Plant-based n-3 polyunsaturated fatty acids (PUFA) possess a prospective antiatherogenic potential. Currant oil from Ribes nigrum L. is one of the few plant oils containing PUFAn-3 (15.3 mol%) in addition to PUFAn-6 (60.5 mol%). This study was aimed at comparing the effects of currant oil with those of lard fat, rich in saturated (43.8 mol%) and monounsaturated (47.0 mol%) fatty acids, on antioxidant parameters, the lipoprotein profile and liver lipids in rats fed on 1 % (w/w) cholesterol diets containing either 10 % of currant oil (COD) or lard fat (LFD). After 3 weeks of feeding, the COD induced a significant decrease in blood glutathione (GSH) and an increase in Cu2+ induced oxidizability of serum lipids, but did not affect liver GSH and t-butyl hydroperoxide-induced lipoperoxidation of liver microsomes. Although the COD did not cause accumulation of liver triacylglycerols as LFD, the lipoprotein profile (VLDL, LDL, HDL) was not significantly improved after COD. The consumption of PUFAn-3 was reflected in LDL as an increase in eicosapentaenoic and docosahexaenoic acid. These results suggest that currant oil affects positively the lipid metabolism in the liver, above all it does not cause the development of a fatty liver. However, adverse effects of currant oil on the antioxidant status in the blood still remain of concern., R. Večeřa, N. Škottová, P. Váňa, L. Kazdová, Z. Chmela, Z. Švagera, D. Walterová, J. Ulrichová, V. Šimánek., and Obsahuje bibliografii
The consequences of increased oxidative stress, measured as the level of malondialdehyde (MDA) during ischemia/reperfusion, were studied in 48 patients in the acute phase of myocardial infarction (AMI) and a control group (21 blood donors). The serum levels of a-tocopherol and b-carotene were followed. Immediately after the treatment onset the level of a-tocopherol started to decrease, reaching a plateau after 24 h. The consumption of b-carotene was delayed by 90 min. Steady decline was detected during the whole time interval studied (48 h). Glutathione peroxidase (GPx) activity, as a representative of antioxidant enzymes, was estimated in whole blood. The influx of oxygenated blood was accompanied by a stimulation of GPx activity, which reached its maximum at the time of completed reperfusion. When comparing the AMI patients with the control group, the levels of MDA were found significantly increased, which indicates that oxidative stress is already increased during ischemia. Lower antioxidant levels found in the patients might either already be the result of vitamin consumption during ischemia or be a manifestation of their susceptibility to AMI. Monitored consumption of a-tocopherol and b-carotene during reperfusion indicated that in the case of patients, whose level of antioxidant vitamins is below the threshold limit, a further substantial decrease of antioxidant vitamins during reperfusion could enhance the oxidative damage of the myocardium., V. Mužáková, R. Kanďár, P. Vojtíšek, J. Skalický, R. Vaňková, A. Čegan, Z. Červinková., and Obsahuje bibliografii
Serum levels of vitamin E (VE), β-carotene (BC) and vitamin C (VC) were determined in 50 patients with the first acute myocardial infarction (AMI) before starting thrombolytical treatment. VE and BC were determined by HPLC, VC spectrophotometrically. The reperfused patients were divided according to vitamin concentrations into four groups. The lowest quartile was compared with the rest of the studied population (VE: group with high (H) > 15.6 μM > group with low (L), BC: H > 0.07 μM > L, VC: H > 25 μM > L) in the following parameters: extent of myocardial damage (area under the curves of troponin I, CK-MB during 48 h), arrhythmia and congestive heart failure occurrence, size of ejection fraction, positivity of ventricular late potentials. No significant differences between groups H and L for either VE, BC or VC were found (P±0.05). As no correlation between serum concentrations of vitamins E, C and β-carotene and the extent and clinical course of AMI was found, the actual vitamin concentrations may be important for prevention of ischemic heart a disease, but they do not play a decisive role in the acute phase of myocardial infarction in humans.
Experimental data on the effect of nicotine on cerebral microvessel thrombosis is lacking. Therefore, this study was carried out to elucidate the effects of nicotine on platelet aggregation in cerebral (pial) microcirculation of the mouse, and the possible protective effect of vitamins C and E. Male TO mice were divided into six groups, and injected i.p. with saline as a control, nicotine (1 mg/kg), vi tamin C alone (100 mg/kg), vitamin E alone (100 mg/kg), nicotine plus vitamin C or nicotine plus vitamin E, all for one week before the experiment. After one week, platelet aggregation in ce rebral microvessels of these groups of mice were studied in vivo . The appearance of the first platelet aggregation and total blood flow stop in arterioles and venules were timed in seconds. In the animals treated with nicotine, venules did not show any alteration in the platelet aggregation time in comparison to the control animals. However, in arterioles platelet aggreg ation time was significantly accelerated (p<0.001) in nicotine-treated animals as compared to controls. Both vitamins C and E prevented the shortening of arteriolar platelet aggregation ti me significantly (p<0.001) when applied with nicotine but not alone. It can be concluded that nicotine enhances the susceptibility to thrombosis in the cerebral arterioles in vivo and that vitamins C and E have alleviating effect on nicotine-induced thrombotic events in mice pial microvessels., M. A. Fahim ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Various reactive oxygen species (ROS) may be produced from normal biochemical, essential metabolic processes or from external sources as exposure to a variety of agents presented in the environment. Lipids, proteins, carbohydrates and DNA are all capable of reacting with ROS and can be implicated in etiology of various human disorders (rheumatoid arthritis, reperfusion injury, atherosclerosis, lung diseases etc.). In the organism damage by ROS is counteracted with natural antioxidants (glutathione peroxidases, superoxide dismutases, catalase, glutathione, ubiquinol, uric acid, and essential minerals) and nutritional antioxidants from diet (i.e. vitamins E, C, carotenoids). Possible mechanisms of nutritional depletion and side effects of high intake are in the article described., Z. Zadák ... [et al.]., and Obsahuje seznam literatury
This study aimed to examine the effect of dietary flavonoid isoquercitrin on ovarian granulosa cells using the immortalized human cell line HGL5. Cell viability, survival, apoptosis, release of steroid hormones 17β-estradiol and progesterone, and human transforming growth factor-β2 (TGF-β2) and TGF-β2 receptor as well as intracellular reactive oxygen species (ROS) generation were investigated after isoquercitrin treatment at the concentration range of 5-100 μg.ml-1 . It did not cause any significant change (p>0.05) in cell viability as studied by AlamarBlue assay in comparison to control. No significant change was observed (p>0.05) in the proportion of live, dead and apoptotic cells as revealed by apoptotic assay using flow cytometry. Similarly, the release of 17β-estradiol, progesterone, TGF-β2 and its receptor were not affected significantly (p>0.05) by isoquercitrin as detected by ELISA, in comparison to control. Except for the highest concentration of 100 μg.ml-1 , which led to oxidative stress, isoquercitrin exhibited antioxidative activity at lower concentration used in the study (5, 10, 25, and 50 μg.ml-1 ) by hampering the production of intracellular ROS, in comparison to control, as detected by chemiluminescence assay (p<0.05). Findings of the present study indicate an existence of the antioxidative pathway that involves inhibition of intracellular ROS generation by isoquercitrin in human ovarian granulosa cells., Adriana Kolesárová, Katarína Michalcová, Shubhadeep Roychoudhury, Simona Baldovská, Eva Tvrdá, Jaromír Vašíček, Peter Chrenek, Ľuboslav Sanisló, Vladimír Křen., and Obsahuje bibliografii
Literature data support that green tea and its major component epigallocatechin gallate (EGCG) have powerful antioxidant effects. Contrary, hepatotoxicity can be induced by high-dose EGCG. The timing of exposure to green tea in relation to administration of hepatotoxic agent plays an import role too. The aim of our work was a verification of antioxidative effect of EGCG on D-galactosamine-induced injury in primary culture of rat hepatocytes. Hepatocytes were incubated with EGCG at concentrations of 1.25-10 μM and toxic D-galactosamine (GalN) for 24 hrs. Alternatively, hepatocytes were pretreated with EGCG for 24 hrs, and then incubated with EGCG and GalN for further 24 hrs. Cytotoxicity was analysed by lactate dehydrogenase activity, functional capacity by albumin production. Oxidative stress was evaluated from a production of malondialdehyde and glutathione content in the cells. EGCG protected hepatocytes against GalN-induced cytotoxicity but preventive treatment of intact hepatocytes with EGCG was required to diminish the development of hepatocyte injury. Oxidative stress induced in our study seems to overcome the ability of hepatocytes to improve GSH depletion and albumin production. Prolongation of the pretreatment with EGCG could be a promising strategy leading to amelioration of its hepatoprotective effect. and Alena Moravcová, Zuzana Červinková, Otto Kučera, Vojtěch Mezera, Halka Lotková