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The exposure to extremely low frequency electromagnetic field (ELF-MF, frequencies less than 200-300 Hz) can alter the transcription and translation of genes, influence the cell proliferation rate and affect enzyme activities. Moreover, the hypothesis that ELF-MF increases free oxygen metabolites generation has been proposed. Since recent in vivo studies suggest that electric and magnetic fields are able to affect adipose cells metabolism. The aim of the study was to examine the effects of ELF-MF (frequency of basic impulse 180-195 Hz, induction 120 µT) on cell proliferation, antioxidative enzyme activities and malondialdehyde (MDA) concentration in 3T3-L1 preadipocyte cell culture. We found that ELF-MF application lasting 36 minutes daily failed to influence cell count after 24h and 48 h of incubation. After 24 h, in the ELF-MF treated group, manganese- and copper-zinc-containing superoxide dismutase (MnSOD and Cu/ZnSOD) isoenzymes media activities were decreased, catalase activity was increased, whereas there were no significant differences in glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-Rd) activities in comparison to the control. After 48 h of incubation, all enzyme activities were reduced, except for GSSG-Rd, in which no changes were noticed. MDA concentration at 24 h after incubation with the exposure to ELF-MF was significantly higher in comparison to the control, without ELF-MF. After 48 h of incubation, MDA levels were significantly lower in both groups with no differences between the groups without and with ELF-MF. We conclude that ELF-MF influences antioxidative enzyme activities and increases lipid peroxidation in 3T3-L1 preadipocyte cultures.
The experimental model of acute gastritis such as water immersion restraint (WRS) stress-induced gastric injury is useful tool in examination of pathomechanism of acute gastritis. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however, the interaction between reactive oxygen species (ROS) and NO on gastric mucosal integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used and the number of gastric lesions was counted in each stomach. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4- hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue levels of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of mucosal levels of MDA and 4-HNE, and it was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction in gastric lesion number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS plays an important role in the action of NO-donors on healing of acute gastric lesions induced by 3.5 h of WRS. NO-donors caused an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by an increase of SOD activity.
The aim of this paper was to study the activity of liver superoxide dismutase and catalase and the concentration of liver malondialdehyde in rats intoxicated with chlorfenvinphos, an organophosphate widely used as an insecticide. The study was carried out on male Wistar rats weighing 180-230 g. The rats were divided into two groups: examined - receiving oil solution of chlorfenvinphos in doses of 0.5 LD50, and 0.1 LD50, and control group - receiving oil. The activity of superoxide dismutase (SOD), catalase (CAT) and concentration of malondialdehyde (MDA) were determined after 1, 24 and 48 hours of intoxication. We observed an increase in the liver activity of SOD in further period of intoxication with chlorfenvinphos in both doses and a decrease of liver SOD activity in the rats intoxicated with the higher dose. The CAT activity in liver of the treated rats increased at the 1st hour of experiment with a dose of 0.5 LD50 and at the Ist hour and the 24th hour after intoxication with a dose 0.1 LD50. Hepatic concentration of MDA showed a decrease at the 24th hour of intoxication with chlorfenvinphos and an increase at the 48th hour of intoxication with the higher dose and returned to control value for the rats intoxicated with the lower dose. SOD and CAT play a major role in the maintaince of the physiological level of reactive form of oxygen. When reactive oxygen species generation exceeds capability of redox degrading systems, MDA levels increase. The results obtained suggest that reactive oxygen species in liver injury might be caused by chlorfenvinphos.
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