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Oxidant Injury (oxidant + injury)
Selected AbstractsGlutathione depletion in hippocampal cells increases levels of H and L ferritin and glutathione S-transferase mRNAsGENES TO CELLS, Issue 5 2007Nadya Morozova Glutathione plays an essential role in maintaining cellular redox balance, protecting cells from oxidative stress and detoxifying xenobiotic compounds. Glutathione depletion has been implicated in neurodegenerative disorders, including Alzheimer's and Parkinson's diseases. Cells of neuronal origin are acutely sensitive to glutathione depletion, providing an avenue for studying the mechanisms invoked for neuronal survival in response to oxidant challenge. We investigated the changes in mRNA profile in HT22 hippocampal cells following administration of homocysteic acid (HCA), a glutathione-depleting drug. We report that HCA treatment of HT22 murine hippocampal cells increases the levels of the mRNAs encoding at least three proteins involved in protection from oxidant injury, the mRNAs encoding heavy (H) and light (L) ferritin and glutathione S-transferase (GST). [source] Isofurans, but not F2 -isoprostanes, are increased in the substantia nigra of patients with Parkinson's disease and with dementia with Lewy body diseaseJOURNAL OF NEUROCHEMISTRY, Issue 3 2003Joshua P. Fessel Abstract F2 -isoprostanes (F2 -IsoPs) are well-established sensitive and specific markers of oxidative stress in vivo. Isofurans (IsoFs) are also products of lipid peroxidation, but in contrast to F2 -IsoPs, their formation is favored when oxygen tension is increased in vitro or in vivo. Mitochondrial dysfunction in Parkinson's disease (PD) may not only lead to oxidative damage to brain tissue but also potentially result in increased intracellular oxygen tension, thereby influencing relative concentrations of F2 -IsoPs and IsoFs. In this study, we attempted to compare the levels of F2 -IsoPs and IsoFs esterified in phospholipids in the substantia nigra (SN) from patients with PD to those of age-matched controls as well as patients with other neurodegenerative diseases, including dementia with Lewy body disease (DLB), multiple system atrophy (MSA), and Alzheimer's disease (AD). The results demonstrated that IsoFs but not F2 -IsoPs in the SN of patients with PD and DLB were significantly higher than those of controls. Levels of IsoFs and F2 -IsoPs in the SN of patients with MSA and AD were indistinguishable from those of age-matched controls. This preferential increase in IsoFs in the SN of patients with PD or DLB not only indicates a unique mode of oxidant injury in these two diseases but also suggests different underlying mechanisms of dopaminergic neurodegeneration in PD and DLB from those of MSA. [source] Enhanced hippocampal F2 -isoprostane formation following kainate-induced seizuresJOURNAL OF NEUROCHEMISTRY, Issue 5 2001Manisha Patel We attempted to obtain evidence for the occurrence of oxidant injury following seizure activity by measuring hippocampal F2 -isoprostanes (F2 -IsoPs), a reliable marker of free radical-induced lipid peroxidation. Formation of F2- IsoPs esterified in hippocampal phospholipids was correlated with hippocampal neuronal loss and mitochondrial aconitase inactivation, a marker of superoxide production in the kainate model. F2 -IsoPs were measured in microdissected hippocampal CA1, CA3 and dentate gyrus (DG) regions at various times following kainate administration. Kainate produced a large increase in F2 -IsoP levels in the highly vulnerable CA3 region 16 h post injection. The CA1 region showed small, but statistically insignificant increases in F2 -IsoP levels. Interestingly, the DG, a region resistant to kainate-induced neuronal death also showed marked (2.5,5-fold) increases in F2 -IsoP levels 8, 16, and 24 h post injection. The increases in F2 -Isop levels in CA3 and DG were accompanied by inactivation of mitochondrial aconitase in these regions. This marked subregion-specific increase in F2 -Isop following kainate administration suggests that oxidative lipid damage results from seizure activity and may play an important role in seizure-induced death of vulnerable neurons. [source] In Vitro evaluation of effects of two ghanaian plants relevant to wound healingPHYTOTHERAPY RESEARCH, Issue 11 2006Abraham Y. Mensah Abstract Commelina diffusa and Spathodea campanulata are used as wound-healing agents in Ashanti traditional medicine in Ghana. The methanol extracts of Commelina diffusa herb and Spathodea campanulata bark showed some level of antimicrobial activity with C. diffusa exhibiting selective antifungal activity against Trichophyton species. The extracts reduced the peroxidation of bovine brain extract with an IC50 value of 1.39 mg/mL and 0.24 mg/mL, respectively. In addition the extracts also exhibited significant antioxidant activity by protecting MRC-5 cells from hydrogen peroxide induced oxidant injury at concentrations between 1 µg/mL and 10 µg/mL. The extracts showed no inhibition of NF- ,B at 100 µg/mL. The antioxidant activities and antimicrobial activities suggest that the use of the plants in wound healing may be based on antioxidant and antiseptic effects of its constituents. Copyright © 2006 John Wiley & Sons, Ltd. [source] Intracellular glutathione in stretch-induced cytokine release from alveolar type-2 like cellsRESPIROLOGY, Issue 1 2004Behrouz Jafari Objective: Ventilator-induced lung injury (VILI) is characterized by release of inflammatory cytokines, but the mechanisms are not well understood. We hypothesized that stretch-induced cytokine production is dependent on oxidant release and is regulated by intracellular glutathione (GSH) inhibition of nuclear factor ,B (NF-,B) and activator protein-1 (AP-1) binding. Methodology: Type 2-like alveolar epithelial cells (A549) were exposed to cyclic stretch at 15% strain for 4 h at 20 cycles/min with or without N-acetylcysteine (NAC) or glutathione monoethylester (GSH-e) to increase intracellular GSH, or buthionine sulfoximine (BSO), to deplete intracellular GSH. Results: Cyclic stretch initially caused a decline in intracellular GSH and a rise in the levels of isoprostane, a marker of oxidant injury. This was followed by a significant increase in intracellular GSH and a decrease in isoprostane. Stretch-induced IL-8 and IL-6 production were significantly inhibited when intracellular GSH was further increased by NAC or GSH-e (P < 0.0001). Stretch-induced IL-8 and IL-6 production were augmented when intracellular GSH was depleted by BSO (P < 0.0001). NAC blocked stretch-induced NF-,B and AP-1 binding and inhibited IL-8 mRNA expression. Conclusions: We conclude that oxidant release may play a role in lung cell stretch-induced cytokine release, and antioxidants, which increase intracellular GSH, may protect lung cells against stretch-induced injury. [source] | |||||||||||||