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 CdCl(2) 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 Na(2)SeO(3) 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.

• MeSH
• antioxidancia metabolismus   farmakologie   MeSH
• chlorid kademnatý metabolismus   toxicita   MeSH
• glutathionperoxidasa metabolismus   MeSH
• glutathiontransferasa metabolismus   MeSH
• játra účinky léků   enzymologie   metabolismus   MeSH
• katalasa metabolismus   MeSH
• krysa rodu Rattus MeSH
• kyselina askorbová metabolismus   MeSH
• látky znečišťující životní prostředí metabolismus   toxicita   MeSH
• ledviny účinky léků   enzymologie   metabolismus   MeSH
• oxidační stres účinky léků   MeSH
• oxidy selenu MeSH
• peroxidace lipidů účinky léků   MeSH
• sloučeniny selenu farmakologie   MeSH
• superoxiddismutasa metabolismus   MeSH
• vitamin E metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• chlorid kademnatý MeSH
• glutathionperoxidasa MeSH
• glutathiontransferasa MeSH
• katalasa MeSH
• kyselina askorbová MeSH
• látky znečišťující životní prostředí MeSH
• oxidy selenu MeSH
• sloučeniny selenu MeSH
• superoxiddismutasa MeSH
• vitamin E MeSH

The effects of nitroglycerine (NTG) are mediated by liberated nitric oxide (NO) after NTG enzymatic bio-transformation in cells. The aim of this study was to evaluate some products of NTG bio-transformation and their consequences on the redox status of rat erythrocytes and reticulocytes, considering the absence and presence of functional mitochondria in these cells, respectively. Rat erythrocyte and 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 NTG (0.1, 0.25, 0.5, 1.0 and 1.5 mM). In rat erythrocytes, NTG did not elevate the concentrations of any reactive nitrogen species (RNS). However, NTG robustly increased concentration of methemoglobin (MetHb), suggesting that NTG bio-transformation was primarily connected with hemoglobin (Hb). NTG-induced MetHb formation was followed by the induction of lipid peroxidation. In rat reticulocytes, NTG caused an increase in the levels of nitrite, peroxinitrite, hydrogen peroxide, MetHb and lipid peroxide levels, but it decreased the level of the superoxide anion radical. Millimolar concentrations of NTG caused oxidative damage of both erythrocytes and reticulocytes. These data indicate that two pathways of NTG bio-transformation exist in reticulocytes: one generating RNS and the other connected with Hb (as in erythrocytes). In conclusion, NTG bio-transformation is different in erythrocytes and reticulocytes due to the presence of mitochondria in the latter.

• MeSH
• erytrocyty účinky léků   metabolismus   MeSH
• hemoglobiny metabolismus   MeSH
• krysa rodu Rattus MeSH
• methemoglobin metabolismus   MeSH
• mitochondrie metabolismus   MeSH
• nitroglycerin farmakologie   MeSH
• oxidace-redukce účinky léků   MeSH
• oxidační stres účinky léků   MeSH
• peroxidace lipidů účinky léků   MeSH
• potkani Wistar MeSH
• reaktivní formy dusíku metabolismus   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• retikulocyty účinky léků   metabolismus   MeSH
• techniky in vitro MeSH
• vazodilatancia farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• hemoglobiny MeSH
• methemoglobin MeSH
• nitroglycerin MeSH
• reaktivní formy dusíku MeSH
• reaktivní formy kyslíku MeSH
• vazodilatancia MeSH

The effects of the sodium nitroprusside (SNP), a nitric oxide (NO) donor clinically used in the treatment of hypertensive emergencies on the energy production of rat reticulocytes were investigated. Rat reticulocyte-rich red blood cell suspensions were aerobically incubated without (control) or in the presence of different concentrations of SNP (0.1, 0.25, 0.5, 1.0 mM). SNP decreased total and coupled, but increased uncoupled oxygen consumption. This was accompanied by the stimulation of glycolysis, as measured by increased glucose consumption and lactate accumulation. Levels of all glycolytic intermediates indicate stimulation of hexokinase-phosphofructo kinase (HK-PFK), glyceraldehyde 3-phosphate dehydrogenase (GAPD) and pyruvate kinase (PK) activities in the presence of SNP. Due to the decrease of coupled oxygen consumption in the presence of SNP, ATP production via oxidative phosphorylation was significantly diminished. Simultaneous increase of glycolytic ATP production was not enough to provide constant ATP production. In addition, SNP significantly decreased ATP level, which was accompanied with increased ADP and AMP levels. However, the level of total adenine nucleotides was significantly lower, which was the consequence of increased catabolism of adenine nucleotides (increased hypoxanthine level). ATP/ADP ratio and adenylate energy charge level were significantly decreased. In conclusion, SNP induced inhibition of oxidative phosphorylation, stimulation of glycolysis, but depletion of total energy production in rat reticulocytes. These alterations were accompanied with instability of energy status.

• MeSH
• donory oxidu dusnatého farmakologie   MeSH
• energetický metabolismus účinky léků   fyziologie   MeSH
• krysa rodu Rattus MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý metabolismus   MeSH
• potkani Wistar MeSH
• retikulocyty účinky léků   metabolismus   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• donory oxidu dusnatého MeSH
• nitroprusid MeSH
• oxid dusnatý MeSH

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.

• MeSH
• antioxidancia metabolismus   MeSH
• erytrocyty chemie   účinky léků   MeSH
• glutathion krev   účinky léků   MeSH
• glutathionperoxidasa krev   účinky léků   MeSH
• glutathionreduktasa krev   účinky léků   MeSH
• glutathiontransferasa krev   účinky léků   MeSH
• hematokrit MeSH
• hemoglobiny analýza   účinky léků   MeSH
• kadmium toxicita   MeSH
• katalasa krev   účinky léků   MeSH
• krysa rodu Rattus MeSH
• kyselina askorbová krev   MeSH
• lipidové peroxidy krev   MeSH
• otrava kadmiem krev   prevence a kontrola   MeSH
• počet erytrocytů MeSH
• potkani Wistar MeSH
• superoxiddismutasa krev   účinky léků   MeSH
• vitamin E krev   farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• glutathion MeSH
• glutathionperoxidasa MeSH
• glutathionreduktasa MeSH
• glutathiontransferasa MeSH
• hemoglobiny MeSH
• kadmium MeSH
• katalasa MeSH
• kyselina askorbová MeSH
• lipidové peroxidy MeSH
• superoxiddismutasa MeSH
• vitamin E MeSH

Four groups of goldfish were exposed to cadmium in a concentration of 20 mg Cd/l water under aquarium conditions. The duration of exposure was 1, 4, 7 and 15 days. It was shown that the activity of superoxide dismutase (SOD) in the red blood cells (RBC) significantly decreased after the first day of cadmium exposure. However, the SOD activity increased after 7 and 15 days of cadmium treatment. Elevated activity of catalase (CAT) was found in erythrocytes of cadmium-treated fishes after 15 days, whereas plasma GOT levels was increased after 7 and 15 days and GPT levels after 1, 4, 7 and 15 days of cadmium treatment. This was accompanied by a significant decrease of blood hemoglobin concentrations (after 15 days) and hematocrit values (after 7 and 15 days). However, the concentration of blood glucose significantly increased after 1, 4, 7 and 15 days of cadmium exposure. These results indicate that cadmium causes oxidative stress and tissue damage in the exposed fishes.

• MeSH
• alanintransaminasa krev   MeSH
• aspartátaminotransferasy krev   MeSH
• erytrocyty enzymologie   MeSH
• hematokrit MeSH
• hemoglobiny analýza   MeSH
• kadmium aplikace a dávkování   toxicita   MeSH
• karas zlatý krev   MeSH
• katalasa krev   MeSH
• kinetika MeSH
• krevní glukóza metabolismus   MeSH
• superoxiddismutasa krev   MeSH
• transaminasy krev   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• alanintransaminasa MeSH
• aspartátaminotransferasy MeSH
• hemoglobiny MeSH
• kadmium MeSH
• katalasa MeSH
• krevní glukóza MeSH
• superoxiddismutasa MeSH
• transaminasy MeSH

Since nitric oxide (NO) in many cells is involved in energy metabolism, the aim of this study was to evaluate the role of isosorbide dinitrate (ISDN), a NO donor, in energy metabolism of rat reticulocytes, particularly due to their high content of hemoglobin--an effective scavenger of NO. Rat reticulocyte-rich red blood cell suspensions were aerobically incubated in the absence (control) or in the presence of different concentrations of ISDN. ISDN decreased total and coupled oxygen consumption (p<0.05) while increased uncoupled oxygen consumption (p<0.05) in a dose- and time-dependent manner. This was followed by enhancement of glycolysis, as measured by increased glucose consumption and lactate accumulation (p<0.05). Levels of all glycolytic intermediates in the presence of ISDN indicate only stimulation of pyruvate kinase activity. ISDN did not alter the concentration of ATP, while increased ADP and AMP levels (p>0.05). In rat reticulocytes under steady-state conditions, 95.4% of overall energy was produced by oxidative phosphorylation but only 4.6% by glycolysis. Due to a reduced coupled oxygen consumption in the presence of ISDN, ATP production via oxidative phosphorylation was significantly diminished. A simultaneous increase of glycolytic ATP production is not enough to ensure constant ATP production. The calculated mean ATP turnover time was prolonged by 199% in the presence of 1.5 mmol/l ISDN. In conclusion, ISDN a) inhibited total and coupled respiration but enhanced uncoupled respiration, b) stimulated glycolysis, c) decreased ATP production and d) prolonged ATP turnover time in rat reticulocytes. These effects were mediated by NO as the effector molecule.

• MeSH
• adenosindifosfát metabolismus   MeSH
• adenosinmonofosfát metabolismus   MeSH
• adenosintrifosfát metabolismus   MeSH
• donory oxidu dusnatého farmakologie   MeSH
• energetický metabolismus účinky léků   MeSH
• glykolýza účinky léků   fyziologie   MeSH
• isosorbiddinitrát farmakologie   MeSH
• krysa rodu Rattus MeSH
• oxid dusnatý metabolismus   MeSH
• oxidativní fosforylace účinky léků   MeSH
• potkani Wistar MeSH
• retikulocyty účinky léků   metabolismus   MeSH
• spotřeba kyslíku účinky léků   fyziologie   MeSH
• vazodilatancia farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adenosindifosfát MeSH
• adenosinmonofosfát MeSH
• adenosintrifosfát MeSH
• donory oxidu dusnatého MeSH
• isosorbiddinitrát MeSH
• oxid dusnatý MeSH
• vazodilatancia MeSH

The goldfish (Carassius auratus gibelio Bloch.) were exposed to cadmium in the concentration of 20 mg Cd/l water under aquarium conditions for 1, 4, 7 and 15 days. After exposure to cadmium, the activities of superoxide dismutase (SOD) and catalase (CAT) were significantly decreased. At the same time, the liver ascorbic acid (AsA) content was increased.

• MeSH
• antioxidancia metabolismus   MeSH
• časové faktory MeSH
• játra účinky léků   enzymologie   metabolismus   MeSH
• kadmium metabolismus   toxicita   MeSH
• karas zlatý metabolismus   MeSH
• katalasa metabolismus   MeSH
• kyselina askorbová metabolismus   MeSH
• spektrofotometrie atomová MeSH
• superoxiddismutasa metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• kadmium MeSH
• katalasa MeSH
• kyselina askorbová MeSH
• superoxiddismutasa MeSH

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 micrograms Se/day/kg), and to cadmium+selenium (15 mg Cd + 7 micrograms 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.

• MeSH
• játra účinky léků   metabolismus   MeSH
• kadmium antagonisté a inhibitory   farmakologie   MeSH
• krysa rodu Rattus MeSH
• kyselina askorbová metabolismus   MeSH
• osmolární koncentrace MeSH
• oxidoreduktasy metabolismus   MeSH
• potkani Wistar MeSH
• selen farmakologie   MeSH
• vitamin E metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• kadmium MeSH
• kyselina askorbová MeSH
• oxidoreduktasy MeSH
• selen MeSH
• vitamin E MeSH