Selenium reduces oxidative stress and calcium entry through TRPV1 channels in the neutrophils of patients with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common inflammatory disease with an uncertain pathogenesis, although one consistent finding is increased neutrophil activity. It has been recently reported that the essential antioxidant element selenium has protective effects on oxidative stress and cytosolic Ca(2+) concentrations in human neutrophil. We aimed to investigate the effects of selenium on oxidative stress and Ca(2+) levels through TRPV1 channels in neutrophils from patients with PCOS. Blood samples were obtained for neutrophil isolation from ten female patients with PCOS and ten healthy female subjects. Neutrophils isolated from PCOS group were investigated in four settings: (1) PCOS, (2) after incubation with TRPV1 channel blocker capsazepine (CPZ), (3) after incubation with selenium (sodium selenite), and (4) with combination (CPZ + selenium) exposure. Intracellular free Ca(2+) concentrations were higher in the patients than those in the controls, although their levels were reduced after CPZ and selenium incubations. The cytosolic Ca(2+) concentrations in neutrophils obtained from PCOS group were further decreased after incubation with CPZ + selenium, as compared with those exposed to neither agent. Lipid peroxidation levels were higher in the PCOS group than those in the control although neutrophil glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) values were decreased. The lipid peroxidation level was lower in the CPZ and selenium groups than that in the PCOS group although GSH and GSH-Px values were higher in the treatment with selenium and CPZ. In conclusion, we observed the importance of Ca(2+) influx into the neutrophils through TRPV1 channels in the pathogenesis of the patients with PCOS. The selenium appeared to provide a protective effect against oxidative stress and Ca(2+) entry through modulation of neutrophil TRPV1 calcium channels.