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 Ca(2+) influx (168%). 3. The protective potency of various oestrogens for these parameters is dependent on the precise oestrogenic structure, with 2-hydroxy-oestradiol-17 beta (2-OH-E(2)) and 4-OH-E(2), both catecholic oestrogens, or diethylstilbesterol (DES) being more potent than oestradiol (E(2)), oestriol or oestradiol-17 alpha, all phenolic oestrogens (P < 0.05). 4. These cytoprotective effects of oestrogens occur at concentrations above 10 micromol/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 [(14)C]-alpha-methyl-D-glucopyranoside (alpha-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 alpha-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 Ca(2+) influx.
The protective effect of caffeic acid (CA) against oxidative stress-induced inhibition of proximal tubule apical transporter was investigated. In the present study, 10 (-4) M H2O2 did not affect cell viability regardless of incubation time. However, it decreased apical transporters' activity such as Na (+)/glucose cotransporter, Na (+)/Pi cotransporter, and Na (+)/H(+) antiporter in the proximal tubule cells. CA (>10(-6) M) prevented H2O2-induced inhibition of apical transporters. Thus, we investigated its action mechanism. CA also prevented H2O2-induced lipid peroxides formation, arachidonic acid (AA) release, and Ca(2+) uptake. In conclusion, CA, in part, prevented H2O2-induced inhibition of apical transporter activity via decrease of AA release and Ca(2+) uptake in primary cultured renal proximal tubule cells.
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