22 research outputs found
āļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°āđāļĨāļ°āđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ Free Radicals and Alzheimerâs Disease
āļāļāļāļąāļāļĒāđāļ āļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°āļāļĢāļ°āļāļāļāļāđāļ§āļĒ ROS āļāļķāđāļāļāļ°āļāļģāļāļāļīāļāļīāļĢāļīāļĒāļēāļāļąāļāļŠāļēāļĢāļāļĩāļ§āđāļĄāđāļĨāļāļļāļĨāļŠāđāļāļāļĨāđāļŦāđāđāļāļīāļāļāļ§āļēāļĄāđāļŠāļĩāļĒāļŦāļēāļĒāđāļāđāļāļāļāđāļāļĢāļ°āļāļāļāļāđāļēāļ āđ āļāļāļāđāļāļĨāļĨāđāđāļāļĢāđāļēāļāļāļēāļĒ āđāļāđāļ āļāļģāļĨāļēāļĒāđāļāļĢāļāļŠāļĢāđāļēāļ DNA āļāļēāļĢāđāļāļĨāļĩāđāļĒāļāļŠāļ āļēāļāđāļāļĢāļāļĩāļāļĢāļ§āļĄāļāļąāđāļāđāļāļĄāļąāļāļāļāļāđāļĒāļ·āđāļāļŦāļļāđāļĄāđāļāļĨāļĨāđ āļāļēāļĢāļŠāļĢāđāļēāļāļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°āļāļģāļāļ§āļāļĄāļēāļāļāļ°āļāđāļāđāļŦāđāđāļāļīāļāļāļēāļĢāļāļēāļāđāļāđāļāļāļāļāđāļāļĨāļĨāđ āļāļķāđāļāđāļāđāļāļāļĨāđāļāļŠāļģāļāļąāļāļāļĩāđāļāđāļāđāļŦāđāđāļāļīāļāļāļĒāļēāļāļīāļŠāļ āļēāļāļāđāļēāļ āđ āļĢāļ§āļĄāļāļąāđāļāđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ āļāļķāđāļāđāļāđāļāđāļĢāļāļāļĩāđāđāļāļīāļāļāļēāļāļāļ§āļēāļĄāđāļŠāļ·āđāļāļĄāļāļāļāļāļĢāļ°āļŠāļēāļ āļĄāļĩāļāļēāļĢāļŠāļ°āļŠāļĄāļāļāļ Ab plaques āđāļĨāļ° NFTs āļĢāļ§āļĄāļāļķāļ oxidative stress āļāļēāļĢāļŠāļ°āļŠāļĄāļāļāļ Ab āļāļēāļāļāļ°āļāļģāđāļāļŠāļđāđāļāļēāļĢāđāļŠāļ·āđāļāļĄāļāļāļāļāļĢāļ°āļŠāļēāļāļāđāļēāļāļāļēāļ oxidative stress āđāļāđāļ āļāļēāļĢāļāļģāļĨāļēāļĒ DNA āđāļĨāļ°āđāļāļĢāļāļĩāļ āļĄāļĩāļāļēāļĢāđāļāļīāđāļĄāļāļāļ lipid peroxidation āđāļāļŠāļĄāļāļāļāļāļāļāļđāđāļāđāļ§āļĒāđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ āđāļāļĒāđāļāļāļēāļ° temporal lobe āļāļĨāļīāļāļāļĨāļāļĩāđāđāļāļīāļāļāļēāļ oxidative stress āđāļāđāđāļāđ HNE āļāļ°āđāļāđāļāļāļīāļĐāļāđāļāđāļāļĨāļĨāđāļāļĢāļ°āļŠāļēāļāđāļĨāļ°āļāļģāđāļŦāđāļāļēāļĢāļāļģāļāļēāļāļāļāļāđāļĄāļĄāđāļāļĢāļāđāļāļĢāļāļĩāļāđāļŠāļĩāļĒ āļāļēāļĢāļāļāļāļāđāļāļāļąāļāļāļāļāđāļāļĢāļāļĩāļāđāļāļĒāļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°āļāļēāļāļĄāļĩāļāļāļāļēāļāđāļāļāļēāļĢāđāļāļīāļāđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ āļĢāļ§āļĄāļāļąāđāļ DNA āļāļĩāđāļāļđāļāļāļģāļĨāļēāļĒāļĄāļēāļāļāļķāđāļāļāļēāļāļāļāļāļāļīāđāļāļāļąāļāđāļāļŠāļĄāļāļāļāļāļāļāļđāđāļāđāļ§āļĒāđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ āđāļāļĒāļāļĩāđ hydroxyl radicals āđāļāļāļĢāļ°āļāļģāļāđāļ DNA āļāļāļāļāļēāļāļāļĩāđ āļĒāļąāļāļāļąāļāļāļģāđāļŦāđāđāļāļīāļāļāļ§āļēāļĄāļāļīāļāļāļāļāļīāļāļāļāđāļĄāđāļāļāļāļāđāļāļĢāļĩāļĒāļāļąāļāđāļāļ·āđāļāļāļāļēāļāļāļēāļĢāļāļĨāļīāļ ROS āļĄāļēāļāļāļīāļāļāļāļāļī āļ āļēāļ§āļ°āļāļąāļāļāļĨāđāļēāļ§āļāļģāđāļŦāđāļŠāļđāļāđāļŠāļĩāļĒāļāļēāļĢāļāļģāļāļēāļāļāļāļāđāļāļĨāļĨāđ āļāļēāļĢāļāļēāļĒāļāļāļāđāļāļĨāļĨāđāđāļĨāļ°āļāļ§āļēāļĄāđāļŠāļ·āđāļāļĄāļāļāļāđāļāļĨāļĨāđāļāļĢāļ°āļŠāļēāļāđāļāļāļđāđāļāđāļ§āļĒāđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđ āļāļģāļŠāļģāļāļąāļ: āļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°, oxidative stress, āđāļĢāļāļāļąāļĨāđāļāđāļĄāļāļĢāđAbstract Free radicals contain ROS which reacts with biomolecules causing damage to various components of the cell. ROS destroys DNA structure and changes proteins and lipids on the cell membrane. A large number of free radicals can cause cell injuries, which are important pathological mechanisms of various diseases including Alzheimer's disease caused by nerve degeneration. The accumulation of Ab plaques and NFTs and oxidative stress lead to pathological progress of Alzheimerâs disease. Ab accumulation may lead to nerve degeneration through oxidative stress, such as DNA and protein destruction. Increased lipid peroxidation in the brain of Alzheimer's patients especially the temporal lobe was found. Oxidative stress products, such as HNE, are toxic to nerve cells and impair the membrane proteins function. Oxidation of proteins by free radicals resulting, increased oxidative damage with hydroxyl radicals acting on the DNA may play a role in Alzheimer's disease. Mitochondrial disorders were caused by abnormal ROS production. These conditions lead to loss of cell function, cell death and degeneration of neurons in patients with Alzheimer's disease. Keywords: free radicals, oxidative stress, Alzheimerâs diseas
āļāļāļāļēāļāļāļāļāļ āļēāļ§āļ°āđāļāļĢāļĩāļĒāļāļāļāļāļāļīāđāļāļāļąāļāđāļāđāļĢāļāļāļēāļĢāđāļāļīāļāļŠāļąāļ The Role of Oxidative Stress in Parkinsonâs Disease
āļāļāļāļąāļāļĒāđāļ āļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°āļāļĢāļ°āļāļāļāļāđāļ§āļĒ reactive oxygen species (ROS) āļāļķāđāļāļāļģāļāļāļīāļāļīāļĢāļīāļĒāļēāļāļąāļāļŠāļēāļĢāļāļĩāļ§āđāļĄāđāļĨāļāļļāļĨāļŠāđāļāļāļĨāđāļŦāđāđāļāļīāļāļāļ§āļēāļĄāđāļŠāļĩāļĒāļŦāļēāļĒāđāļāđāļāļāļāđāļāļĢāļ°āļāļāļāļāđāļēāļ āđ āļāļāļāđāļāļĨāļĨāđāđāļāļĢāđāļēāļāļāļēāļĒ āđāļāđāļ āļāļģāļĨāļēāļĒāđāļāļĢāļāļŠāļĢāđāļēāļ DNA āļāļēāļĢāđāļāļĨāļĩāđāļĒāļāļŠāļ āļēāļāđāļāļĢāļāļĩāļāļĢāļ§āļĄāļāļąāđāļāđāļāļĄāļąāļāļāļāļāđāļĒāļ·āđāļāļŦāļļāđāļĄāđāļāļĨāļĨāđ āļŠāļģāļŦāļĢāļąāļāļ āļēāļ§āļ°āđāļāļĢāļĩāļĒāļāļāļāļāļāļīāđāļāļāļąāļ (oxidative stress) āđāļāđāļāļ āļēāļ§āļ°āļāļēāļĢāđāļŠāļĩāļĒāļŠāļĄāļāļļāļĨāļĢāļ°āļŦāļ§āđāļēāļ ROS āļāļĩāđāļāļĨāļīāļāđāļāļĒāļāļĢāļ°āļāļ§āļāļāļēāļĢāļāļĩāļ§āđāļāļĄāļĩāđāļĨāļ°āļāļ§āļēāļĄāļŠāļēāļĄāļēāļĢāļāļāļāļāļĢāļ°āļāļāļāļēāļāļāļĩāļ§āļ°āđāļāļāļēāļĢāļāļģāļĨāļēāļĒ reactive intermediates āļāļķāđāļ ROS āļāļģāđāļŦāđāđāļāļīāļāļāļ§āļēāļĄāđāļŠāļĩāļĒāļŦāļēāļĒāļāđāļāđāļĄāđāļĨāļāļļāļĨāđāļĨāļ°āļāļēāļĢāļāļēāļĒāļāļāļāđāļāļĨāļĨāđ āļāļķāđāļāļŦāļēāļāļāļĒāļēāļāļīāļŠāļ āļēāļāļāļĩāđāđāļāļīāļāļāļĩāđāļŠāļĄāļāļāļŠāđāļ§āļ basal ganglia āļāđāļāļ°āļāļģāđāļāļŠāļđāđāļāļēāļĢāđāļāļīāļāđāļĢāļāļāļēāļĢāđāļāļīāļāļŠāļąāļ āđāļāļĒāļāļ§āļēāļĄāđāļŠāļ·āđāļāļĄāļĄāļĩāļĨāļąāļāļĐāļāļ°āđāļāđāļāļāļ·āļ āļāļēāļĢāļŠāļ°āļŠāļĄāđāļāļĢāļāļĩāļāļāļīāļāļāļĢāļ°āđāļ āļ (misfolded proteins) āļ āļēāļĒāđāļāđāļāļĨāļĨāđ āđāļĨāļ° Lewy bodies āļāļģāđāļŦāđāļŠāļđāļāđāļŠāļĩāļĒāđāļāļĨāļĨāđāļāļĢāļ°āļŠāļēāļāđāļāļāļēāļĄāļīāđāļāļāļĢāđāļāļīāļ āļāļķāđāļāļāļēāļāļĨāļāļāļģāļāļ§āļāļŦāļĢāļ·āļāđāļāļīāļāļāļ§āļēāļĄāļāļāļāļĢāđāļāļāđāļāļāļēāļĢāļāļĨāđāļāļĒāļŠāļēāļĢāļŠāļ·āđāļāļāļĢāļ°āļŠāļēāļāđāļāļāļēāļĄāļĩāļ āļāļēāļāļēāļĢāļāļāļāđāļĢāļāļāļēāļĢāđāļāļīāļāļŠāļąāļāļāļķāļāđāļāļīāļāļāļķāđāļ āđāļāđāđāļāđ āļāļēāļāļēāļĢāļŠāļąāđāļ āđāļāļĨāļ·āđāļāļāđāļŦāļ§āļāđāļē  āđāļāđāļāđāļāļĢāđāļ āđāļĨāļ°āļāļąāļāļŦāļēāļāļāļāļāļēāļĢāļāļĢāļāļāļąāļ§āđāļĨāļ°āđāļāļīāļāļĨāļģāļāļēāļāļāļēāļĢāđāļāļīāļ āđāļāļĒāļāļēāļĢāđāļāļīāļ oxidative stress āđāļāļŠāļĄāļāļāđāļāļ·āđāļāļāļāļēāļ dopamine metabolism, āļĢāļ°āļāļąāļāđāļŦāļĨāđāļāđāļĨāļ°āđāļāļĨāđāļāļĩāļĒāļĄāļāļĩāđāļŠāļđāļāđāļ substantia nigra, mitochondria dysfunction, neuroinflammation āđāļĨāļ° genetic mutations āļŠāđāļāļāļĨāđāļŦāđāđāļāļīāļāļāļēāļĢāļāļģāļĨāļēāļĒāđāļāļĨāļĨāđāļāļĢāļ°āļŠāļēāļāļāđāļ§āļĒāļāļĨāđāļāļŦāļĨāļēāļāļŦāļĨāļēāļĒ āđāļāđāļ āļĄāļĩāļāļēāļĢāđāļāļīāđāļĄ oxidation āļāļāļāđāļāļāļēāļĄāļĩāļāđāļĨāļ°āļāļēāļĢāđāļāļīāļ neuromelanin, āļĄāļĩāļāļēāļĢāđāļāļīāđāļĄāļāļ§āļēāļĄāđāļāđāļĄāļāđāļāļāļāļāđāļŦāļĨāđāļ āđāļĨāļ°āļĨāļāļāļēāļĢāļāļĨāļīāļ reduced glutathione āđāļĨāļ°āđāļāļīāđāļĄ oxidized glutathione āļāļģāđāļāļŠāļđāđāļāļēāļĢāđāļŠāļ·āđāļāļĄāđāļĨāļ°āļāļēāļĢāļāļēāļĒāļāļāļāđāļāļĨāļĨāđāļāļĢāļ°āļŠāļēāļāđāļāļāļđāđāļāđāļ§āļĒāļāļēāļĢāđāļāļīāļāļŠāļąāļ āļāļģāļŠāļģāļāļąāļ: āļ āļēāļ§āļ°āđāļāļĢāļĩāļĒāļāļāļāļāļāļīāđāļāļāļąāļ, āļāļāļļāļĄāļđāļĨāļāļīāļŠāļĢāļ°, āđāļĢāļāļāļēāļĢāđāļāļīāļāļŠāļąāļAbstract Reactive oxygen species (ROS) as free radicals interact with biomolecules resulting in damage to the composition of the cells in the body, such as the destruction of the DNA structure, the transformation of proteins and lipids of the cell membrane. Oxidative stress is an imbalance between ROS produced by biochemical processes and the biochemical system's ability to destroy reactive intermediates, leading to ROS accumulation which could cause molecular damage and cell death. Such neurodegeneration in the basal ganglia could lead to the reduction or defect of dopaminergic neurons which results in the reduction in dopamine release. Specific mechanisms involve the accumulation of misfolded proteins within the cells and Lewy bodies. With the reduced release of dopamine, symptoms of Parkinson's are apparent including bradykinesia, rest tremor, rigidity and postural instability. Oxidative stress in the brain is due to dopamine metabolism, high iron and calcium levels in substantia nigra, mitochondria dysfunction, neuroinflammation and genetic mutations. This results in the destruction of neurons by a variety of mechanisms such as increased dopamine oxidation and the occurrence of neuromelanin, increased iron concentrations, reduced glutathione production and increased oxidized glutathione, leading to degeneration and death of neurons in Parkinson's patients. Keywords: oxidative stress, free radicals, Parkinsonâs diseas
Formulation and evaluation of gels containing coconut kernel extract for topical application
The biological activity of coconut (Cocos nucifera L.) extracts from its kernels and various parts was reported by many previous studies, it is therefore believable that the extracts of its kernels might show some activities in topical formulations. Among several kernel extracts, the TC06 extract prepared by soaking the steamed coconut kernels in hot water showed the highest total phenolic content (6.98âŊÂąâŊ0.30âŊmg GAE/g extract) and the strongest antioxidant activity as determined using FRAP and DPPH methods with a reducing power value of 4.12âŊÂąâŊ0.16âŊmg AAE/g of extract and an SC50 value of 2.38âŊÂąâŊ0.14âŊmg/ml, respectively. In addition, this extract did not display any cytotoxic effects in the concentration range of 50â3200âŊÂĩg/ml. Meanwhile, it revealed cytoprotective effects against t-BHP-induced cytotoxicity in HaCaT cells at concentrations higher than 400âŊÂĩg/ml. The results of phytochemical investigations including a chemical color test, TLC, 1H NMR and FTIR suggested that the TC06 extract was mainly composed of flavonoids and terpenoids. Furthermore, the concentrations of heavy metals including As, Cd, Hg, and Pb in the TC06 extract were below permissible limits. According to the solubility, the TC06 extract was incorporated into gels using Carbopol Ultrez 21 as a gelling agent. The formulated gel containing 3% (w/w) TC06 extract was stable at 4 °C and 25 °C with 75% RH throughout the storage period. It was found that the Carbopol Ultrez 21-based hydroalcoholic gel containing an aqueous extract of coconut kernels exhibited antioxidant activities in the two assays and showed a sufficient consistency, a pleasing color, and a non-oily perception during the period of observation. Keywords: Coconut kernel, Extract, Gel, Antioxidant activity, Phytochemical screenin
A novel approach to analyze gene expression data demonstrates that the ÎF508 mutation in CFTR downregulates the antigen presentation pathway
Gene array studies comparing cystic fibrosis (CF) and non-CF genotypes should reveal factors that explain variability in CF lung disease progression, yielding insights that lead to improved CF care. To date, studies have reached conflicting conclusions, perhaps due to experimental differences and divergent statistical approaches. This review aims: 1) to summarize the findings of four recent gene studies comparing CF and non-CF genotypes, and 2) to reanalyze original data using a recently developed statistical approach, with the aim of identifying genes and paths consistently regulated by the CF genotype. We identified four studies evaluating the effect of the ÎF508-CFTR mutation on human airway epithelial cell gene expression, restricting our investigation to human airway epithelial cell studies whose data were accessible in NCBI's Gene Expression Omnibus or the European Bioinformatic Institute's ArrayExpress. Gene expression patterns showed consistent repression of MHC class I antigen presentation genes in CF human airway epithelia, suggesting a novel mechanistic explanation for poor clearance of viral and bacterial infections by CF patients. We also examined proinflammatory and NF-ΚB genes, whose induction is widely accepted as a hallmark of the CF genotype, but found little evidence of induction, consistent with a recent review (Machen TE, Am J Physiol Cell Physiol 291: C218âC230, 2006.). In conclusion, our analysis suggests that the CF genotype may impair immune function in airway epithelial cells but may not increase inflammation. Additional studies are required to determine whether MHC class I gene repression in CF reduces antigen presentation at the protein level and whether repression impairs immune function
Emerging Evidence for the Importance of Phosphorylation in the Regulation of NADPH Oxidases
The NADPH oxidase (Nox) enzyme family generates reactive oxygen species (ROS) that contribute to cell signaling, innate immune responses, proliferation, and transcription. The signaling mechanisms that regulate this important enzyme family are only beginning to be understood. Evidence is emerging which suggests that phosphorylation of Nox and/or their regulatory components may be important means of modulating their activity. We describe here the evidence for Nox regulation through the action of kinases, and speculate on how such regulatory mechanisms might contribute to the development of pathological disease states. Antioxid. Redox Signal. 11, 2429â2441