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The objective of this study was to investigate the effects of inoculum concentration, plant post-inoculation incubation temperature and exogenous hydrogen peroxide (H2O2) on the induction of the hypersensitive response (HR) in Nicotiana tabacum against Xanthomonas perforans. Inoculation of leaves with X. perforans at a concentration of 108 CFU · ml–1 and incubation of plants at 30°C resulted in the strongest HR elicitation. Furthermore, an exogenous supply of H2O2 accelerated X. perforans-induced HR, whereas in planta H2O2 removal by application of catalase led to a delay in HR development. Our data suggest that H2O2 has an important role in HR of N. tabacum against X. perforans.
An enhanced formation of nitric oxide (NO) by the inducible NO synfhase (iNOS) may contribute to the pathophysiology of hemorrhagic shock. This study investigates the effect of a novel, potent and selective inhibitor of iNOS activity (GW274150) on the circulatory failure and the organ injury and dysfunction associated with hemorrhagic shock in the anesthetised rat. Hemorrhage (sufficient to lower mean arterial blood pressure to 45 mmHg for 90 min) and subsequent resuscitation with shed blood resulted (within 4 h after resuscitation) in a delayed fall in blood pressure, renal and liver injury and dysfunction as well as the pancreatic injury. Pre-treatment of rats with GW274150 (5 mg/kg at 30 min prior to the onset of hemorrhage) attenuated the renal dysfunction as well as the liver and pancreatic injury caused by hemorrhage and resuscitation. Interestingly, GW274150 did not reduce the delayed fall in blood pressure associated with hemorrhagic shock. We propose that an enhanced formation of NO from iNOS contributes to the organ injury and dysfunction in hemorrhagic shock, and that highly selective inhibitors of iNOS activity, such as GW274150, may represent a novel therapeutic approach for the therapy of hemorrhagic shock.
Deficiencies in superoxide dismutases (Cu,Zn-SOD or Mn-SOD) strongly shorten the life span of yeast cells. The effects of these deficiencies are additive. In contrast, deficiencies in catalases do not influence life span. Our results confirm that free radical processes may be involved in aging.
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.
Cardiac ischemia/reperfusion leads to coronary endothelial dysfunction, mediated by superoxide anion (O2-), but not hydroxyl radical (.OH). Ischemic preconditioning and mitochondrial ATP-dependent potassium channel opener (diazoxide) protect endothelium in the mechanism involving attenuation of O2- burst at reperfusion. We hypothesize that the endothelial protection involves upregulation of myocardial anty-O2- defense. Langendorff-perfused guinea-pig hearts were subjected to global ischemia/reperfusion (IR) or were preconditioned prior to IR with three cycles of ischemia/reperfusion (IPC) or infusion/washout of 0.5 µM diazoxide. Coronary flow responses to acetylcholine were measures of endothelium-dependent vascular function. Myocardial outflow of O2- and of .OH during reperfusion and myocardial activities of superoxide dismutase (SOD) and catalase were measured. IR impaired acetylcholine response and augmented cardiac O2- and .OH outflow. IPC, diazoxide, and SOD (150 IU/ml) attenuated O2- outflow, increased .OH outflow and protected endothelium. There were no differences in Cu/Zn-SOD, Mn-SOD and catalase activities between sham-perfused and IR hearts and only catalase activity was increased in the IPC hearts. We speculate that: (i) IPC and diazoxide endothelial protection involves activation of some SOD-like anti-O2- mechanism resulting in attenuation of O2- burst and increase in .OH burst, (ii) improved SOD activity might have not been detected because it was confined to a small, although functionally important, enzyme fraction, like that bound to the endothelial glycocalyx.
Sulphide-2-chloroethyl-3-chloropropyl is an alkylating agent. It posssesses mutagenic and carcinogenic properties, participates in oxidative processes and can induce lipid peroxidation.The aim of our investigation was to define antioxidative activity of natural anthocyanins after single experimental intoxication with sulphide-2-chloroethyl-3-chloropropyl in mice. Catalase activity in hemolysate, thiobarbituric acid reacting substances (TBARS) concentration in hemolysate and selected organs were determined. The study confirms increased lipid peroxidation as a result of sulphide-2-chloroethyl-3-chloropropyl intoxication, but natural anthocyanines derived from Aronia Melanocarpa also seem to play a protective role as an antioxidative agent.
The effects of the exposure of human erythrocytes to different concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin were studied. Particular attention was paid to lipid peroxidation, haemoglobin oxidation, and changes in the activity of catalase and glutathione peroxidase. Human erythrocytes at a 5% haematocrit were incubated with 2,3,7,8-TCDD at concentrations of 0.2 ppm to 1.6 ppm (ng-mg/ml erythrocytes) for 1 hour. The results obtained show that 2,3,7,8-TCDD induces the generation of lipid peroxides and the oxidation of Hb, and decreases the activity of catalase and glutathione peroxidase. This supports the thesis that TCDD causes oxidative stress in erythrocytes.
Hydrogen peroxide (H₂O₂) formation in surface waters is initiated by the absorption of sunlight by dissolved organic matter (DOM). The fraction of the DOM pool that interacts with sunlight, referred to as chromophoric dissolved organic matter, impacts the optical properties of surface waters. Second source of H₂O₂ is wet and dry deposition of photogenerated substance in the atmosphere and biological production. The study examined the concentration of hydrogen peroxide in water from the surface microlayer (SM) (<100 m) and subsurface water (SSW) (25 cm) in the typical eutrophic (TOC 5–15 mg dm⁻³; chlorophyll 5–26 g dm⁻³, water transparency 0.6–1.0 m) lake as well as the impact of this compound on occurrence and survivorship of catalase-positive and catalase-negative bacteria isolated and cultured on the TSA medium (Difco). The experimental H₂O₂ concentrations ranged between 500–5000 nM. The concentration of H₂O₂ in analyzed water samples clearly increased in day-time hours and was different in May, July and October. The highest natural concentration of H₂O₂ (700 nM) was observed in SM water in summer in afternoon hours. During that period, 100% of bacterial populations found in SM water produced catalase. The experiments confirmed that environmental concentrations of H₂O₂ caused no considerable decrease in survivorship of culturable bacteria, while concentrations exceeding 1000 nM were lethal for the majority of catalasenegative bacteria, but not for catalase-positive bacteria.
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