Oxidative stress and changes in antioxidative defense system in erythrocytes of preeclampsia in women.

The present study was designed to investigate whether oxidative stress occurred to erythrocytes in preeclampsia and was related to disease. Indicative markers of oxidative stress and changes in antioxidant defense system were assayed in the erythrocytes of 22 healthy pregnant and 20 women with preeclampsia. Results of our work indicated high concentration of hydrogen peroxide, nitrite, peroxynitrite and lipid peroxides in preeclampsia compared to healthy pregnant women. Concentration of superoxide anion was lower in preeclamptic women. There were no differences in concentrations of vitamin E, reduced glutathione and oxidized glutathione. Activity of glutathione-S-transferase (GST) was higher while activities of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) were lower in preeclamptic women. There were no differences in glutathione peroxidase (GSH-Px) activity between the two investigated groups. These results suggest that preeclampsia was characterized by oxidative stress and alteration of antioxidative defense system by disbalance in oxidative/antioxidative status of erythrocytes.

A comparative study of the effects of molsidomine and 3-morpholinosydnonimine on the redox status of rat erythrocytes and reticulocytes.

After enzymic biotransformation, molsidomine (MO) acts via the metabolite 3-morpholinosydnonimine (SIN-1) through spontaneous liberation of nitric oxide (NO) and superoxide (O(2)(.-)). The aim of this study was to compare the effects of MO and its active metabolite SIN-1 on the redox status of rat erythrocytes and reticulocytes. Rat erythrocyte as well as reticulocyte-rich red blood cell (RBC) suspensions were aerobically incubated (2 h, 37 degrees C) without (control) or in the presence of different concentrations of MO or SIN-1. In rat erythrocytes, biotransformation of MO resulted in the production of NO and nitroxyl (NO(-)). Endogenous superoxide anion (O(2)(.-)) participated in peroxynitrite generation. SIN-1 simultaneously liberated NO and O(2)(.-), which formed peroxynitrite (at least in part), but the liberated NO predominantly reacted with haemoglobin, forming methaemoglobin in erythrocytes. In reticulocytes, MO and SIN-1 caused an increase in the levels of both nitrite and 3-nitrotyrosine (an indicator of peroxynitrite), whereas they decreased the level of O(2)(.-). In reticulocytes, MO was metabolized into SIN-1 which led to the generation of NO, which reacted with O(2)(.-) (endogenous or exogenous) forming reactive nitrogen species. In conclusion, there are two metabolic pathways for MO biotransformation: one causing NO and NO(-) generation predominantly in erythrocytes and the other, via SIN-1 metabolism, in reticulocytes. The main difference between the action of MO and SIN-1 was that the latter caused oxidative damage in RBCs.

Combined effects of coenzyme Q(10) and Vitamin E in cadmium induced alterations of antioxidant defense system in the rat heart.

Our study investigated the possible protective effects of coenzyme Q(10) (CoQ(10)) and Vitamin E (Vit E) alone or in combination against cadmium (Cd) induced alterations of antioxidant defense system in the rat heart. Male Wistar rats were injected with a single dose of CdCl(2) (0.4mg Cd/kg BW i.p.), CoQ(10) (20mg CoQ(10)/kg BW i.m.) and Vit E (20IU Vit E/kg BW i.m.), alone or in combination. Acute intoxication of rats with Cd were followed by significantly increased activity of antioxidant defense enzymes (CuZn SOD, GSH-Px, GST and GR), while the activity of Mn SOD was decreased in the heart. The treatment with Cd significantly decreased Vit C and Vit E concentrations. Treatment with CoQ(10) and Vit E reversed Cd-induced alterations of antioxidant defense system. The obtained results support the assumption that CoQ(10) and Vit E functions cooperatively with endogenous antioxidants and diminished toxic effects of Cd in rat heart.

The activity of antioxidant defence enzymes in the mussel Mytilus galloprovincialis from the Adriatic Sea.

The activity of the antioxidant defence enzymes superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), glutathione peroxidase (GSH-Px, EC 1.11.1.9), glutathione reductase (GR, EC 1.6.4.2) and the phase II biotransformation enzyme glutathione-S-transferase (GST, EC 2.5.1.18) in whole mussels (Mytilus galloprovincialis) were studied. The mussels were collected in winter and in spring at two localities in the Adriatic Sea: Bar Port and Tivat Bay. Our results show that the activities of SOD, GSH-Px and GST were seasonally dependent with higher activities in winter. GR activity was also higher in winter, but only in mussels from Bar Port. In mussels from Tivat Bay, GR activity was lower in winter compared to spring. In addition, a decrease in CAT activity in mussels from Bar Port compared to those from Tivat Bay was found. It can be concluded that seasonal variations should be incorporated into interpretation of biomonitoring studies in mussels.

Seasonal variations of cytosolic antioxidant enzyme activities in the liver and white muscle of thinlip gray mullet (Liza ramada Risso) from the Adriatic Sea.

The activity of cytosolic antioxidative defence enzymes in the liver and white muscle of thinlip gray mullet (Liza ramada Risso) were compared in winter and spring in the Adriatic Sea. Activity of antioxidative enzymes is functionally organized due to metabolic demands: analyses of variance and correlation analysis revealed tissue- and seasonal- specific organization of antioxidative enzymes. In winter GST activity increased in both tissues compared with spring. At the same time decreased GSH-Px and GR activities were observed and this effect was more pronounced in liver then in white muscle. From correlation analyses it is concluded that the antioxidative components correlate, but the composition of the antioxidative defence system is different in respect to season and tissue. This means that the antioxidative defence system reorganizes its structure due to oxidative demands and to protect the tissues against reactive oxygen species and to establish homeostasis. Discriminant analyses separated groups according to the complete organization of individual components of the system very well and identified individual components (CAT, GST and GR) which contribute most to the differences. Statistical differences were observed between enzyme activities in tissues (liver and muscle) in both winter and spring, and between seasons (winter and spring) for liver tissue only. Since environmental parameters, such as temperature and oxygen concentration in the sea differ with season, we conclude that in this species the tissues examined expressed their antioxidative defence systems in different ways in respect of external/environmental conditions. We propose that tissue- and seasonal- specific levels of antioxidant enzyme activities should be considered in the interpretation of data from future biomonitoring field studies, especially in relation to low temperature.

[Effects of molsidomine on changes in oxidant/antioxidant status of rat erythrocytes]. / Promene oksidaciono-antioksidacionog statusa eritrocita pacova u prisustvu molsidomina.

INTRODUCTION: Molsidomine (MO) is an established drug in treatment of coronary heart disease. Considering that MO is a donor of nitric oxide (NO) and a superoxide anion radical (O2*-), which forms peroxynitrite, a very toxic radical, the aim of this study was further elucidation of molecular mechanisms of MO action, particularly effects on prooxidative-antioxidative status of rat erythrocytes. MATERIAL AND METHODS: Rat (Wistar albino, male, 250-300 g of b.m.) erythrocyte suspensions were aerobically incubated (120 min, 37 degrees C) without (control) or with MO (0.1, 0.25, 0.5, 1.0 and 1.5 mM). Concentrations of reactive oxygen species, methemoglobin, Heinz bodies, lipid peroxides, vitamins and glutathione, as well as activities of enzymes of the antioxidative defense system (AOS) were evaluated using standard techniques. RESULTS AND DISCUSSION: Molsidomine increases nitrite concentrations (indicating NO+ level), hydroxylamine (indicating NO- level), 3-nitro-tyrosine (indicating ONOO- level) and H2O2, but decreases O2*- level in a dose-dependent manner (changes are statistically significant only with high doses of molsidomine--1.0 and 1.5 mM). These alterations were followed by partial cells damage, increased formation of Heinz bodies, but there were no changes in MetHb and lipid peroxide levels. The defense response of erythrocytes to evident oxidative stress includes increased Vitamin E and Vitamin C concentrations (nonenzymatic components ofAOS), as well as decreased glutathione (reduced and oxidized) levels. Activities ofAOS enzymes remain unchanged. CONCLUSION: Experimental doses of MO induce oxidative stress in rat erythrocytes. However, the first line of AOS is successful in the cellular defence response.