Showing papers in "Free Radical Biology and Medicine in 2008"

TL;DR: This review focuses on mechanisms for sensing and transmitting redox signals, from the perspective of their chemical reactivity with specific oxidants, and discusses substrate preferences for different oxidants and how the kinetics of these reactions determines how each oxidant will react in a cell.

TL;DR: It is found that interfering with free radical metabolism with antioxidants may hamper useful adaptations to training and exercise itself can be considered an antioxidant.

TL;DR: The mechanisms by which particulate pollutants exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed and the importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will be discussed.

TL;DR: Signal transduction and the chemical biology of NO in terms of the direct and indirect reactions are discussed, with general results that promote cell survival and proliferation, whereas higher levels favor cell cycle arrest, apoptosis, and senescence.

TL;DR: Some of the recent findings that illuminate the significance of redox signaling and exciting future perspectives are reviewed to highlight some of the current pitfalls and the approaches needed to advance this important area of biochemical and biomedical research.

TL;DR: The newly discovered role of p53 in regulating cellular ROS generation and how ROS modulate selective transactivation of certain p53 target genes are examined, with a focus on interlinks between ROS and p53.

TL;DR: This review article summarizes some of the biochemical and toxicological properties of CYP2E1 and briefly describes the use of cell lines developed to constitutively express CYP1-dependent and cytochrome P450 2E1 knockout mice in assessing the actions of CYE1.

TL;DR: The vulnerability of the body to oxidative stress and diseases is significantly enhanced in a sedentary compared to a physically active lifestyle, which means that the well-known beneficial effects of exercise are due to the capability of exercise to produce increased levels of ROS.

TL;DR: Thiol/disulfide pathway, redox potential, and rate information are summarized as a basis for kinetic modeling of sulfur switches and indicates that systems biology could encourage novel therapeutic approaches to protect against oxidative stress by identifying specific redox-sensitive sites which could be targeted for intervention.

TL;DR: Since chronic oxidative stress plays a major role in the pathophysiology of several chronic inflammatory diseases, it is hypothesized that telomere length is reducing at a faster rate during oxidative stress, therefore, assessment of telomeres length might be a useful biomarker of disease progression.

TL;DR: The measurement of anthocyanins and flavanols in the brain following blueberry supplementation may indicate that changes in spatial working memory in aged animals are linked to the effects of flavonoids on the ERK-CREB-BDNF pathway.

TL;DR: An overview of the involvement of ROS-induced oxidative damage in Alzheimer's disease, Parkinson’s disease, and Huntington's disease is provided and the potential therapeutic effects of antioxidant enzymes and compounds that activate the Nrf2-ARE pathway are discussed.

TL;DR: The factors determining protein 3-nitrotyrosine formation, the functional and biological outcome associated with protein tyrosine nitration, and the fate of the nitrated proteins are analyzed.

TL;DR: The "two-hit" or "multi- hit" hypothesis, the role of mitochondrial bioenergetic defects and oxidant stress, the interplay between NO and mitochondria in fatty liver disease, genetic risk factors and oxidative stress-responsive genes, and the feasibility of antioxidants for treatment are discussed.

TL;DR: Long-chain nonesterified ("free") fatty acids and some of their derivatives and metabolites can modify intracellular production of reactive oxygen species (ROS) and be, at least partly, responsible for their proapoptotic effects in several types of cells.

TL;DR: The data suggest that Nox4 is responsible for basal H2O2 production, while O2*- production in nonstimulated and AngII-stimulated cells depends on Nox1, and the difference in the products generated by Nox 1 and Nox 4 may help to explain the distinct roles of these NADPH oxidases in cell signaling.

TL;DR: Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

TL;DR: ROS is identified as endogenous mediators of muscle fatigue and the importance of future research to define the cellular mechanism of ROS action and develop antioxidants as novel therapeutic interventions for treating fatigue is highlighted.

TL;DR: In this article, the authors investigated the role of oxidative stress in the early stages of Alzheimer's disease in a triple-transgenic mouse model and showed that the levels of antioxidants, namely, reduced glutathione and vitamin E, are decreased and the extent of lipid peroxidation is increased.

TL;DR: The evidence presented strongly suggests that free radicals generated during mild to moderate endurance-type exercise actually form part of the mechanism of exercise adaptation that includes extensive biogenesis of muscle mitochondria, increased muscle blood supply, and altered fuel consumption patterns.

TL;DR: Novel quantitative methods of ROS and NO detection help dissect the mechanisms of alcohol-induced neurodegeneration by uncovering the basic mechanisms of oxidative neuronal injury and will serve as the basis for development of new therapies.

TL;DR: In different mammalian cell lines exposed to physiological H( 2)O(2) levels, increased endogenous P5CS and P5CR expression was observed, indicating that upregulation of proline biosynthesis is an oxidative stress response.

TL;DR: This mini-review will discuss the main mechanisms and gene targets for nuclear factor kappaB and mitogen-activated protein kinase signaling pathways during exercise and the biological significance of the adaptation.

TL;DR: The use of environmental agents such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, rotenone, paraquat, dieldrin, and maneb in toxicant-based models of PD has become increasingly popular, and the neurotoxic properties of these compounds are discussed with specific focus on the induction of oxidative stress.

TL;DR: This review will outline what is known about the location and behaviour of tocols in phospholipid bilayers to assist researchers when designing new experiments and when critically assessing the results, in turn providing a more thorough understanding of the biochemistry of to cols.

TL;DR: It is suggested that acute hypoxia may distinctively activate Nox to increase [ROS](i) through the mitochondrial ROS-PKCepsilon signaling axis, providing a positive feedback mechanism to contribute to the hypoxic increase in [-ROS] and [Ca(2+)](i) as well as contraction in PASMCs.

TL;DR: Early onset of oxidative stress suggests that the initial therapeutic window following TBI appears to be relatively short, and it may be necessary to stagger selective types of antioxidant therapy to target specific oxidative components.

TL;DR: In this paper, a proteomic analysis of human brain postmortem samples obtained from striatum and cortex of patients with Huntington disease compared to samples of age and sex-matched controls was performed.

TL;DR: It is shown that antioxidant enzymes, including superoxide dismutase 1 and 2, catalase, and heme oxygenase 1, are markedly upregulated in active demyelinating MS lesions compared to normal-appearing white matter and white matter tissue from nonneurological control brains.

TL;DR: A conceptual framework for understanding CO biology in terms of this physiological-pathological hierarchy is provided and a brief overview of the fundamental responses to CO is provided.