The potential protective roles of zinc, selenium and glutathione on hypoxia-induced TRPM2 channel activation in transfected HEK293 cells.

Hypoxia induces cell death through excessive production of reactive oxygen species (ROS) and calcium (Ca2+) influx in cells and TRPM2 cation channel is activated by oxidative stress. Zinc (Zn), selenium (Se), and glutathione (GSH) have antioxidant properties in several cells and hypoxia-induced TRPM2 channel activity, ROS and cell death may be inhibited by the Zn, Se, and GSH treatments. We investigated effects of Zn, Se, and GSH on lipid peroxidation (LPO), cell cytotoxicity and death through inhibition of TRPM2 channel activity in transfected HEK293 cells exposed to hypoxia defined as oxygen deficiency.We induced four groups as normoxia 30 and 60 min evaluated as control groups, hypoxia 30 and 60 min in the HEK293 cells. The cells were separately pre-incubated with extracellular Zn (100 µM), Se (150 nM) and GSH (5 mM). Cytotoxicity was evaluated by lactate dehydrogenase (LDH) release and the LDH and LPO levels were significantly higher in the hypoxia-30 and 60 min-exposed cells according to normoxia 30 and 60 min groups. Furthermore, we found that the LPO and LDH were decreased in the hypoxia-exposed cells after being treated with Zn, Se, and GSH according to the hypoxia groups. Compared to the normoxia groups, the current densities of TRPM2 channel were increased in the hypoxia-exposed cells by the hypoxia applications, while the same values were decreased in the treatment of Zn, Se, and GSH according to hypoxia group. In conclusion, hypoxia-induced TRPM2 channel activity, ROS and cell death were recovered by the Se, Zn and GSH treatments.

Evaluation of Relationship Between SOD1 50-bp Deletion Gene Polymorphism, Cu, Zn Level, and Viscosity in Postmenopausal Osteoporosis Patients with Vertebral Fractures.

Oxidative stress plays a role in the pathogenesis of bone loss, causing low bone mineral density (BMD) and associated osteoporotic fractures. In our study, we aimed to investigate the relationship of SOD1 50-bp insertion(Ins)/deletion(Del) polymorphism that is involved in oxidative stress metabolism, Cu and Zn element concentrations, and plasma viscosity level, with postmenopausal osteoporosis and related vertebral fractures. The study included 167 voluntary individuals. The 50-bp Ins/Del polymorphism of SOD1 was determined by allele-specific PCR. Plasma Cu and Zn levels were measured by atomic absorption spectrophotometry (AAS). The plasma viscosity was determined using the Harkness Capillary Viscometer device. In our study, the distribution of SOD1 promoter 50-bp Ins/Del polymorphism did not indicate a significant difference between the groups and in postmenopausal osteoporosis patients with and without fractures (p > 0.05). The Ins/Ins genotype was found to be common in individuals in both groups. The Cu and Zn levels of the study group were found to be between the normal reference values (p > 0.05). It was determined that plasma viscosity increased significantly in the group of osteoporotic patients and in patients with postmenopausal osteoporosis with fractures (p < 0.01). In addition, plasma viscosity was found to significantly increase in patients with Ins/Ins genotype and fractures (p < 0.01). Postmenopausal osteoporosis and associated vertebral fracture were found not to be directly related to SOD1 50-bp polymorphism and Cu and Zn element levels. Plasma viscosity levels were found to increase due to the increase in oxidative stress products. Further studies are needed to clarify the roles and relationships of SOD genes and trace elements in the development of postmenopausal osteoporosis and vertebral fracture.

Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells.

There is a widespread use of 2.4 GHz electromagnetic radiation emitting devices especially in communication and education. Recent studies show the adverse effects of electromagnetic fields (EMF) such as oxidative stress, cellular damage and apoptosis on tissues. Selenium (Se) has an antioxidant properties by inhibiting oxidative damage being within the structure of antioxidant enzymes like glutathione peroxidase (GSH-Px) and it has also regulatory function for cell cycle and apoptosis. The aim of this study was to investigate the effect of Se on 2.4 GHz frequency EMF exposed human embryonic kidney cells (HEK293) by means of alterations in apoptotic and oxidative stress parameters. Our study was planned as control, EMF, 100 nM Se + EMF, 200 nM Se + EMF groups. EMF groups were exposed to 2.4 GHz EMF for 1 h, element groups were incubated with two different doses of Se added cell culture medium for 48 h before EMF exposure. MDA levels were significantly higher whereas SOD and GSH-Px activities were significantly lower in EMF compared to control. 100 and 200 nM Se + EMF application decreased MDA levels, increased SOD and GSH-Px activities than EMF. Apoptosis and caspase-3 were statistically significantly higher but bcl-2 was lower in EMF than control. Apoptosis and caspase-3 were lower in 100 and 200 nM Se + EMF, although bcl-2 were higher than EMF. In conclusion, Se has protective effects against 2.4 GHz EMF-induced oxidative stress by reducing lipid peroxidation, regulating SOD and GSH-Px activity. Also, Se has inhibitory effect on 2.4 GHz EMF induced apoptosis by increasing the expression of anti-apoptotic protein bcl-2 and suppressing apoptosis regulatory protein caspase-3.