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  • 1
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The present study was conducted to examine the involvement of oxidative stress in bee venom-induced inhibition of the Na+/glucose cotransporter (α-methyl-d-glucopyranoside (α-MG) uptake), a typical functional marker of proximal tubules, in primary cultured rabbit renal proximal tubule cells (PTC).2. Bee venom (≥ 1 μg/mL) increased lipid peroxide (LPO) formation over 30 min. The increase in [3H]-arachidonic acid (AA) release and LPO formation and the inhibition of α-MG uptake induced by bee venom (1 μg/mL) and melittin (a major component of bee venom; 0.5 μg/mL) were blocked by N-acetyl-l-cysteine, vitamin C and vitamin E, anti-oxidants.3. Bee venom- and melittin-induced increases in LPO formation and inhibition of α-MG uptake were significantly prevented by mepacrine and AACOCF3, phospholipase A2 inhibitors. In addition, nordihydroguaiareic acid (a lipoxygenase inhibitor) and econazole (a cytochrome P-450 epoxygenase inhibitor), but not indomethacin (a cyclo-oxygenase inhibitor), prevented bee venom- and melittin-induced increases in LPO formation and inhibition of α-MG uptake.4. Nordihydroguaiareic acid prevented bee venom- and melittin-induced increases in Ca2+ uptake. Moreover, anti- oxidants significantly prevented bee venom- and melittin-induced increases in Ca2+ uptake.5. In conclusion, bee venom inhibits α-MG uptake via the phospholipase A2–oxidative stress–Ca2+ signalling cascade in primary cultured rabbit renal proximal tubule cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The present study was undertaken in order to examine the effect of various oestrogens on tert-butyl hydroperoxide (t-BHP)-induced cell injury and changes in apical transporters in primary cultured rabbit renal proximal tubule cells.2. Compared with control, t-BHP (0.5 mmol/L; 1 h) decreased cell viability (62%) and glutathione (GSH) content (60%) and increased lipid peroxide (LPO) formation (309%), arachidonic acid (AA) release (193%) and Ca2+ influx (168%).3. The protective potency of various oestrogens for these parameters is dependent on the precise oestrogenic structure, with 2-hydroxy-oestradiol-17β (2-OH-E2) and 4-OH-E2, both catecholic oestrogens, or diethylstilbesterol (DES) being more potent than oestradiol (E2), oestriol or oestradiol-17α, all phenolic oestrogens (P 〈 0.05).4. These cytoprotective effects of oestrogens occur at concentrations above 10 μmol/L and are not dependent on classical oestrogen receptors and gene transcription and translation. In addition, various oestrogens have different preventative effects against t-BHP-induced inhibition of [14C]-α-methyl-D-glucopyranoside (α-MG), inorganic phosphate (Pi) and Na+ uptake, consistent with the results of cell injury. In contrast, the potency against t-BHP-induced changes in cell viability, LPO, GSH content and transporter function of the anti-oxidants taurine and vitamin C is similar to that of phenolic oestrogens, whereas that of the iron chelators deferoxamine and phenanthroline is similar to that of catecholic oestrogens.5. In conclusion, various oestrogens have differential cytoprotective potential against t-BHP-induced cell injury and decreases in α-MG, Na+ and Pi uptake. These effects are due, in part, to both the basic chemical properties of the compounds and the maintenance of endogenous GSH or inhibition of AA release and Ca2+ influx.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2018-04-26
    Description: Mitochondrial NADP + -dependent isocitrate dehydrogenase deficiency increases cisplatin-induced oxidative damage in the kidney tubule cells Mitochondrial NADP〈sup〉+〈/sup〉-dependent isocitrate dehydrogenase deficiency increases cisplatin-induced oxidative damage in the kidney tubule cells, Published online: 25 April 2018; doi:10.1038/s41419-018-0537-6 Mitochondrial NADP + -dependent isocitrate dehydrogenase deficiency increases cisplatin-induced oxidative damage in the kidney tubule cells
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
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