Does the platelet-activating factor affect the antioxidant defense system? (original) (raw)
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Biological Trace Element Research, 2000
The platelet-activating factor (PAF) is an inflammatory mediator and it may exert some of its effects by reactive oxygen species (ROS). We investigated the effects of PAF and hyperbaric oxygenation (HBO) on copper (Cu) and zinc (Zn) levels in plasma and the intracellular antioxidant enzyme activities of rats. PAF administiration caused a decrease in erythrocyte catalase (CAT) and glutathione peroxidase (GPx) activities and in the plasma zinc level. Following PAF administration, exposure to HBO also caused a decrease in erythrocyte GPx activity. These results support the hypothesis that PAF may produce free oxygen radicals and HBO enhances this effect. The enzyme activities of the antioxidant defense system were found to be affected by these oxidative processes. This is likely to be the result of excessive production of ROS or overutilization and/or inhibition of the antioxidant enzymes.
International Journal of Angiology, 1994
Platelet-activating factor (PAF) is released in numerous clinical situations. PAF primes or directly activates polymorphonuclear (PMN) leukocytes, which results in release of oxyradicals (O2, H2Oz, .OH) and hypochlorous acid (HOC1). The authors investigated the effects of PAF (1 ixg/kg IV) in the absence and in the presence of antioxidants (superoxide dismutase [SOD], catalase [CAT], dimethylthiourea [DMTU]) and methionine, a quencher of HOC1, on cardiac function and contractility; blood lactate, gases, and pH levels; serum creatine kinase activity (CK); chemiluminescent activity of PMN leukocytes; and cardiac tissue malondialdehyde (MDA) in anesthetized dogs. Hemodynamic measurements and collection of blood samples for various biochemical measurements were made before and at various intervals up to two hours after PAF administration in the presence and absence of various antioxidants. PAF produced a decrease in indices of cardiac function and contractility and an increase in systemic and pulmonary vascular resistance. There were decreases in the blood pH and PMN leukocyte chemiluminescence and increases in blood lactate, serum CK activity, and tissue MDA content. SOD plus catalase or DMTU plus methionine reduced the effects of PAF on cardiac function and contractility, blood lactate and pH, serum CK, and cardiac tissue MDA. The antioxidants only partially antagonized the deleterious effects of PAF. The combination of SOD + CAT was superior to that of DMTU + methionine in reducing the deleterious effects of PAF. These results suggest that PAF-induced depression of cardiac function and contractility, and the increase in systemic and pulmonary vascular resistance, may be partly mediated by the release of oxyradicals and HOCI from PMN leukocytes. Antioxidants may be beneficial in reducing the deleterious effects of PAF on the cardiovascular system.
Clinical Biochemistry, 2005
Objectives: The aim of the study was to investigate whether a single hyperbaric oxygen exposure causes oxidative stress in isolated platelets. Design and methods: Isolated horse platelets were exposed to 100% oxygen at 2.2 atmospheres, or 100% oxygen under normobaric conditions, or air under normobaric conditions for 90 min. Results: There were no differences in platelet SOD activity between conditions, but there was a rise in SOD in all cases after 24 h (in control platelets at 24 h, SOD was 11.9 T 1.9 nmol/min/mg protein compared to initial background levels of 8.2 T 1.9 nmol/min/mg protein) (P < 0.05). Neither platelet catalase activity nor platelet GSH concentration changed over time, nor between conditions (catalase activity remained at around 12 units/mg protein, and GSH at around 1.58 nmol/mg protein). Conclusions: These data suggest that a single HBO exposure has no detrimental effect on platelet biochemistry, and does not cause overt oxidative stress in vitro.
Polish Hyperbaric Research
Hyperbaric oxygen (HBO) treatment is generally a relatively safe therapy for various conditions. However, there are some adverse side effects. For example HBO tratment has been reported to increase the production of free oxygen radicals(FRs). Furthermore, to our knowledge, no previous clinical research has been carried out to study the involvement of platelet-activating factor(PAF)as the lipid oxidative stressor in patients undergoing HBO treatment. A total of 45 patients included in this study were first given clinical assessment and laboratory measurements before starting HBO treatment and were named group baseline. After the HBO treatment, the same clinical and laboratory measurements from the same patients were repeated and this was named group sesion >20.As expected, long-term HBO treatment had no effect on oxLDL (oxidized low-density lipoprotein), a lipid oxidative stress(OS) marker. However, the mean PAF values in the second group showed a statistically significant increas...
Journal of Experimental and Integrative Medicine, 2011
The aim of this study is to provide comprehensive information on the relationship between clinically used hyperbaric oxygen (HBO) protocols and its oxidative effects. In order to enlighten this issue, we investigated the effects of various HBO pressure modalities on oxidant and antioxidant parameters in the rat lung. Methods: Sixty male Sprague-Dawley rats were divided into 6 groups. Group 1 was used as control. Groups 2 to 6 were subjected to 100% oxygen at a pressure of 1, 1.5, 2, 2.5, and 3 ATA (atmosphere absolute) respectively for 2 hours. The lungs were taken immediately after exposure. Oxidation products of lipids (thiobarbituric acid reactive substances, TBARS) and proteins (carbonyl formation, PCO), and antioxidant enzyme levels (superoxide dismutase, SOD; catalase, CAT, glutathione peroxidase, GSH-Px) were determined. Results: TBARS, PCO, SOD and CAT levels increased concordantly with pressure. Significant change of TBARS levels started from 100% oxygen exposure at 1 ATA (normobaric), but PCO and CAT levels were affected first after 1.5, and SOD activity after 2 ATA. A significant correlation exists between exposure pressure and oxidative parameters. GSH-Px activity was not affected significantly. Conclusion: The oxidative effect of HBO in rat lung presents a positive correlation with increasing exposure pressure.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1995
Iron overload was developed in rats by ip injection of iron-dextran. Iron concentration in plasma increased 12-fold after 20 h of iron supplementation and unsaturated iron binding capacity (UIBC) drastically decreased in iron overloaded compared to control rats (69 + 36 and 177 _+ 19/xg/dl, respectively). Lipid peroxidation in plasma increased by 285% and plasma a-tocopherol content decreased by 40% after 20 h of iron overload, a-Tocopherol supplementation decreased by 30% the measured increase in TBARS content in plasma after iron injection. On the other hand, both iron and TBARS content in erythrocytes were not significantly different in control and iron loaded rats. However, red blood cells from iron treated rats exposed to pro-oxidant conditions showed a significant increase in TBARS content as compared to control erythrocytes, a-Tocopherol pretreatment prevented this increase. Moreover, red blood cells from iron loaded rats showed a higher content of TBARS after incubation with plasma from iron-dextran injected rats than after incubation with plasma from control animals. This measured increase was partially prevented by a-tocopherol supplementation. Neither the activity of antioxidant enzymes nor the content of a-tocopherol in red blood cells were affected by iron overload. Total thiols content was significantly lower (30%) in erythrocytes isolated from iron treated rats. The data presented here suggest that free radical generation catalyzed by metal ions may lead to consumption of thiols. The decrease in thiols content in erythrocytes could afford an appropriate degree of protection and avoid other oxidative damage to these cells.
Biological Trace Element Research, 2008
The aim of this study was to evaluate the lipid peroxidation, nitric oxide (NO), and free radical scavenging enzyme activities in erythrocytes of zinc (Zn)-deficient rats and to investigate the relationship among these parameters in either group. Sixteen male rats with a weight of 40–50 g were used for the experiment. The rats were divided into control (n = 8) and Zn-deficient groups. At the end of the experiment, the animals were anesthetized with ketamine–HCl (Ketalar, 20 mg/kg−1, i.p.), and the blood was collected by cardiac puncture after thoracotomy. Blood samples were collected in vacutainer tubes without and with K3-EDTA as anticoagulant. Erythrocyte catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GRD), glutathione-S-transferase (GST), superoxide dismutase (SOD) activities, total (enzymatic plus nonenzymatic) superoxide scavenger activity (TSSA), nonenzymatic superoxide scavenger activity (NSSA), antioxidant potential (AOP), and serum zinc (Zn) values in the Zn-deficient group were significantly lower than those of the control group, whereas NO and malondialdehyde (MDA) levels were significantly higher than those of the control group. The results show that Zn deficiency causes a decrease in antioxidant defense system and an increase in oxidative stress in erythrocyte of rats.
Oxidative Stress Induced Cell Damage and Antioxidant Enzyme Response in Human Lymphocytes
International Journal of Pharmaceutical & Biological Archive, 2017
Human lymphocytes were subjected to oxidative stress by exposing to hydrogen peroxide at concentrations varying from 0-250μM for time duration of 0-24h to evaluate cell viability. Trypan blue dye exclusion test indicated a loss of ˂5% cell viability on incubation with hydrogen peroxide for 24h; however MTT assay signified a decline of 55% activity after 12h or long with 200μM concentration. Redox status and activities of antioxidant enzymes were examined after incubation with hydrogen peroxide up to 200μM for 4h. Reduced glutathione level decreased with concentration dependent increase in lipid peroxidation, measured as MDA produced. Increase in LDH leakage from the cells with increasing hydrogen peroxide concentration in medium indicated considerable cell membrane damage. SOD and catalase activities increased at lower concentration of 50μM but at higher stress, a decline in activities of SOD, catalase and GST was observed. GPx increased with increasing hydrogen peroxide in incubati...