The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl2 for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na2SeO3 for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage., B. I. Ognjanović, S. D. Marković, S. Z. Pavlović, R. V. Žikić, A. Š. Štajn, Z. S. Saičić., and Obsahuje bibliografii a bibliografické odkazy
The aim of the study was to char acterize a) the lipofuscin-like pigment (LFP) accumulation (an indicator of ROS production) in the rat heart during early postnatal period and b) possible antioxidative role of selenium. Experimental animals received Na 2 SeO 3 in drinking water during gravidity and up to day 15 post partum . Two fluorophores of LFP in the hearts of 1-, 4-, 7- and 15-day-old rats were evaluated by fluorescent analysis. The highest level of heart/body weight ratio in control rats was observed on day 4, in the Se-supplemented rats on day 7. Cardiac LFP content in controls increased from postnatal day 4, in the hearts of Se-supplemented rats the LFP content increased already from day 1. As compared with the Se-supplemented group the LFP content of control hearts was significantly higher on day 1 but significantly lower on day 4. LFP concentration in control hearts decreased from postnatal day 1 to 4; this decrease was followed by significant increa se until day 7 and decrease to day 15. LFP concentration in the Se-supplemented hearts was the highest on postnatal day 7; it differed from controls on day 1 and 4. Significant changes of LF P suggest an important role of ROS during critical ontogenetic period., I. Ošťádalová, Z. Charvátová, J. Wilhelm., and Obsahuje bibliografii
Increased oxidative stress in the brain during the course of Alzheimer’s disease (AD) leads to an imbalance of antioxidants and formation of free radical reaction end-products which may be detected in blood as fluorescent lipofuscin-like pigments (LFPs). The aim of this study was to evaluate and compare LFPs with plasma selenium concentrations representing an integral part of the antioxidant system. Plasma samples from subjects with AD dementia (ADD; n=11), mild cognitive impairment (MCI; n=17) and controls (n=12), were collected. The concentration of selenium was measured using atomic absorption spectroscopy. LFPs were analyzed by fluorescence spectroscopy and quantified for different fluorescent maxima and then correlated with plasma selenium. Lower levels of selenium were detected in MCI and ADD patients than in controls (P=0.003 and P=0.049, respectively). Additionally, higher fluorescence intensities of LFPs were observed in MCI patients than in controls in four fluorescence maxima and higher fluorescence intensities were also observed in MCI patients than in ADD patients in three fluorescence maxima, respectively. A negative correlation
between selenium concentrations and LFPs fluorescence was observed in the three fluorescence maxima. This is the first study focused on correlation of plasma selenium with specific lipofuscin-like products of oxidative stress in plasma of patients with Alzheimer´s disease and mild cognitive impairment.
Effect of selenium on leaf senescence was studied in oilseed rape plants treated with 10 μM Na2SeO4 at a rosette growth stage. In addition to developmental senescence, N deficiency and leaf detachment were used for induction of senescence. Nonphotochemical quenching declined in old leaves as senescence became more advancing but rose progressively in the plants supplied by Se. The total carbohydrate and protein pools decreased with leaf age, while increased by the Se treatment. However, during senescence induced by N deficiency, Se did not change remarkably the C and N metabolism, but delayed senescence mainly through protection of plants from photoinhibitory effects. After detachment, untreated leaves became chlorotic and necrotic, while the Se-treated ones remained fairly green. Our results demonstrated that Se delayed leaf senescence by a maintaining or even improving photochemical activities. During developmental senescence, the Se effect on the extending life span of the leaves was additionally linked to the metabolic regulation of senescence., S. Rahmat, R. Hajiboland, N. Sadeghzade., and Obsahuje bibliografii
Total superoxide dismutase (total SOD), copper zinc containing superoxide dismutase (CuZn SOD), and manganese superoxide dismutase (Mn SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione- S-transferase (GST) activities as well as ascorbic acid (AsA), and vitamin E (vit E) concentrations were analysed in the liver of rats exposed to cadmium (15 mg Cd/day/kg), selenium (7 fig Se/day/kg), and to cadmium + selenium (15 mg Cd + 7 ptg Se/day/kg), and in control animals. Cadmium caused a decrease of total SOD, Mn SOD, CAT and GSH-Px but an increase of GST activity in the liver of rats. Contrary to cadmium, selenium caused a significant increase of the activity of these enzymes except for GSH-Px. By concomitant exposure to both cadmium and selenium, the toxic effects of cadmium on the activity of mentioned enzymes we abolished. In all exposed groups, the activity of enzyme glutathione-S-transferase was enhanced, indicating its increased role in prevention of lipid peroxidation. Cadmium decreased the concentration of AsA and increased the concentration of vitamin E in the liver, while selenium increased the concentration of both vitamins. However, by concomitant administration of cadmium and selenium, these changes were diminished and tended to reach control values.
For more than sixty years lith ium carbonate has been used in medicine. However, during its administration different side effects including oxidative stress can occur. Selenium belongs to essential elements possessing antioxidant properties. This study aimed at evaluating if selenium co uld be used as a protective adjuvant in lithium therapy. The experiment was performed on four groups of Wistar rats: I (control), II (Li), III (Se), IV (Li + Se) treated with saline, lithium carbonate (2.7 mg Li/kg b.w.), sodium selenite (0.5 mg Se/kg b.w.) and lithium carbonate (2.7 mg Li/kg b.w.) + sodium selenite (0.5 mg Se/kg b.w.), respectively. All substances were administered as water solutions by stomach tube for 3 or 6 weeks. Catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GP x) as well as malonyldialdehyde (MDA) were determined in brain homogenates. Lithium slightly enhanced MDA and depressed CAT and SOD after 6 weeks as well as GPx after 3 weeks. Selenium co -administration show ed tendency to restore the disturbed parameters. Selenium alone and given with lithium significantly increased GPx vs. Li- treated group after 3 weeks. Having regarded the outcomes of this study, the research on application of selenium during lithium treatment seems to be worth continuation., M. Kiełczykowska, J. Kocot, A. Lewandowska, R. Żelazowska, I. Musik., and Obsahuje bibliografii
Intrahepatic cholestasis of pregnancy (ICP) is a disorder of liver function, commonly occurring in the third trimester but sometimes also as soon as the end of the second trimester of pregnancy. Symptoms of this disorder include pruritus, plus abnormal values of bile acids and hepatic transaminases. After birth, symptoms disappear and liver function returns to normal. Though ICP is relatively non-complicated and often symptomatically mild from the point-of-view of the mother, it presents a serious risk to the fetus, making this disease the subject of great interest. The etiology and pathogenesis of ICP is multifactorial and as yet not fully elucidated. Hormonal factors likely play a significant role, along with genetic as well as exogenous factors. Here we summarize the knowledge of changes in steroid hormones and their role in the development of intrahepatic cholestasis of pregnancy. In addition, we consider the role of exogenous factors as possible triggers of steroid hormone changes, the relationship between metabolic steroids and bile acids, as well as the combination of these factors in the development of ICP in predisposed pregnant women., A. Pařízek, M. Dušková, L. Vítek, M. Šrámková, M. Hill, K. Adamcová, P. Šimják, A. Černý, Z. Kordová, H. Vráblíková, B. Boudová, M. Koucký, K. Malíčková, L. Stárka., and Obsahuje bibliografii
The protective role of nutrition factors such as calcium, vitamin D and vitamin K for the integrity of the skeleton is well understood. In addition, integrity of the skeleton is positively influenced by certain trace elements (e.g. zinc, copper, manganese, magnesium, iron, selenium, boron and fluoride) and negatively by others (lead, cadmium, cobalt). Deficiency or excess of these elements influence bone mass and bone quality in adulthood as well as in childhood and adolescence. However, some protective elements may become toxic under certain condition s, depending on dosage (serum concentration), duration of treatment and interactions among individual elements. We review the beneficial and toxic effects of key elements on bone homeostasis., I. Zofkova, M. Davis, J. Blahos., and Obsahuje bibliografii