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Redox Ratio (redox + ratio)
Selected AbstractsEffects of Fusaric Acid on Reactive Oxygen Species and Antioxidants in Tomato Cell CulturesJOURNAL OF PHYTOPATHOLOGY, Issue 10 2001E. Ku Generation of O2, and H2O2 as well as the activities of superoxide dismutase, catalase, ascorbate peroxidase, guaiacol peroxidase, dehydroascorbate reductase and ascorbate content were studied in tomato cell cultures in response to fusaric acid , a nonspecific toxin of phytopathogenic Fusarium species. Toxin treatment resulted in decreased cell viability which was preceded by culture medium alkalinization up to 0.65 pH unit and enhanced extracellular O2, production. The H2O2 level was not significantly affected. In toxin-treated cultures, a transient, significant increase occurred in intracellular superoxide dismutase, catalase, guaiacol peroxidase and ascorbate peroxidase activities. Fusaric acid-induced ascorbate turnover modulation led to up to a twofold increase in dehydroascorbic acid accumulation, and a decrease in the associated ascorbate redox ratio. It was concomitant with a significant decrease in dehydroascorbate reductase activity. These results support previous observations that the pro- and anti-oxidant systems are involved in response to fusaric acid treatment although differential response of H2O2 and its metabolism-related enzymes between the whole leaf and cell culture assays was found. [source] Influence of Different Hemodialysis Membranes on Red Blood Cell Susceptibility to Oxidative StressARTIFICIAL ORGANS, Issue 1 2000Leonardo Lucchi Abstract: Oxidative stress is crucial in red blood cell (RBC) damage induced by activated neutrophils in in vitro experiments. The aim of the study was to evaluate whether the bioincompatibility phenomena occurring during hemodialysis (HD) (where neutrophil activation with increased free radical production is well documented) may have detrimental effects on RBC. We evaluated RBC susceptibility to oxidative stress before and after HD in 15 patients using Cuprophan, cellulose triacetate, and polysulfone membrane. RBC were incubated with t-butyl hydroperoxide as an oxidizing agent both in the presence and in the absence of the catalase inhibitor sodium azide. The level of malonaldehyde (MDA), a product of lipid peroxidation, was measured at 0, 5, 10, 15, and 30 min of incubation. When Cuprophan membrane was used, the MDA production was significantly higher after HD, indicating an increased susceptibility to oxidative stress in comparison to pre-HD. The addition of sodium azide enhanced this phenomenon. Both cellulose triacetate and polysulfone membranes did not significantly influence RBC susceptibility to oxidative stress. Neither the level of RBC reduced glutathione nor the RBC glutathione redox ratio changed significantly during HD with any of the membranes used. The RBC susceptibility to oxidative stress was influenced in different ways according to the dialysis membrane used, being increased only when using the more bioincompatible membrane Cuprophan, where neutrophil activation with increased free radical production is well documented. The alterations found in this study might contribute to the reduced RBC longevity of HD patients where a bioincompatible membrane is used. [source] Protective Effect of Sesamol against 3-Nitropropionic Acid-Induced Cognitive Dysfunction and Altered Glutathione Redox Balance in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Puneet Kumar It is a well-known antioxidant, currently being tried against several neurological disorders. The present study was designed to evaluate the potential of sesamol treatment against 3-nitropropionic acid (3-NP)-induced cognitive impairment and oxidative damage in striatal, cortex and hippocampal regions of the rat. The memory performance was assessed by Morris water maze and elevated plus maze paradigms. The oxidative damage was assessed by estimating the total glutathione, reduced glutathione, oxidized glutathione levels and glutathione redox ratio. Glutathione- S -transferase and lactate dehydrogenase enzymes were also measured in different brain areas. 3-NP significantly impaired memory performance as assessed in Morris water maze and elevated plus maze, which was significantly attenuated by sesamol (5, 10 and 20 mg/kg) pre-treatment. On the other hand, 3-NP significantly induced oxidative stress and depleted total glutathione, reduced glutathione, glutathione- S -transferase, lactate dehydrogenase enzyme levels and redox ratio in the striatum, cortex and hippocampal regions as compared to the vehicle-treated group. Sesamol pre-treatment restored oxidative defence possibly by its free radical scavenging activity as compared to the 3NP-treated group. The present study suggests that sesamol could be used as an effective agent in the management of Huntington's disease. [source] | ||||||||||