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  • 1
    Electronic Resource
    Electronic Resource
    Distribution of Neuropeptide Receptors (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 757 (1995), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1995.tb17497.x
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  • 2
    Electronic Resource
    Electronic Resource
    Effect Of Various Oestrogens On Cell Injury And Alteration Of Apical Transporters Induced By Tert-Butyl Hydroperoxide In Renal Proximal Tubule Cells (2002)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 29 (2002), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03603.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of ATP on Ca2+ uptake in the presence of high glucose in renal proximal tubule cells (2003)
    Oxford, UK : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 30 (2003), S. 0 
    Details
    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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.2003.03895.x
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  • 4
    Electronic Resource
    Electronic Resource
    Involvement Of Oxidative Stress In Bee Venom-Induced Inhibition Of Na+/Glucose Cotransporter In Renal Proximal Tubule Cells (2002)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 29 (2002), S. 0 
    Details
    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
    URL: http://dx.doi.org/10.1046/j.1440-1681.2002.03685.x
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of 7-Nitroindazole, a Selective Neuronal Nitric Oxide Synthase Inhibitor, on Parvalbumin Immunoreactivity after Cerebral Ischaemia in the Hippocampus of the Mongolian Gerbil (1999)
    Oxford, UK : Blackwell Science, Ltd
    Anatomia, histologia, embryologia 28 (1999), S. 0 
    Details
    ISSN: 1439-0264
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Previous studies have demonstrated that a loss of parvalbumin-immunoreactive (PV-ir) neurones is observed in the hippocampus after transient cerebral ischaemia. However, whether the loss of parvalbumin (PV) immunoreactivity is related to the over-production of nitric oxide (NO) during cerebral ischaemia has not been evaluated. This study was designed to test the effect of 7-nitroindazole pre-treatment (7-NI, 50 mg/kg), a selective neuronal NO synthase inhibitor, on PV immunoreactivity and its cellular activity following forebrain ischaemia. PV-ir neurones in the hippocampus of the control group were widely distributed in the pyramidal cell layer and stratum oriens of CA1 and CA3, and the granular cell layer of dentate gyrus. 7-NI pre-treatment completely suppressed the reduction of PV immunoreactivity in CA1 that was observed in the ischaemia-induced group. Subsequently, 7-NI pre-treatment also protected against the structural loss of microtubule-associated protein 2 (MAP2) immunoreactivity in CA1 after ischaemic insult. In addition, the Fos-defined neuronal activity of PV-ir neurones was slightly increased by the 7-NI pre-treatment 3 h after ischaemia. Based on these data, we conclude that the neuronal toxicity of NO may be involved in the loss of PV-ir neurones after cerebral ischaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1439-0264.1999.00218.x
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