Home About us Contact
|
Home About us Contact | ||
|
|
||
Membrane Lipid Peroxidation (membrane + lipid_peroxidation)
Selected AbstractsBid-dependent generation of oxygen radicals promotes death receptor activation,induced apoptosis in murine hepatocytesHEPATOLOGY, Issue 2 2004Wen-Xing Ding Activation of tumor necrosis factor receptor 1 or Fas leads to the generation of reactive oxygen species, which are important to the cytotoxic effects of tumor necrosis factor , (TNF-,) or Fas ligand. However, how these radicals are generated following receptor ligation is not clear. Using primary hepatocytes, we found that TNF-, or anti,Fas antibody,induced burst of oxygen radicals was mainly derived from the mitochondria. We discovered that Bid,a pro-death Bcl-2 family protein activated by ligated death receptors,was the main intracellular molecule signaling the generation of the radicals by targeting to the mitochondria and that the majority of oxygen radical production was dependent on Bid. Reactive oxygen species contributed to cell death and caspase activation by promoting FLICE-inhibitory protein degradation and mitochondrial release of cytochrome c. For the latter part, the oxygen radicals did not affect Bak oligomerization but instead promoted mitochondrial cristae reorganization and membrane lipid peroxidation. Antioxidants could reverse these changes and therefore protect against TNF-, or anti,Fas-induced apoptosis. In conclusion, our studies established the signaling pathway from death receptor engagement to oxygen radical generation and determined the mechanism by which reactive oxygen species contributed to hepatocyte apoptosis following death receptor activation. (HEPATOLOGY 2004;40:403,413.) [source] Wheat Cellular Membrane Thermotolerance Under Heat StressJOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 2 2010A. S. Dias Abstract Four genotypes of Triticum aestivum L. and Triticum turgidum subsp. durum chosen according to their genetic background diversity were subjected to heat stress after anthesis. Membrane permeability, lipid peroxidation and fatty acids (C14:0, C16:0, C16:1c, C16:1t, C18:0, C18:1, C18:2 and C18:3) were quantified. The estimation of the quantum yield of non-cyclic photosynthetic electron transport was used as well as a test system to further evaluate the implications on thylakoid functioning. It was found differences within bread and durum wheat species concerning the capability to cope with high temperatures at the stage of grain filling. The genotype Sever showed high thermal sensitivity concerning membrane lipid peroxidation and membrane permeability, as evaluated by the increased production of ethylene and MDA, as well as by the impact on TFA (at the middle term of grain filling). In the durum wheat genotypes, differences were also found, with TE 9306 displaying high membrane stability, with no increases on membrane permeability, MDA and ethylene content. In this way, the observed changes on TFA in this genotype might have constituted a mechanism to allow qualitative lipid changes, reflected in lower unsaturation level of membrane FAs which is a positive trait under high temperatures. [source] Methyl tert -butyl ether (MTBE)-induced cytotoxicity and oxidative stress in isolated rat spermatogenic cellsJOURNAL OF APPLIED TOXICOLOGY, Issue 1 2007Dongmei Li Abstract Methyl tert -butyl ether (MTBE) is a class of synthetic organic chemical. In the USA, MTBE pollution is regarded as a serious environmental problem. The objective of the present study was to investigate the cytotoxic effects and oxidative stress induced by MTBE in isolated rat spermatogenic cells. In cytotoxic experiments, spermatogenic cells isolated from the testes of adult Sprague-Dawley rats by a mechanical procedure without the use of trypsin were incubated with medium alone (control), 0.5, 5, 50 mm MTBE, respectively, for 6, 12 and 18 h. MTT assay, staining with fluorescein diacetate (FDA) and propidium iodide (PI) and flow cytometric analyses were used. In oxidative stress experiments, the spermatogenic cells were incubated with medium alone (control) and with 0.5, 50 ,m, 5 mm MTBE. For 1, 2, 6, 12, 18 h incubation, ROS production was tested using a 2,,7,-dichlorofluorescein diacetate (DCHF-DA) probe; for 1, 3, 6, 12, 18 h incubation, cytosolic superoxide dismutase (SOD) and extracellular SOD (SODEX) activity was assessed; and for 18 h incubation, lipid peroxidation was assessed. The results showed that MTBE at high doses significantly decreased the spermatogenic cell viability and increased plasma membrane damage and the ratio of necrotic cells compared with the control. Assessment of the MTBE-induced oxidative stress revealed that MTBE increased the production of reactive oxygen species (ROS) and enhanced lipid peroxidation. In addition, although SODEX activity increased at a high dose level, cytosolic SOD activity decreased. These results suggest that an increase of MTBE-induced ROS production and an enhancement of membrane lipid peroxidation may play an important role in its cytotoxicity in isolated rat spermatogenic cells. Copyright © 2006 John Wiley & Sons, Ltd. [source] Some photosynthetic responses to salinity resistance are transferred into the somatic hybrid descendants from the wild soybean Glycine cyrtoloba ACC547PHYSIOLOGIA PLANTARUM, Issue 3 2007Yong Yang The somatic hybrid descendants between a cultivated soybean Glycine max Melrose and a wild species Glycine cyrtoloba ACC547 were found to possess some salinity-resistant traits of the wild soybean. Under salt stress, two of the descendants as well as their wild parent grew better than their cultivated parent. In addition, salinity-induced decline in the net photosynthetic rate and the maximum photochemical efficiency was much less in the wild species and the descendants than in Melrose when stressed for more than 5 days. Analysis of the postillumination transient increase in chlorophyll fluorescence and the dark rereduction of the oxidized primary electron donor in photosystem I (PSI) (P700+) indicated that salinity induced a significant upregulation of the cyclic electron flow around PSI (CEF1) in the wild species and the hybrid descendants. Similar to their wild parent, the descendants maintained higher non-photochemical dissipation of excess excitation energy than their cultivated parent under salt stress. As a consequence, there were lower levels of superoxide radical and membrane lipid peroxidation in the plants of the descendants and the wild species. Based on these results, we proposed that the high salinity resistance of the descendants might be because of, at least partially, the trait inherited from the wild species of the enhanced CEF1 which contributed to the sufficient dissipation of excess excitation energy to protect photosynthetic apparatus from the damage of reactive oxygen species. [source] Allelochemical stress causes inhibition of growth and oxidative damage in Lycopersicon esculentum MillPLANT CELL & ENVIRONMENT, Issue 11 2006AURORA LARA-NUÑEZ ABSTRACT The aim of this study was to analyse the effect of allelochemical stress on Lycopersicon esculentum growth. Our results showed that allelochemical stress caused by Sicyos deppei aqueous leachate inhibited root growth but not germination, and produced an imbalance in the oxidative status of cells in both ungerminated seeds and in primary roots. We observed changes in activity of catalase (CAT), ascorbate peroxidase (APX), superoxide dismutase (SOD), glutathione reductase (GR) and the plasma membrane NADPH oxidase, as well as in the levels of H2O2 and O2,, in seeds at 12 and 24 h, and in primary roots at 48 and 72 h of treatment, which could account for the oxidative imbalance. There were changes in levels of expression of the mentioned enzymes, but without a correlation with their respective activities. Higher levels of membrane lipid peroxidation were observed in primary roots at 48 and 72 h of treatment. No effect on the expression of metacaspase and the PR1 was observed as indicators of cell death or induction of plant defence. This paper contributes to the understanding of plant,plant interactions through the phytotoxic allelochemicals released in an aqueous leachate of the weed S. deppei, which cause a negative effect on other plants. [source] Enhancing the natural defences and barrier protection of aquaculture speciesAQUACULTURE RESEARCH, Issue 3 2010John W Sweetman Abstract The promotion of nutritional strategies that optimize natural defence mechanisms in fish is of critical importance in producing robust juveniles and adult fish. These animals are more capable of minimizing the impact of opportunistic pathogen attack, thus improving liveability and performance characteristics. The importance of the piscine gastrointestinal tract as a major endocrine and osmoregulatory organ is well reported as is its function as a defensive barrier to pathogen attack. Investigations using the inclusion of a specific structural form of mannan oligosaccharide have been shown to improve the performance parameters, immune status, and gut morphology and improve an important aspect of barrier protection through the enhancement of mucal production in a number of aquaculture species. The selenium status of an animal is pivotal in determining the success of the innate and adaptive immune response of the animal, and the use of an organic selenium source, in the form of a selenoyeast, has been shown to improve enzyme function and tissue uptake. The antioxidant role of many of the selenoptroteins and the role of selenium in the glutathione peroxidase enzyme pathways involved in the control of oxidative stress is critical if oxidative damage and cell membrane lipid peroxidation are to be prevented. The use of these compounds as feed additives has important implications for health management in commercial aquaculture facilities. Further research is needed to evaluate the benefits offered by a range of commercial products. [source] Erythrocyte Susceptibility to Oxidative Stress in Chronic Renal Failure Patients Under Different Substitutive TreatmentsARTIFICIAL ORGANS, Issue 1 2005Leonardo Lucchi Abstract:, An increased oxidative stress is now considered one of the major risk factors in chronic renal failure (CRF) patients that may be exacerbated by dialysis. It has been postulated that this increased oxidative stress might cause an augmented red blood cell (RBC) membrane lipid peroxidation with the consequent alteration in membrane deformability. The aim of this study was to evaluate RBC susceptibility to an in vitro induced oxidative stress and RBC antioxidant potential in different groups of CRF patients undergoing different substitutive treatment modalities. Fifteen end-stage CRF patients were evaluated in conservative treatment, 23 hemodialysis (HD) patients, 15 continuous ambulatory peritoneal dialysis (CAPD) patients, 15 kidney transplanted patients, and 16 controls. Their RBCs were incubated with the oxidative stress-inducing agent tert-butylhydroperoxide both in the presence and in the absence of the catalase inhibitor sodium azide, and the level of malondialdehyde (MDA) (a product of lipid peroxidation), was measured at 0, 5, 10, 15, and 30 min of incubation. In addition, the RBC content of reduced glutathione (GSH) was measured by HPLC. As opposed to the controls, RBCs from end-stage CRF patients exhibited an increased sensitivity to oxidative stress induced in vitro, both in the absence and presence of a catalase inhibitor, as demonstrated by a significantly higher level of MDA production at all the incubation times (P < 0.05). Different substitutive treatments had different impacts on this phenomenon; CAPD and kidney transplantation were able to normalize this alteration while HD was not. GSH appeared to be related to the increase in RBC susceptibility to oxidative stress; its content being significantly elevated in end-stage CRF and HD patients as compared with CAPD and transplanted patients and controls (P < 0.05). No significant changes were observed in the RBC glutathione content during the HD session. The increase of GSH in RBCs of end-stage CRF and HD patients seems to indicate the existence of an adaptive mechanism under increased oxidative stress occurring in vivo. Unlike HD, the beneficial effect of CAPD on the anemia of dialysis patients might partly be due to a condition of lower oxidative stress that might in addition counterbalance the cardiovascular negative effects of dislipidemia ,of, CAPD, patients. [source] Protective effects of N-acetyl- L -cysteine against acute carbon tetrachloride hepatotoxicity in ratsCELL BIOCHEMISTRY AND FUNCTION, Issue 1 2008Yu. Z. Maksimchik Abstract In recent years, N-acetyl- L -cysteine (NAC) has been widely investigated as a potentially useful protective and antioxidative agent to be applied in many pathological states. The aim of the present work was further evaluation of the mechanisms of the NAC protective effect under carbon tetrachloride-induced acute liver injuries in rats. The rat treatment with CCl4 (4,g/kg, intragastrically) caused pronounced hepatolysis observed as an increase in blood plasma bilirubin levels and hepatic enzyme activities, which agreed with numerous previous observations. The rat intoxication was accompanied by an enhancement of membrane lipid peroxidation (1.4-fold) and protein oxidative damage (protein carbonyl group and mixed protein-glutathione disulphide formations) in the rat liver. The levels of nitric oxide in blood plasma and liver tissue significantly increased (5.3- and 1.5-fold, respectively) as blood plasma triacylglycerols decreased (1.6-fold). The NAC administration to control and intoxicated animals (three times at doses of 150,mg/kg) elevated low-molecular-weight thiols in the liver. The NAC administration under CCl4 -induced intoxication prevented oxidative damage of liver cells, decreased membrane lipid peroxidation, protein carbonyls and mixed protein-glutathione disulphides formation, and partially normalized plasma triacylglycerols. At the same time the NAC treatment of intoxicated animals did not produce a marked decrease of the elevated levels of blood plasma ALT and AST activities and bilirubin. The in vitro exposure of human red blood cells to NAC increased the cellular low-molecular-weight thiol levels and retarded tert -butylhydroperoxide-induced cellular thiol depletion and membrane lipid peroxidation as well as effectively inhibited hypochlorous acid-induced erythrocyte lysis. Thus, NAC can replenish non-protein cellular thiols and protect membrane lipids and proteins due to its direct radical-scavenging properties, but it did not attenuate hepatotoxicity in the acute rat CCl4 -intoxication model. Copyright © 2007 John Wiley & Sons, Ltd. [source] Lipid peroxidation, vitamins C, E and reduced glutathione levels in patients with pulmonary tuberculosisCELL BIOCHEMISTRY AND FUNCTION, Issue 1 2004M. Vijayamalini Abstract The present study examined the relationship between lipid peroxidation and vitamin C, vitamin E and reduced glutathione levels in plasma, erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients and an equal number of age-and sex-matched healthy subjects. Enhanced plasma, erythrocytes and erythrocyte membrane lipid peroxidation with concomitant decline in vitamin C, vitamin E and reduced glutathione levels were found in pulmonary tuberculosis patients. The elevated lipid peroxidation and decreased vitamin C, vitamin E and reduced glutathione levels indicate the potential of oxidative damage to erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients. Copyright © 2003 John Wiley & Sons, Ltd. [source] | ||||||||||||||||