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Ethanol chronic

Barbiturates Carbamazepine Ethanol, chronic ingestion Phenytoin... [Pg.804]

Most abundant isoform wide substrate range inhibited by cimetidine, macrolides, azoles, and ethanol (acute) induced by general P450 inducers such as carbamazepine, phenobarbital, phenytoin, and rifampin and by ethanol (chronic). [Pg.300]

Giovannini L, Guglielmi G, Casini T, et al. 1992. Effect of ethanol chronic use on hepatotoxicity in rats exposed to tetrachloroethylene. Int J Tiss Reac XIV(6) 281-285. [Pg.255]

Claudin-5 =AD [43] fMPS III [37], animal models ofischemia [70], toxic injmy [71], ethanol chronic intake [64], cortical cold injury [72], and EAE [73]... [Pg.247]

Occludin =Embolic stroke in rats despite BBB breakdown lAnimal models of PD [28], cerebral ischemia [55], methamphetamine toxicity, toxic injmy [40], ethanol chronic intake, cortical cold injury, patients with MPS III [53] and cerebral malaria [65]... [Pg.247]

In several studies, chronic ethanol treatment has been associated with PKC upregulation. In PCI 2 cells, increased levels of PKCg and e were found (25-200 mM ethanol, 2-8 days of treatment) which was associated with increased PKC-mediated phosphorylation. [Pg.485]

Subunit changes are other mechanisms that alter the physiology of GABA synapses and account for plastic changes seen following chronic ethanol treatment. [Pg.485]

Chronic administration of ethanol may up-regulate L-type and N-type VGCCs—an effect that may contribute to ethanol withdrawal symptoms (Kahkonen and Bondarenko 2004 McMahon et al. 2000), probably through involvement of NMDA receptors and other neural circuitry (Calton et al. 1999). [Pg.16]

Goldstein DB, Hungund BL, Lyon RC Increased surface glycoconjugates of synaptic membranes in mice during chronic ethanol treatment. Br J Pharmacol 78 8-10, 1983... [Pg.45]

Bernstein, J., Videla, L. and Israel, Y. (1973). Metabolic alterations produced in the liver by chronic ethanol administration changes related to energy parameters of the cell. Biochem. J. 134, 515-521. [Pg.161]

Boveris, A., Fraga, C.G., Varsavsky, A.I. and Koch, O.I. (1983). Increased chemiluminescence and superoxide production in the liver of chronic ethanol-treated rats. Arch. Biochem. Biophys. 227, 534-541. [Pg.162]

French, S.W., Benson, N.C. and Sun, P.S. (1984). Cen-trilobular liver necrosis induced by hypoxia in chronic ethanol-fed rats. Hepatology 4, 912-917. [Pg.163]

Kawase, T., Kato, S. and Lieber, C.S. (1989). Lipid peroxidation and antioxidant defence systems in rat liver after chronic ethanol feeding. Hepatology 10, 815-820. [Pg.165]

Klein, S.M., Cohen, G., Lieber, C.S. and Cederbaum, A.l. (1983). Increased microsomal oxidation of hydroxyl scavenging agents and ethanol after chronic consumption of ethanol. Arch. Biochem. Biophys. 223, 425-432. [Pg.166]

Chronic excessive ingestion of ethanol causes progressive liver damage because both ethanol and its metabolic products are direct hepatotoxins. [Pg.323]

See other pages where Ethanol chronic is mentioned: [Pg.1212]    [Pg.253]    [Pg.62]    [Pg.62]    [Pg.69]    [Pg.131]    [Pg.114]    [Pg.866]    [Pg.866]    [Pg.1033]    [Pg.1212]    [Pg.253]    [Pg.62]    [Pg.62]    [Pg.69]    [Pg.131]    [Pg.114]    [Pg.866]    [Pg.866]    [Pg.1033]    [Pg.530]    [Pg.316]    [Pg.444]    [Pg.484]    [Pg.484]    [Pg.485]    [Pg.485]    [Pg.485]    [Pg.486]    [Pg.486]    [Pg.520]    [Pg.10]    [Pg.13]    [Pg.14]    [Pg.47]    [Pg.212]    [Pg.183]    [Pg.154]    [Pg.155]    [Pg.155]    [Pg.238]    [Pg.238]   
See also in sourсe #XX -- [ Pg.214 ]



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Ethanol chronic ingestion

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