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www.mdpi.com/journal/ijms Exploring the Role of Genetic Variability and Lifestyle in Oxidative Stress Response for Healthy Aging and Longevity
, 2013
"... Abstract: Oxidative stress is both the cause and consequence of impaired functional homeostasis characterizing human aging. The worsening efficiency of stress response with age represents a health risk and leads to the onset and accrual of major age-related diseases. In contrast, centenarians seem t ..."
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Abstract: Oxidative stress is both the cause and consequence of impaired functional homeostasis characterizing human aging. The worsening efficiency of stress response with age represents a health risk and leads to the onset and accrual of major age-related diseases. In contrast, centenarians seem to have evolved conservative stress response mechanisms, probably derived from a combination of a diet rich in natural antioxidants, an active lifestyle and a favorable genetic background, particularly rich in genetic variants able to counteract the stress overload at the level of both nuclear and mitochondrial DNA. The integration of these factors could allow centenarians to maintain moderate levels of free radicals that exert beneficial signaling and modulator effects on cellular metabolism. Considering the hot debate on the efficacy of antioxidant supplementation in promoting healthy aging, in this review we gathered the existing information regarding genetic variability and lifestyle factors which potentially modulate the stress response at old age. Evidence reported here suggests that the integration of lifestyle factors (moderate physical activity and healthy nutrition) and genetic background could shift the balance in favor of the antioxidant cellular machinery by activating appropriate defense mechanisms in
osteoarthritis
, 2008
"... Nitric oxide in inflammation and pain associated with ..."
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Nitric oxide in inflammation and pain associated with
Effects of acute and chronic endurance exercise on intracellular nitric oxide and superoxide in circulating CD34+ and CD34– cells
- J. Appl. Physiol
, 2011
"... of acute and chronic endurance exercise on intracellular nitric oxide in putative endothelial progenitor cells: role of NADPH oxidase. Am J Physiol Heart Circ Physiol 297: H1798–H1805, 2009. First published August 28, 2009; doi:10.1152/ajpheart.00347.2009.—We sought to delineate the effects of acute ..."
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of acute and chronic endurance exercise on intracellular nitric oxide in putative endothelial progenitor cells: role of NADPH oxidase. Am J Physiol Heart Circ Physiol 297: H1798–H1805, 2009. First published August 28, 2009; doi:10.1152/ajpheart.00347.2009.—We sought to delineate the effects of acute and chronic exercise on the regulation of intracellular nitric oxide (NOi) production in putative endothelial progenitor cells (EPCs). Putative EPC colony-forming units (CFU-EC) were cultured from blood drawn before and after 30 min of treadmill exercise at 75 % of maximal oxygen uptake in active (n 8) and inactive (n 8) men. CFU-EC were similar between groups at baseline, but increased after exercise in active men only (P 0.04). CFU-EC expressed lower NADPH oxidase subunit gp91phox mRNA and elevated endothelial nitric oxide synthase mRNA in active rela-tive to inactive men at baseline (P 0.05). Acute exercise reduced gp91phox mRNA in CFU-EC of both groups (P 0.05), whereas
www.mdpi.com/journal/ijms Endothelial Aging Associated with Oxidative Stress Can Be Modulated by a Healthy Mediterranean Diet
, 2013
"... Abstract: Aging is a condition which favors the development of atherosclerosis, which has been associated with a breakdown in repair processes that occurs in response to cell damage. The dysregulation of the biological systems associated with aging are produced partly through damage which accumulate ..."
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Abstract: Aging is a condition which favors the development of atherosclerosis, which has been associated with a breakdown in repair processes that occurs in response to cell damage. The dysregulation of the biological systems associated with aging are produced partly through damage which accumulates over time. One major source of this injury is oxidative stress, which can impair biological structures and the mechanisms by which they are repaired. These mechanisms are based on the pathogenesis of endothelial dysfunction, which in turn is associated with cardiovascular disease, carcinogenesis and aging. The dependent dysfunction of aging has been correlated with a reduction in the number and/or functional activity of endothelial progenitor cells, which could hinder the repair and regeneration of the endothelium. In addition, aging, inflammation and oxidative stress are endogenous factors that cause telomere shortening, which is dependent on oxidative cell damage. Moreover, telomere length correlates with lifestyle and the consumption of a healthy diet. Thus, diseases associated with aging and age may be caused by the long-term effects of oxidative damage, which are modified by genetic and environmental factors. Considering that diet is a very important source of antioxidants, in this review we will
Vascular function and circulating progenitor cells in thrombangitis obliterans (Buerger’s disease) and arteriosclerosis. Hypertension
"... Abstract—Thromboangitis obliterans (TAO; Buerger’s disease) and atherosclerosis obliterans (ASO) are associated with endothelial dysfunction. The purpose of this study was to evaluate the role of circulating progenitor cells (CPCs) in endothelial function in patients with TAO and ASO. We measured fl ..."
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Abstract—Thromboangitis obliterans (TAO; Buerger’s disease) and atherosclerosis obliterans (ASO) are associated with endothelial dysfunction. The purpose of this study was to evaluate the role of circulating progenitor cells (CPCs) in endothelial function in patients with TAO and ASO. We measured flow-mediated vasodilation (FMD), nitroglycerine-induced vasodilation, and circulating CPCs in 30 patients with TAO and 30 age- and sex-matched healthy subjects and in 40 patients with ASO. FMD was smaller in both the TAO group and ASO group than in the control group (6.62.7%, 5.73.3 % versus 9.53.1%, P0.0001, respectively). There was no significant difference in FMD between the TAO group and ASO group. Nitroglycerine-induced vasodilation was similar in the 3 groups. The number of and migration of circulating CPCs were similar in the TAO group and control group, whereas the number of and migration of circulating CPCs were significantly lower in the ASO group than in other groups (ASO 553297/mL versus TAO 963543/mL; control 1063426/mL and ASO 3618/hpf versus TAO 6223/hpf; control 6818/hpf, P0.0001, respectively). There was a significant relationship between the number of and migration of CPCs and FMD (r0.43 and r0.40, P0.0001, respectively). FMD was impaired in patients with TAO as well as in patients with ASO compared to that in normal control subjects, and the number of and function of circulating CPCs were not decreased in patients with TAO. These findings may partially explain why there are differences in cardiovascular morbidity and mortality rates between patients with TAO and patients with ASO. (Hypertension. 2011;57:70-78.) ● Online Data Supplement
Factors That Contribute to the Misidentification of Tyrosine Nitration by Shotgun Proteomics*□S
"... The high selectivity and throughput of tandemmass spec-trometry allow for rapid identification and localization of various posttranslational protein modifications from com-plex mixtures by shotgun approaches. Although sequence database search algorithms provide necessary support to process the poten ..."
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The high selectivity and throughput of tandemmass spec-trometry allow for rapid identification and localization of various posttranslational protein modifications from com-plex mixtures by shotgun approaches. Although sequence database search algorithms provide necessary support to process the potentially enormous quantity of MS/MS spectra generated from large scale tandem mass spec-trometry experiments, false positive identifications of peptide modifications may exist even after implementa-tion of stringent identification criteria. In this report, we describe factors that lead to misinterpretation of MS/MS spectra as well as common chemical and experimental artifacts that generate false positives using the proteom-ics-based identification of tyrosine nitration as an exam-ple. In addition to the proposed manual validation criteria,
www.mdpi.com/journal/ijms Hormesis in Aging and Neurodegeneration—A Prodigy Awaiting Dissection
, 2013
"... Abstract: Hormesis describes the drug action of low dose stimulation and high dose inhibition. The hormesis phenomenon has been observed in a wide range of biological systems. Although known in its descriptive context, the underlying mode-of-action of hormesis is largely unexplored. Recently, the ho ..."
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Abstract: Hormesis describes the drug action of low dose stimulation and high dose inhibition. The hormesis phenomenon has been observed in a wide range of biological systems. Although known in its descriptive context, the underlying mode-of-action of hormesis is largely unexplored. Recently, the hormesis concept has been receiving increasing attention in the field of aging research. It has been proposed that within a certain concentration window, reactive oxygen species (ROS) or reactive nitrogen species (RNS) could act as major mediators of anti-aging and neuroprotective processes. Such hormetic phenomena could have potential therapeutic applications, if properly employed. Here, we review the current theories of hormetic phenomena in regard to aging and neurodegeneration, with the focus on its underlying mechanism. Facilitated by a simple mathematical model, we show for the first time that ROS-mediated hormesis can be explained by the addition of different biomolecular reactions including oxidative damage, MAPK signaling and autophagy stimulation. Due to their divergent scales, the optimal hormetic window is sensitive to each kinetic parameter, which may vary between individuals. Therefore, therapeutic utilization of hormesis requires quantitative characterizations in order to access the optimal hormetic
Mechanisms of Oxidative Damage in Multiple Sclerosis and Neurodegenerative Diseases: Therapeutic Modulation via
, 2012
"... Abstract: Oxidative stress plays a crucial role in many neurodegenerative conditions such as Alzheimer’s disease, amyotrophic lateral sclerosis and Parkinson’s as well as Huntington’s disease. Inflammation and oxidative stress are also thought to promote tissue damage in multiple sclerosis (MS). Rec ..."
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Abstract: Oxidative stress plays a crucial role in many neurodegenerative conditions such as Alzheimer’s disease, amyotrophic lateral sclerosis and Parkinson’s as well as Huntington’s disease. Inflammation and oxidative stress are also thought to promote tissue damage in multiple sclerosis (MS). Recent data point at an important role of anti-oxidative pathways for tissue protection in chronic-progressive MS, particularly involving the transcription factor nuclear factor (erythroid-derived 2)-related factor 2 (Nrf2). Thus, novel therapeutics enhancing cellular resistance to free radicals could prove useful for MS treatment. Here, fumaric acid esters (FAE) are a new, orally available treatment option which had already been tested in phase II/III MS trials demonstrating beneficial effects on relapse rates and magnetic resonance imaging markers. In vitro, application of dimethylfumarate (DMF) leads to stabilization of Nrf2, activation of Nrf2-dependent transcriptional activity and abundant synthesis of detoxifying proteins. Furthermore, application of FAE involves direct modification of the inhibitor of Nrf2, Kelch-like ECH-associated protein 1. On cellular levels, the application of FAE enhances neuronal survival and protects astrocytes against oxidative stress. Increased levels of Nrf2 are
Neurocysticercosis: A Review
- The Scientific World Journal
, 2012
"... Neurocognitive effects of repetitive transcranial magnetic ..."
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Neurocognitive effects of repetitive transcranial magnetic
G: Potential role of nitric oxide in contractionstimulated glucose uptake and mitochondrial biogenesis in skeletal muscle. Clin Exp Pharmacol Physiol 2008
"... mitochondrial biogenesis in skeletal muscle ..."
