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  • 1
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Chronic alcohol treatment has been reported to be associated with liver and kidney damage. The insulin-like growth factor (IGF) is the major growth factor related to alcohol consumption. However, the effect of alcohol on the IGF system in the liver and kidney has not been fully elucidated. Thus, the present study was conducted to investigate this issue.2. Alcohol reduced the level of IGF-I in a dose-dependent manner in the serum, liver and kidney. Alcohol also decreased the level of IGF-II in the liver. In contrast, alcohol increased the level of IGF-II in the serum and kidney. These observations were correlated with IGF-I and IGF-II mRNA expression in the liver and kidney.3. To examine the effect of alcohol on IGF receptors in the liver and kidney, IGF-I receptor mRNA was measured. Alcohol decreased IGF-I receptor mRNA in the liver and kidney.4. In experiments performed to examine the regulation of IGF-binding proteins (IGFBP), alcohol increased serum levels of IGFBP-1. However, alcohol had no effect on serum levels of IGFBP-2, -3 and -4. These effects were also observed in the liver and kidney.5. In conclusion, alcohol alters the IGF system in rat liver and kidney in a tissue-specific manner, which may contribute to the metabolic dysfunction following chronic alcohol consumption.
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  • 2
    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.
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  • 3
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Calcium regulation has been reported to be associated with the development of diabetic nephropathy. Thus, changes in Ca2+ uptake induced by ATP, an important regulator of Ca2+ uptake, in the diabetic condition and related signal pathways were examined in primary cultures of rabbit renal proximal tubule cells (PTC).2. Under low (5 mmol/L) glucose conditions, 10−4 mol/L ATP inhibited Ca2+ uptake early on (〈 30 min), whereas Ca2+ uptake was stimulated at later time points (〉 2 h). However, under high (25 mmol/L) glucose conditions, ATP stimulated both the early and late uptake of Ca2+.3. The adenylate cyclase inhibitor SQ 22536, the protein kinase (PK) A inhibitor PKI amide 14–22, Rp-cAMP, staurosporine, bisindolylmaleimide I and H-7 (PKC inhibitors) blocked the change in ATP effect on Ca2+ uptake in the presence of 25 mmol/L glucose. However, none one of these drugs blocked the effect of ATP on Ca2+ uptake in the presence of 5 mmol/L.4. At 25 mmol/L, glucose increased cAMP content and PKC activity, whereas ATP had no effect on either parameter.5. In conclusion, high glucose levels alter ATP-induced Ca2+ uptake via cAMP and PKC pathways in the PTC.
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  • 4
    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.
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