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Hepatic induction

Rifapentine is an analogue of rifampin that is active against M. tuberculosis and M. avium. Rifapentine s mechanism of action, cross-resistance, hepatic induction of P450 enzymes, drug interactions, and toxic profile are similar to those of rifampin. It has been used in the treatment of tuberculosis caused by rifampin-susceptible strains. [Pg.562]

Cherrington NJ, Hartley DP, Li N, et al. Organ distribution of multidrug resistance proteins 1, 2, and 3 (Mrpl, 2, and 3) mRNA and hepatic induction of Mrp3 by constitutive androstane receptor activators in rats. J Pharmacol Exp Ther 2002 300 97-104. [Pg.203]

Rifampin Inhibits DNA-dependent RNA polymerase (nucleic acid synthesis inhibitor) Resistance via change in enzyme Hepatitis Induction of P450 Red-orange metabolites... [Pg.193]

Stamp et al, (48 ) suggested that plasma calcium concentrations among epileptics may be regulated by effects of anticonvulsants on mechanisms other than those concerning vitamin D, i.e. that it is not related to hepatic induction of vitamin D-metabolizing enzymes as has been thought. [Pg.50]

Historical Inhalation Agents. Diethyl ether produces excellent surgical anesthesia, but it is flammable (see Ethers). Chloroform is a nonflammable, sweet smelling, colorless Hquid which provides analgesia at nonanesthetic doses and can provide potent anesthesia at 1% (see Chlorocarbons AND CHLOROHYDROCARBONs). However, a metabohte causes hepatic cell necrosis. Tdlene, a nonflammable colorless Hquid, has a slower onset and recovery and a higher toxicity and chemical reactivity than desirable. Cyclopropane is a colorless gas which has rapid induction (2 —3 min) and recovery characteristics and analgesia is obtained in the range of 3—5% with adequate skeletal muscle relaxation (see Hydrocarbons). The use of cyclopropane has ceased, however, because of its flammabiHty and marked predisposition to cause arrhythmias. [Pg.408]

Intoxicated patients surviving for 28 hours to 9 days had hepatocytes free in central or hepatic veins this finding was described as mobilization of liver cells. The role of methyl parathion in the induction of all of these lesions is unclear. [Pg.65]

Dubois M, Plaisance H, Thome JP, et al. 1996. Hierarchical cluster analysis of environmental pollutants through P450 induction in cultured hepatic cells. Ecotoxicol Environ Saf 34 205-215. [Pg.202]

Keeffe EB, Dieterich DT, Han SH, Jacobson IM, Martin P, Schiff ER, Tobias H, Wright TL (2006) A treatment algorithm for the management of chronic hepatitis B virus infection in the United States an update. Clin Gastroenterol Hepatol 4 936-962 Kim KI, Sasase N, Taniguchi M, Mita K, Kinoshita K, Togitani T, Shikata M, Kimura N, Izawa S, Ohtani A, Nakao K, Muramoto Y, Kim SR, Nabeshima S, Ishii F, Tanaka K, Hayashi Y (2005) Interferon-beta induction/interferon-alpha2b plus ribavirin therapy in patients with chronic hepatitis C. Int J Clin Pharmacol Res 25 71-76... [Pg.236]

A broad and vigorons T cell response generally accompanies elimination of HBV as well as HCV infection. By contrast, patients with chronic hepatitis B or C tend to have late, transient, or narrow T cell responses. In a long-term follow-up of HBV-infected patients receiving HPC transplants from HBV-immune individuals, 20 of 31 recipients cleared their HBV infection (Hui et al. 2005). In principle, these results encourage the development of adoptive T cell transfer strategies for the treatment of chronic viral hepatitis. However, it is still controversial whether induction of an efficient T cell response is the cause or the consequence of viral clearance. Furthermore, T cell responses do not only contribute to virus control but also to disease pathology (Rehermann and Nascimbeni 2005). [Pg.284]

Agarwal et al. 1978), the quantification of these specific enzymes may indicate that exposure to endosulfan has occurred. Blood tests, such as decay curves for aminopyrine in plasma, which are semiquantitative indices of liver enzyme induction, have been used successfully in the past to demonstrate enzyme induction in pesticide-exposed workers. Because numerous chemicals found at hazardous waste sites also induce these hepatic enzymes, these measurements are not specific for endosulfan exposure. However, measurements of enzyme activity, together with the detection of the parent compound or its metabolites in tissue or excreta, can be useful indicators of exposure. All of these potential biomarkers require further verification in epidemiological studies. Further studies with focus on the development of methods to separate and measure the estrogenicity of endosulfan in in vitro assays would be valuable since these assays are more sensitive and discriminative than other conventional biomarkers. Preliminary results have been presented by Sonnenschein et al. (1995). [Pg.196]

Dubois M, Pfohl-Leszkowicz A, De Waziers I, etal. 1996. Selective induction of the cyp3a family by endosulfan and DNA-adduct formation in different hepatic and hepatoma cells. Environmental Toxicology and Pharmacology l(4) 249-256. [Pg.283]

Tyagi SR, Sing Y, Srivastava PK, et al. 1984. Induction of hepatic mixed function oxidase system by endosulfan in rats. Bull Environ Contam Toxicol 32 550-556. [Pg.316]

Donohoe, R.M. and Curtis, L.R. (1996). Estrogenic activity of chlordecone, o,p -DDT and o,p -DDE in juvenile rainbow trout Induction of vitellogenesis and interaction with hepatic estrogen binding sites. Aquatic Toxicology 36, 31-52. [Pg.344]

Guyan et al. 1990) have used several markers of lipid peroxidation (9-cis-, 11-tmns-isomer of linoleic acid, conjugated dienes and ultraviolet fluorescent products) to demonstrate significant increases in the duodenal aspirate after secretin stimulation in patients with acute and clinic pancreatitis. They interpreted this as indicating induction of hepatic and pancreatic drug-metabolizing enzymes in the face of a shortfidl of antioxidant defences, more marked in chronic pancreatitis. Subsequent studies in patients with chronic pancreatitis have confirmed decreased serum concentrations of selenium, -carotene and vitamin E compared with healthy controls (Uden et al., 1992). Basso aol. (1990) have measured increases in lipid peroxides in the sera of patients with chronic... [Pg.152]

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. [Pg.243]

As noted above, many of the AEDs induce hepatic microsomal enzyme systems and thus reduce the effectiveness of hormonal contraceptives. Women taking AEDs that may reduce the effectiveness of hormonal contraceptives should be encouraged to also use other forms of birth control. Due to induction or inhibition of sex hormone metabolism and changes in binding of hormones to sex hormone binding globulin, some AEDs may reduce fertility. For example, valproate has been associated with a drug-induced polycystic ovarian syndrome. Women who experience difficulties with fertility should seek the advice of health care professionals with expertise in fertility. [Pg.459]

Keto con azole Inhibits several 200 mg twice reactions develops with continued use. Hematologic disturbances and hypothyroidism also seen. Generally well High potential for drug interactions due to potent induction of hepatic enzymes. Effective in a majority of causes ... [Pg.697]


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