Impaired hypotensive effects of centrally acting oxytocin in SHR and WKY rats exposed to chronic mild stress.

The present study was designed to determine the role of centrally acting oxytocin (OT) in the regulation of blood pressure during chronic mild stress (CMS) in spontaneously hypertensive (SHR; n = 36) and normotensive Wistar-Kyoto (WKY; n = 38) rats. The rats were implanted with osmotic minipumps for intracerebroventricular infusions of 0.9% NaCl, OT, and oxytocin receptor antagonist (OTANT) and divided into two groups: SHR and WKY 1) exposed to 4-wk CMS and 2) not exposed to stress (controls). After 4 wk, hemodynamic parameters were recorded at rest and after an application of acute stressor [air-jet stress (AJS)]. Resting mean arterial blood pressure (MAP) was significantly lower in CMS-exposed SHR and WKY infused with OT than in the corresponding groups receiving saline. Exposure to CMS exaggerated the AJS-dependent pressor response in WKY receiving saline but not in the corresponding group of SHR. OT infusion reduced the AJS-dependent pressor response in both CMS-exposed and not exposed SHR and in CMS-exposed WKY. Intracerebroventricular infusion of OTANT potentiated the AJS-dependent pressor response in both stressed and not stressed WKY rats but not in SHR. The results show that centrally delivered OT decreases resting MAP during CMS in both SHR and WKY rats and that in SHR it reduces pressor responses to AJS under control and CMS conditions, whereas in WKY this effect is significant only after CMS exposure. The study indicates that endogenous centrally acting OT may play an essential role in buffering pressor responses to AJS in CMS-exposed and not exposed WKY rats and that this function is significantly impaired in SHR.

Lipid peroxidation as a predictive biomarker of the early stage of cancer.

Prostate cancer continues to be a major cause of morbidity and mortality in men around the world. The data concerning the antioxidant status and the degree of lipid peroxidation at the moment of the initiation of cancer is limited. The aim of this research is to assess the effect of selected minerals (zinc, selenium, iron, copper and calcium) on the growth of the neoplastic process and the concentrations of selected biomarkers of the oxidative damage in rats with implanted prostate cancer cells. It was found that the diet supplementation with selected minerals (zinc, selenium, iron, copper and calcium) affect the occurrence of prostate tumor growth in the examined rats. The intraperitoneal implantation of prostate cancer cells resulted in the occurrence of prostatic adenoma in 71% of the examined rats. In the rats that were additionally supplemented with selenium and with copper, the cancer cell aggregates constituted, respectively, 25% and 38% of the cases. As a result of implantation of cancer cells, the level of biomarkers of lipid peroxidation increased both in the urine and in tissues of the examined animals (rat group without supplementation). No relationship was found between the process of lipid peroxidation due to the supplementation with selenium and copper, and the lower incidence of cancer and the induction of apoptosis. The reduced activity of antioxidative enzymes (catalase, superoxide dismutase and glutathione peroxidase) creates favorable conditions for the formation of cancer cell aggregates, which was shown in the rats whose diet was supplemented with iron. In summary, we conclude that lipid peroxidation represents a fruitful approach to early stage cancer prevention. Supplementation of rats with trace elements correlated with the risk of developing cancer, but the mechanisms of this action is complicated and dose-dependent.