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W pracy oceniano potencjał anty oksydacyjny kwercetyny wykorzystując w tym celu metodę Total Antioxidant Status (TAS) i Peroxyl Radical Trapping Capacity (PRTC).
W pracy przedstawiono wyniki badań wpływu regulatora wzrostu roślin - stymulenu indukcję różnych form molekularnych cytochromu P-450 w wątrobie szczurów.
The aim of study was estimate the effects of acetazolamid administration on arterial acid-base equilibrium and electrolyte concentrations and electrocardiograms in dogs. The study was carried out on 10 mixed-breed dogs, which were administered acetazolamid over 3 days in doses of 30 mg/kg b.w. twice a day. Administration of acetazolamid caused a decrease in pH levels, partial pressure of carbon oxide, bicarbonates in the blood and ions of potassium in the serum. An increase of chloride and sodium concentration in serum was also observed. These results indicate hypochloremic metabolic acidosis associated with hypokalemia. Electrocardiography recordings in the examined dogs were abnormal. Prolonged QT intervals, depression of ST segments and the appearance of a paroxysmal, polymorphous type of ventricular tachycardia were also recorded.
The aim of the study was an evaluation of changes in protein level and activity of SOD isoenzymes, and the participation of AP-1 and NF-κB in subsequent stages of colorectal cancer development. Studies were conducted on 65 colorectal cancers. Controls were unchanged colon regions. Activity of SOD isoenzymes, lipid peroxidation level (TBARS), and protein level of SOD1, SOD2, AP-1 and NF-κB were determined. We found that the protein level and activity of SOD isoenzymes and protein level of AP-1 and NF-κB change in subsequent stages of clinical advancement of colorectal cancer, according to UICC (I-IV), and in grades of tumor cells differentiation (G1-G3). These results indicate adaptation of colorectal cancer cells to oxidative stress, and show that the observed changes of SOD activity and protein level depend on gradual progression of colorectal cancer, and suggest an impairment of processes regulated by AP-1 and NF-κB which are critical for tumor progression (proliferation, differentiation and apoptosis).
We investigated glutathione level, activities of selenium independent GSH peroxidase, selenium dependent GSH peroxidase, GSH S-transferase, GSH reductase and the rate of lipid peroxidation expressed as the level of malondialdehyde in liver tissues obtained from patients diagnosed with cirrhosis or hepatocellular carcinoma. GSH level was found to be lower in malignant tissues compared to adjacent normal tissues and it was higher in cancer than in cirrhotic tissue. Non-Se-GSH-Px activity was lower in cancer tissue compared with adjacent normal liver or cirrhotic tissue, while Se-GSH-Px activity in cancer was found to be similar to its activity in cirrhotic tissue and lower compared to control tissue. An increase in GST activity was observed in cirrhotic tissue compared with cancer tissue, whereas the GST activity in cancer was lower than in adjacent normal tissue. The activity of GSH-R was similar in cirrhotic and cancer tissues, but higher in cancer tissue compared to control liver tissue. An increased level of MDA was found in cancer tissue in comparison with control tissue, besides its level was higher in cancer tissue than in cirrhotic tissue. Our results show that the antioxidant system of cirrhosis and hepatocellular carcinoma is severely impaired. This is associated with changes of glutathione level and activities of GSH-dependent enzymes in liver tissue. GSH and enzymes cooperating with it are important factors in the process of liver diseases development.
The aim of the present study was to determine antioxidant defence mechanisms in the rat and Hymenolepis diminuta after long-term infestation. We determined levels of oxidative stress markers, and activity of antioxidant enzymes in the rat small intestine and in particular parts of H. diminuta. Observed changes in antioxidant enzymes activity in H. diminuta and the rat intestine indicate the defence against parasitic infestation and probably allowed parasite to adapt and live in oxidative stress.
The aim of the study was the evaluation of cadmium effects on the activity of antioxidant enzymes in rat hepatocytes. The studies were conducted with isolated rat hepatocytes incubated for 1 or 2 hours in a modified (deprived of carbonates with phosphates) Williams’ E medium (MWE) in the presence of cadmium chloride (25, 50 and 200 μM). Hepatocytes incubated in the MWE medium without cadmium chloride were used as a control. The application of the modified Williams’ E medium allowed for the appearance of cadmium compounds in a soluble form that is indispensable for suitable estimation of its toxic action. There were evaluated markers of the oxidative stress such as: concentration of thiobarbiturate reactive substances (TBARS) – proportional to the level of lipid peroxidation, concentration of reduced glutathione (GSH), and the activity of antioxidant enzymes, including superoxide dismutase (SOD1 and SOD2), catalase (CAT), total glutathione peroxidase (GSHPx), selenium – dependent glutathione peroxidase (SeGSHPx), glutathione transferase (GST) and glutathione reductase (GSHR). Alterations of antioxidant enzymes activity, the level of TBARS and GSH in isolated rat hepatocytes caused by cadmium in vitro, were shown to depend on the concentration and time of exposure of cells to this metal. The increased level of TBARS and GSH was observed as well as changes in the activity of antioxidant enzymes. The activity of SOD isoenzymes and CAT was increased, whereas GSHPx and GST were decreased. These results indicate that cadmium induces oxidative stress followed by alterations in the cellular antioxidant enzyme system in isolated rat hepatocytes.
The aim of the study was to evaluate the effect of cadmium on the antioxidant enzyme activity in rat hepatocytes. The experiments were conducted on isolated rat hepatocytes, which were incubated for two hours in modified Williams’ E medium (MWE) with 25, 50, and 200 µM cadmium chloride (CdCl₂). Hepatocytes incubated in MWE medium without cadmium chloride were used as a control. The activity of antioxidant enzymes - superoxide dismutases (SOD1 and SOD2), catalase (CAT), total glutathione peroxidase (tot. GSHPx), selenium-dependent glutathione peroxidase (Se-GSHPx), glutathione S-transferase (GST) and glutathione reductase (GSHR) - and the values of the studied oxidative stress markers - the concentration of tiobarbituric-acid-reacting substances (TBARS) and reduced glutathione (GSH) - indicate that cadmium induces oxidative stress in rat hepatocytes, which impairs antioxidative mechanisms.
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