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The aim of the present study was to investigate the effects of cadmium (Cd) (5 and 50 mg Cd/l in drinking water) and ethyl alcohol (ethanol, EtOH) (5 g EtOH/kg b.wt., intragastrically), administered alone or simultaneously, on the concentrations of pro-inflammatory (interleukin-1, IL-1?; interleukin-6, IL-6; tumor necrosis factor-?, TNF? and interferon ?, INF?) and anti-inflammatory (interleukin-4, IL-4) cytokines in the serum of rats. In order to estimate the involvement of Cd- or/and EtOH-induced oxidative stress in damage to cytokines, the concentration of protein carbonyl groups (PC), as a marker of oxidative protein damage, was also determined. Exposure to 5 and 50 mg Cd/l, alone or in combination with EtOH, led to an increase in the serum concentrations of IL-1?, TNF? and INF? with a simultaneous decrease in IL-4 concentration, compared to the control. The concentration of IL-6 was elevated only after administration of 50 mg Cd/l, both alone and in combination with EtOH. The exposure to EtOH alone resulted in increased concentrations of TNF? and INF?, as well as in decreased concentrations of IL-4. In rats co-exposed to Cd and EtOH, the changes observed in the concentrations of the cytokines, except in IL-6, were more advanced, compared to the animals treated with these xenobiotics alone. Exposure to Cd and EtOH, both alone and in combination, caused an increase in the serum PC concentration. The concentration of PC positively correlated with the concentrations of IL-1?, IL- 6, TNF? and INF? and negatively with IL-4 concentration. The results suggest that changes in the cytokines examined are more enhanced after combined exposure to Cd and EtOH, especially at higher Cd dosage. Moreover, it can be hypothesized that oxidative stress may be involved in the mechanism leading to changes in the concentration of cytokines after exposure to Cd and EtOH alone and in combination.
Badano wpływ chlorfenwinfosu na aktywność aminotransferaz (AspAT, AlAT) w surowicy krwi i frakcjach homogenatu wątroby szczurów otrzymujących insektycyd w dawce 0,5 LD50 bądź 0,1 LD50 Stwierdzono wzrost aktywności AlA T w surowicy krwi (1 i 24 h) oraz przejściowy wzrost aktywności Asp A T, a także zmiany aktywności badanych aminotransferaz we frakcjach homogenatu wątroby.
The effect of continuous exposure to lead (Pb) and ethanol on Pb turnover and zinc (Zn), copper (Cu), iron (Fe), calcium (Ca) and magnesium (Mg) body status was studied in male Wistar rats. The animals received an aqueous solution of 10% (w/v) ethanol and/or 500 μg Pb/cm³ as the only drinking fluid for 12 weeks. Exposure to Pb as well as ethanol alone influenced the body status of Zn, Cu, Fe, Ca and Mg. Disturbances in their metabolism were reflected in decreased bioavailability, changes in serum and/or tissue concentrations and urinary excretion. The most serious disorders under Pb influence were observed in Fe metabolism, while ethanol alone disturbed mainly Fe, Cu and Zn body status. In the conditions of co-exposure to Pb and ethanol some changes were more or less evident and sometimes they had different direction than at separate intoxication. Moreover, simultaneous exposure to Pb and ethanol led to changes in the concentrations of Cu, Fe and Mg, which were not observed in the case of separate administration. The independent action of Pb and/or ethanol as well as the interactive effect of both substances involving the modifying influence of ethanol on Pb turnover could explain the changes in the metabolism of bioelements under combined exposure to Pb and ethanol. Our results seem to indicate that Pb-exposed human subjects abusing ethanol may be more vulnerable to the accumulation of Pb in body organs and metabolic disorders of some bioelements, which may in consequence enhance the risk of health injury.
The aim of this study was to examine the influence of oral intoxication with cadmium and ethanol separately or together on zinc concentrations in liver and kidney of rats. Cadmium was administered at a concentration of 50 mg Cd/dm3 in drinking water for 8 weeks. Ethanol was given in a dose of 5 g/kg of body weight (as a 25% solution) every 12 h for the last 108 h of the experiment. The conducted study has shown that intoxication with cadmium and ethanol alone as well as in combination leads to an increase in zinc concentrations in the liver and kidney. The elevation of zinc levels is highest when the rats are co-exposed to cadmium and ethanol. The deposition of zinc in the liver and kidney of cadmium intoxicated rats is associated with cadmium accumulation and induction of metallothionein synthesis in these organs. Ethanol is also able to induce metallothionein synthesis and an elevation of zinc concentrations in the liver and kidney. As a result, in conditions of co-exposure these effects sum up.
The involvement of some low-molecular thiol compounds in the mechanisms of peroxidative action of cadmium (Cd) and ethanol (EtOH) was studied. Concentrations of reduced glutathione (GSH), metallothionein (Mt) and thiol (-SH) groups in protein and non-protein fractions were assessed in the homogenates of the liver and kidney of rats exposed to Cd (50 Cd/dm³ of drinking water) and EtOH (5 g EtOH/kg body weight/24 h, intragastrically), singly or in combination, for 12 weeks. Exposure to Cd caused a reduction in the concentration of GSH and non-protein SH groups in the liver and kidneys with a simultaneous increase in Mt level in these organs. The concentration of total SH groups increased only in kidneys. Administration of EtOH had no effect on Mt concentration in both organs, but caused a reduction in the concentration of GSH and non-protein SH groups. A reduction in the level of total SH groups following exposure to EtOH was also noted in the liver. In the group of rats with a simultaneous exposure to Cd and EtOH, GSH concentration was decreased in the liver compared to the control and Cd-exposed animals, and in the kidney in comparison to the control and EtOH-receiving rats. Following the combined exposure to Cd and EtOH, the concentration of non-protein SH groups decreased in the liver and kidneys in comparison to the control and Cd-exposed rats, and in the liver also in comparison to the EtOH group. Mt concentration increased in the liver and kidneys of animals exposed to a combination of Cd and EtOH, compared to the control and EtOH group, but was reduced compared to the Cd group. Combined administration of Cd and EtOH caused an increase in the concentration of total SH groups in the kidneys compared to the control, Cd and EtOH groups. A negative correlation was found between GSH concentration and malondialdehyde (MDA) levels and positive correlation between Mt and MDA. The intensity of lipid peroxidation as well as GSH and Mt concentrations influencing this process in the state of combined exposure to Cd and EtOH results both from independent actions of these substances and interactions between them. The study outcome seems to indicate that the Cd- and EtOH-induced reduction in GSH and non-protein SH groups in the liver and kidneys may be one of the mechanisms that leads to lipid peroxidation in these organs.
Inhibition by ethanol of the activities of lysosomal exoglycosidases in stomach, small intestine, liver and brain of rats exposed to cadmium (Ca ) was determined. Out of the glycosidases tested the most distinct effect of Cd2+ and ethanol administered to the rats in vivo was observed in the small intestinal mucosa in a decreasing orden N-acetyl-^-hexosaminidase, p-galactosidase and a-fucosidase.
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