Home About us Contact
|
Home About us Contact | ||
|
|
||
Oxidative Stress Hypothesis (oxidative + stress_hypothesis)
Selected AbstractsOxidative status in iron-deficiency anemiaJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2009Jong-Ha Yoo Abstract Oxidative stress is an imbalance between free radicals and antioxidant molecules that can play an important role in the pathogenesis of iron-deficiency anemia (IDA). The aim of this study was to investigate oxidative status in patients with IDA and alteration of oxidative status after iron treatment. Thirty-three female patients with IDA and 25 healthy controls were included in this study. Oxidant and total antioxidant capacity were determined using free oxygen radicals test and free oxygen radicals defence (Form CR 3000, Callegari, Parma, Italy). Catalase activity was measured by spectrophotometer using a commercially available kit (Bioxytech Catalase-520, OxisResearch, Portland, OR). Oxidant activity in patients with IDA was significantly higher than controls (P<0.05), while total antioxidant and catalase activity were significantly lower (P<0.05). After treatment, oxidant, antioxidant, and catalase activity reached the levels of the control group, and no significant differences were observed among groups (P>0.05). In conclusion, our data indicate that blood reactive oxygen species was lower and total antioxidant and catalase activity were higher after rather than before treatment in patients with IDA. The results of our study support the higher oxidative stress hypothesis in IDA; however, due to the limited number of cases included, more studies may be required to confirm the results. J. Clin. Lab. Anal. 23:319,323, 2009. © 2009 Wiley-Liss, Inc. [source] Advances in vertebrate aging research 2007AGING CELL, Issue 2 2008Steven Austad Summary Among this year's highlights in vertebrate aging research, we find a study in which, contrary to the oxidative stress hypothesis of aging, reduced expression of a major cellular antioxidant, glutathione peroxidase 4, led to a small increase in mouse lifespan. By contrast, a large comparative proteomic analysis discovered a remarkably robust and previous unsuspected inverse association between species lifespan and relative frequency of cysteine residues in mitochondrially encoded respiratory chain proteins only, which the authors attribute to cysteine's ease of oxidation. Another study evaluated more cleanly than any previous work the hypothesis that blood glucose concentration is a key mediator of aging, and concluded that it wasn't. Several new mouse longevity mutants were also reported this year, some (PAPP-A, IRS-1, and IRS-2 knockouts) supporting previous work on the importance of insulin/insulin-like growth factor-1 signaling and aging. However, there were inconsistencies between laboratories in some of the results, which merit further investigation. Also, somewhat inconsistent with these findings, over-expression of insulin-like growth factor-1 in heart only lengthened life. From a completely new direction, type 5 adenylyl cyclase knockout mice were observed to live more than 30% longer than controls. Finally, a new program for evaluating potential pharmaceutical interventions in aging and longevity made its appearance, and is notable at this point chiefly for the excellence of its experimental design. A similar program for the disinterested evaluation of reported longevity mutations in mice would be a service to the community of vertebrate aging researchers. [source] A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's diseaseMOVEMENT DISORDERS, Issue 11 2010Barry J. Snow MD Abstract Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double-blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD. © 2010 Movement Disorder Society [source] Challenging conventional wisdom: The etiologic role of dopamine oxidative stress in Parkinson's diseaseMOVEMENT DISORDERS, Issue 3 2005J. Eric Ahlskog PhD Abstract Oxidative stress is well documented in Parkinson's disease (PD) and has been attributed to dopamine oxidative metabolism. However, evidence of oxidative stress is found in a variety of neurodegenerative disorders, suggesting that more general factors are responsible or that cytodestructive processes secondarily generate oxyradical products. Increasing evidence points away from dopamine metabolism as an important contributor to PD neurodegeneration. Predictions from the dopamine oxidative stress hypothesis of PD reveal multiple inconsistencies. Although the clinical and therapeutic importance of the nigrostriatal dopaminergic system is undeniable, PD neuropathology is much more widespread. © 2004 Movement Disorder Society [source] Nigral glutathione deficiency is not specific for idiopathic Parkinson's diseaseMOVEMENT DISORDERS, Issue 9 2003Paul S. Fitzmaurice PhD Abstract The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [,30%], PSP [,21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [,20%]). GSH levels were normal in all examined normal and degenerating extra-nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (,19 to ,30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD. © 2003 Movement Disorder Society [source] | ||||||||||