Both types of reaction can take place in hepatic microsomal preparations at low oxygen tensions. Cytochrome P450 can catalyze both types of reduction. If a substrate is bound to P450 in the... [Pg.41]

Under anaerobic conditions, p,p -DDT is converted to p,p -DDD by reductive dechlorination, a biotransfonnation that occurs postmortem in vertebrate tissues such as liver and muscle and in certain anaerobic microorganisms (Walker and Jefferies 1978). Reductive dechlorination is carried out by reduced iron porphyrins. It is carried out by cytochrome P450 of vertebrate liver microsomes when supplied with NADPH in the absence of oxygen (Walker 1969 Walker and Jefferies 1978). Reductive dechlorination by hepatic microsomal cytochrome P450 can account for the relatively rapid conversion of p,p -DDT to p,p -DDD in avian liver immediately after death, and mirrors the reductive dechlorination of other organochlorine substrates (e.g., CCI4 and halothane) under anaerobic conditions. It is uncertain to what extent, if at all, the reductive dechlorination of DDT occurs in vivo in vertebrates (Walker 1974). [Pg.104]

Fent, K., Woodin, B.R., and Stegeman, J.J. (1998). Effects of triphenyl tin and other organotins on hepatic monooxygenase system in fish. In D.R. Livingstone and J.J. Stegeman (Eds.) Forms and Functions of Cytochrome P450, 277-288. [Pg.346]

Rosenberg, D.W. and Drummond, G.S. (1983). Direct in vitro effects of TBTO on hepatic cytochrome P450. Biochemical Pharmacology 32, 3823-3829. [Pg.366]

Ticlopidine inhibits the P2Yj2 platelet ADP receptor, thus inhibiting ADP-dependent activation of the GP Ilb/IIIa receptor. It has a slow onset of action and takes 3-7 days to reach its maximal antiplatelet effect. It is inactive in vitro and must undergo activation by the hepatic cytochrome p450 enzyme system. Secondary prevention trials have found that ticlopidine-treated patients have an estimated RRR of 33% for the composite endpoint of stroke, myocardial infarction, or vascular death after ischemic stroke. Significant adverse effects include bone marrow depression, rash, diarrhea, and thrombotic thrombocytopenic purpura. No clinical trials have studied ticlopidine for the treatment of stroke in the acute phase. [Pg.148]

The cytochrome P-450-dependent metabolism of trichloroethylene was studied in hepatic microsomal fractions from 23 different humans (Lipscomb et al. 1997). CYP2E1 was the predominant form of P-450 responsible for the metabolism of trichloroethylene in humans. Incubations of trichloroethylene with the microsomal preparations resulted in hyperbolic plots consistent with Michaelis-Menton kinetics. The values ranged from 12 to 55.7 pM, and were not normally distributed, and the values range from 490 to 3,455 pmol/min/mg protein and were normally distributed. The study authors concluded that the human variability in metabolism of trichloroethylene via P-450-dependent pathways was within a 10-fold range. [Pg.116]

Costa AK, Katz ID, Ivanetich KM. 1980. Trichloroethylene Its interaction with hepatic microsomal cytochrome P-450 in vitro. Biochem Pharmacol 29 433-439. [Pg.259]


See other pages where Hepatic cytochrome is mentioned: [Pg.66]    [Pg.67]    [Pg.139]    [Pg.699]    [Pg.892]    [Pg.1498]    [Pg.76]    [Pg.52]    [Pg.167]    [Pg.181]    [Pg.130]    [Pg.144]    [Pg.221]    [Pg.446]    [Pg.278]    [Pg.627]    [Pg.120]    [Pg.156]    [Pg.239]    [Pg.239]    [Pg.240]    [Pg.204]    [Pg.150]    [Pg.222]   
See also in sourсe #XX -- [ Pg.304 ]

See also in sourсe #XX -- [ Pg.551 ]




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Cytochrome P450, hepatic microsomal

Cytochrome P450-mediated hepatic metabolism

Cytochrome hepatic microsomal, effects

Cytochrome hepatic, characteristics

Hepatic cytochrome P450 enzymes

Hepatic microsomal cytochrome

Hepatic microsomal cytochrome antioxidants

Nuclear Receptor Regulation of Hepatic Cytochrome

Nuclear Receptor Regulation of Hepatic Cytochrome P450 Enzymes

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