CYP2E1 and CYP3A1/2 gene expression is not associated with the ursodeoxycholate effect on ethanol-induced lipoperoxidation

Nguyen, T.D.; Oliva, L.; Villard, Pierre-Henri; Puyoou, F.; Sauze, C.; Montet, Anne-Marie; Lacarelle, Bruno; Durand, Alain; Montet, Jean-Claude

doi:10.1016/s0024-3205(99)00344-6

Cited by 5 publications

(6 citation statements)

References 28 publications

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“…In contrast, in studies in vivo UDCA acts as an effective antioxidant. In rats with alcoholic steatosis UDCA decreased mitochondrial 19 and microsomal 9 end-products of lipid peroxidation, prevented oxidation of polyunsaturated fatty acids and stabilized liver cell membranes 20 also suggestive of an antioxidant effect of UDCA. UDCA decreased products of lipid peroxidation in the liver of rats with bile duct ligation.…”

Section: Discussionmentioning

confidence: 91%

“…Several authors believe that the protective action of UDCA in alcoholic liver disease could be realized via an improvement in mitochondrial structure and functions, 21 a normalization of prostaglandin production and essential fatty acid content 20 and an antioxidant effect of UDCA. 9 The antioxidant effects of UDCA have been studied intensively during the last decade. Investigators have not found an effect of UDCA either on superoxide anion production in monocytes of UDCA-treated patients with cholestatic liver disease or on the cells of healthy persons preincubated with UDCA.…”

Section: Discussionmentioning

confidence: 99%

“…8 Recently published data from different laboratories have characterized clear-cut antioxidative properties of UDCA. [9][10][11] The work described in the present paper was undertaken to assess if UDCA as an antioxidant and a membrane protector could be effective in reducing morphological and functional alterations in pancreatic islet -cells in a rat model of alloxan-induced diabetes.…”

Section: Introductionmentioning

confidence: 99%

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The protective effect of ursodeoxycholic acid in alloxan‐induced diabetes

Lukivskaya

Лис

Егоров

et al. 2003

Cell Biochemistry & Function

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The purpose of this work was to study the effect of ursodeoxycholic acid (UDCA) on the morphological and functional alterations in pancreatic islet beta-cells in rats with diabetes induced by alloxan (150 mg kg(-1), i.p.). UDCA (40 mg kg(-1), i.g.) was administered daily from the fifth to the 35th day after the alloxan treatment. The treatment of diabetic rats with UDCA improved the pancreatic morphology disturbed by the alloxan treatment: UDCA increased the number of pancreatic islets and beta-cells, the beta-/alpha-cell ratio and decreased the number of alpha-cells. As the morphometric data suggest, the treatment of diabetic animals with UDCA significantly increased the area of beta-cell cytoplasmatic granules stained by paraldehyde-fuchsin. The concentration of blood glucose in diabetic rats was gradually decreased after the UDCA treatment, and at the end of the experiment reached the control value. The treatment with UDCA raised the serum insulin level in diabetic rats about 2.5-fold, but this concentration was significantly lower as compared to the control group. The content of lipid peroxidation end-products, hydroxyalkenals and malondialdehyde, was significantly elevated in the alloxan-treated rats, whereas the treatment with UDCA normalized these parameters. The present data indicate that UDCA acts as an effective antidiabetic agent in alloxan-induced diabetes and its beneficial effects in diabetic rats can be related to the antioxidant properties of UDCA.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The protective effect of ursodeoxycholic acid in alloxan‐induced diabetes

Lukivskaya

Лис

Егоров

et al. 2003

Cell Biochemistry & Function

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“…[4][5][6][7] Ursodeoxycholic acid (UDCA) (Figure 1) is a nontoxic bile acid that has been reported to protect hepatocytes, hepatoma cells, osteogenic sarcomas and HeLa cells from apoptosis induced by okadaic acid, hydrogen peroxide, ethanol, and more hydrophobic bile acids, for example, DCA. [8][9][10][11][12][13][14][15] Other investigators found that UDCA promoted apoptosis in some systems. 16,17 These diverse reports prompted an examination of the effects of UDCA on PDT-induced apoptosis in cell culture.…”

Section: Introductionmentioning

confidence: 99%

A mechanism for the proapoptotic activity of ursodeoxycholic acid: effects on Bcl-2 conformation

2004

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Ursodeoxycholic acid (UDCA), a relatively nontoxic bile acid, enhanced the apoptotic response of tumor cells to both photosensitizers that cause photodamage to Bcl-2 and to the nonpeptidic Bcl-2/Bcl-x L antagonist HA14-1. The latter agent binds to the surface pocket formed by the BH1, BH2 and BH3 domains of Bcl-2 and Bcl-x L . Fluorescence polarization studies indicated that affinity of HA14-1 for Bcl-2 was enhanced in the presence of UDCA. Moreover, Bcl-2 photodamage was promoted by UDCA using a photosensitizing agent with affinity for the endoplasmic reticulum, a site of Bcl-2 localization. Fluorescence resonance energy transfer (FRET) studies revealed that the proximity of Bcl-2 to a hydrophobic photosensitizing agent embedded in liposomes was enhanced by UDCA. Since photodamage will occur only if a protein is in close contact with a photosensitizing agent, we propose that these findings support the hypothesis that UDCA causes a conformational change in Bcl-2, promoting HA14-1 binding and enhancing affinity for certain membrane-bound photosensitizers. Cell Death and Differentiation (2004) 11, 906-914. doi:10.1038/sj.cdd.4401433 Keywords: apoptosis; Bcl-2; CPO; NPe6; SnET2; photodynamic therapy (PDT)Abbreviations: CPO, 9-capronyloxy-tetrakis(methoxyethyl) porphycene; DCA, deoxycholic acid; DEVD-R110, asp-glu-valasp-rhodamine 110 (fluorogenic caspase-3 substrate); ER, endoplasmic reticulum; flu-Bak, 5-carboxyfluorecein coupled to the N terminus of a peptide GQVGRQLAIIGDDINR derived from the BH3 domain of Bak; HA14-1, ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; HO342, Höchst dye HO33342; mTHPC, meta-(tetrahydroxyphenyl) chlorin; NPe6, N-aspartyl chlorin e6; P, fluorescence polarization value; PDT, photodynamic therapy; SnET2, tin etiopurpurin; UDCA, ursodeoxycholic acid.

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“…The potent shawii R. may be attributed to its high content of phenolic compounds [15]. Hepatoprotective effects of various natural compounds were proved to be related to their antioxidant activities [13,26] (Table 1).…”

Section: Results and Discussion (3)mentioning

confidence: 99%