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      Effects of Sex Hormones on Na +/Glucose Cotransporter of Renal Proximal Tubular Cells following Oxidant Injury

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          It was reported that reactive oxygen metabolites play an important role in the pathogenesis of several renal diseases including glomerulonephritis, ischemia and acute tubular necrosis. However, the effect of oxidants and protective effect of sex steroid hormones on Na<sup>+</sup>/glucose cotransporter of renal proximal tubular cells is not yet elucidated. In the present study, we examined the effect of sex steroid hormones against tert-butyl hydroperoxide (t-BHP)-induced alteration of Na<sup>+</sup>/glucose cotransporter activity in primary cultured rabbit renal proximal tubule cells (PTCs). t-BHP inhibited α-methyl- D-glucopyranoside (α-MG) uptake in a dose-dependent manner. t-BHP-induced inhibition of α-MG uptake was due not to K<sub>m</sub> but to the decrease of V<sub>max</sub>. 0.5 m M t-BHP-induced inhibition of α-MG uptake was significantly blocked by estradiol-17β, but not by progesterone and testosterone. This protective effect was not blocked by estrogen receptor antagonist or transcription and translation inhibitor. In addition, 0.5 m M t-BHP increased [<sup>3</sup>H]-arachidonic acid (AA) release and Ca<sup>2+</sup> uptake. These effects of t-BHP were also significantly blocked by estradiol-17β, but not by progesterone and testosterone. Protective efficacy of estradiol-17β on t-BHP-induced inhibition of α-MG uptake is exhibited between antioxidants and iron chelators. In conclusion, estradiol-17β, but not progesterone and testosterone, partially prevented t-BHP-induced inhibition of α-MG uptake through its antioxidant activity dependent upon phenol structures and inhibition of AA release and Ca<sup>2+</sup> influx.

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          Most cited references 10

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          17-beta estradiol protects neurons from oxidative stress-induced cell death in vitro.

           T Trapp,  M Widmann,  C Behl (1995)
          The potential antioxidant activity of 17-beta estradiol and other steroid hormones in neuronal cells was investigated by studying oxidative stress-induced cell death caused by the neurotoxins amyloid beta protein, hydrogen peroxide and glutamate in the clonal mouse hippocampal cell line HT22. Preincubation of the cells with 10(-5) M 17-beta estradiol prior to addition of the neurotoxins prevented oxidative stress-induced cell damage and ultimately cell death, as detected with cell viability (MTT) and cell lysis (trypan blue exclusion/cell counting; propidium iodide staining) assays. At the DNA level, 17-beta estradiol blocked the DNA degradation caused by glutamate. Other steroid hormones, such as progesterone, aldosterone, corticosterone and the steroid precursor cholesterol, did not protect the cells. The neuronal protection afforded by 17-beta estradiol was estrogen receptor-independent. These data demonstrate a potent neuroprotective activity of the antioxidant 17-beta estradiol, which may have implications for the prevention and treatment of Alzheimer's disease.
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            Characterization of primary rabbit kidney cultures that express proximal tubule functions in a hormonally defined medium

            Primary cultures of rabbit-kidney epithelial cells derived from purified proximal tubules were maintained without fibroblast overgrowth in a hormone-supplemented serum-free medium (Medium RK-1). A hormone- deletion study indicated that the primary cultures derived from purified rabbit proximal tubules required all of the three supplements in Medium RK-1 (insulin, transferrin, and hydrocortisone) for optimal growth but did not grow in response to EGF and T3. In contrast, the epithelial cells in primary cultures derived from an unpurified preparation of rabbit kidney tubules and glomeruli grew in response to EGF and T3, as well as insulin, transferrin, and hydrocortisone. These observations suggest that kidney epithelial cells derived from different segments of the nephron grow differently in response to hormones and growth factors. Differentiated functions of the primary cultures derived from proximal tubules were examined. Multicellular domes were observed, indicative of transepithelial solute transport by the monolayers. The proximal tubule cultures also accumulated alpha- methylglucoside (alpha-MG) against a concentration gradient. However, little or no alpha-MG accumulation was observed in the absence of Na+. Metabolic inhibitor studies also indicated that alpha-MG uptake by the primaries is an energy-dependent process, and depends upon the activity of the Na+/K+ ATPase. Phlorizin at 0.1 mM significantly inhibited 1 mM alpha-MG uptake whereas 0.1 mM phloretin did not have a significant inhibitory effect. Similar observations have been made concerning the Na+-dependent sugar-transport system located on the lumenal side of the proximal tubule, whereas the Na+-independent sugar transporter on the peritubular side is more sensitive to inhibition by phloretin than phlorizin. The cultures also exhibited PTH-sensitive cyclic AMP synthesis and brush-border enzymes typical of proximal cells. However, the activities of the enzymes leucine aminopeptidase, alkaline phosphatase, and gamma-glutamyl-transpeptidase were lower in the cultures than in purified proximal-tubule preparations from which they are derived.
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              Effect of Bee Venom and Its Melittin on Apical Transporters of Renal Proximal Tubule Cells

              Renal failure by bee venom may be related to a malfunction of renal transporters. However, the effects of bee venom on apical membrane transporters of renal proximal tubular cells are not yet known. The aim of this study was to examine the effects of dried bee venom of Apis mellifera and its melittin on apical transporter activity of primary cultured rabbit kidney proximal tubule cells. Bee venom (1 μg/ml) decreased the cell viability and increased lactate dehydrogenase activity over 30–min treatments. Its effect was blocked by mepacrine or AACOCF 3 (10 –6 M; phospholipase A 2 inhibitors). However, there was no effect on cell viability at a concentration of 0.01 μg/ml of bee venom. Thus, we investigated the effect of bee venom (1 μg/ml) on the activity of renal transporters at 30 min. Bee venom inhibited α–methyl– D –glucopyranoside, Pi, and Na + uptakes, but increased Ca 2+ uptake. These effects of bee venom were blocked by mepacrine or AACOCF 3 (10 –6 M ), and bee venom–induced stimulation of Ca 2+ uptake was also blocked by methoxyverapamil and nifedipine ( L –type calcium channel blockers). In addition, bee venom increased [ 3 H]–arachidonic acid release by 216 % of that of control. In all experiments, bee venom melittin (0.5 μg/ml) had an identical effect to that of bee venom itself. In conclusion, bee venom inhibited, in part, α–MG, Pi, and Na + uptakes through its melittin which increased Ca 2+ uptake and arachidonic acid release in primary cultured rabbit renal proximal tubule cells.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                29 August 2001
                : 24
                : 3
                : 159-165
                aDepartment of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Kwangju, and bCollege of Veterinary Medicine, School of Agricultural Biotechnology, Seoul National University, Seoul, Korea
                54223 Kidney Blood Press Res 2001;24:159–165
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 6, Tables: 1, References: 32, Pages: 7
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/54223
                Original Paper

                Cardiovascular Medicine, Nephrology

                Calcium, Transporter, Estradiol-17β, t-BHP, Kidney, Arachidonic acid


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