Showing papers in "Free Radical Biology and Medicine in 2012"

TL;DR: A critical analysis of the challenges and limitations of the most widely used fluorescent probes for detecting and measuring reactive oxygen and nitrogen species and proposed guidelines that will help present and future researchers with regard to the optimal use of selected fluorescent probes and interpretation of results are presented.

TL;DR: Stimulation of mitochondrial function may also prevent NASH development, protecting the cell against the increased flux of reduced substrates to the ETC and ROS generation.

TL;DR: The main objective of this review is to examine the role of endogenous reactive oxygen/nitrogen species (ROS) in the aging process and proposes the "redox stress hypothesis", which proposes that aging-associated functional losses are primarily caused by a progressive pro-oxidizing shift in the redox state of the cells, which leads to the overoxidation of redox-sensitive protein thiols and the consequent disruption of theredox-regulated signaling mechanisms.

TL;DR: These processes act to maintain the number and quality of synaptic connections in key brain regions and thus flavonoids have the potential to prevent the progression of neurodegenerative pathologies and to promote cognitive performance.

TL;DR: The possibility that drugs modulating the pathway could be used as potential tools in tumor therapy is discussed, and the latest discoveries relating the activity of the pentose phosphate pathway to various aspects of tumor metabolism are summarized.

TL;DR: In human lung carcinoma A549 cells, Ir induced a time-dependent increase in the mitochondrial ROS level, and it was found that the cells in the G2/M phase had a higher mitochondrial content and cellular oxidative stress level than cells inThe G1 or S phase, regardless of whether the cells were irradiated.

TL;DR: Existing evidence suggests a role for glutathione metabolism, the transmethylation cycle, and the transsulfuration pathway, although these findings should be interpreted with caution, and larger, more standardized studies are warranted.

TL;DR: The literature on mechanisms of multimodal regulation of CcO activity by a wide spectrum of physiological and pathological factors is reviewed and an array of literature on the direct or indirect roles of CCO in reactive oxygen species production is reviewed.

TL;DR: These important interactions indicate a critical potential role for tumor suppressor genes in the cellular response against oxidative stress and emphasize links between ROS and tumor suppressionor genes that might be therapeutic targets in oxidative damage-associated diseases.

TL;DR: This analysis of the literature is consistent with the view that reactive oxygen and nitrogen species contribute significantly to the diverse vascular responses in inflammation and supports efforts that are directed at targeting these highly reactive species to maintain normal vascular health in pathological conditions that are associated with acute or chronic inflammation.

TL;DR: In this paper, the authors discuss the evidence for oxidative stress as a primary mechanism linking obesity and metabolic disorders and whether alteration of antioxidant status in laboratory rodents can significantly alter the development of insulin resistance or diabetes.

TL;DR: It is shown that acute exercise stress results in activation of Nrf2/ARE (antioxidant response element) signaling and subsequent enhancement of antioxidant defense pathways in wild-type mouse hearts, while oxidative stress, along with blunted defense mechanisms, was observed in NRF2-/- mice.

TL;DR: Findings of oxidative stress, altered redox signaling, and associated cell/tissue dysfunction in cell and animal models of zinc deficiency highlight the relevant role of zinc in the preservation of cell redox homeostasis.

TL;DR: This data imply that Prdx1 can function as a peroxide receptor in response to extracellular H(2)O(2), receiving the peroxide signal and transducing it into a disulfide bond that is subsequently transmitted to the substrate, ASK1, resulting in p38 phosphorylation.

TL;DR: In conclusion, flavonoid-rich apples and nitrate-rich spinach can independently augment nitric oxide status, enhance endothelial function, and lower blood pressure acutely, outcomes that may benefit cardiovascular health.

TL;DR: The multifaceted role of inflammation in carcinogenesis in the context of altered cellular redox signaling is highlighted and identified as the key molecular event in linking inflammation and cancer.

TL;DR: There exists distinct utilization ofKeap1 cysteine residues by different chemicals that trigger the response of the Keap1-Nrf2 system, and this results substantiate the notion that there are multiple sensing mechanisms within Keap 1 cysteining residues.

TL;DR: A review of recent advances in metal-induced generation of ROS and the related mechanisms; the relationship between metal-mediated ROS generation and carcinogenesis; and the signaling proteins involved inMetal-induced carcinogenesis, especially intracellular reduction-oxidation-sensitive molecules are reviewed.

TL;DR: GKT137831 is a potent inhibitor of fibrosis and hepatocyte apoptosis and a promising therapeutic agent for future translational studies, and plays a key role in liver fibrosis.

TL;DR: High ALDH3A1 expression and activity have been correlated with cell proliferation, resistance against aldehydes derived from lipid peroxidation, and resistance against drug toxicity, such as oxazaphosphorines.

TL;DR: This review focuses on the mechanisms of glycocalyx degradation during hepatic ischemia/reperfusion, the molecular and cellular players involved in the degradation process, and its implications for hepatic pathophysiology.

TL;DR: It is indicated that lutein or zeaxanthin modulates inflammatory responses in cultured RPE in response to photooxidation, and similar mechanisms may explain salutary effects of luteIn and zeaxAnthin in reducing the risk for AMD.

TL;DR: Treatment with RA but not P for 12 months was associated with improvement in liver enzymes, insulin resistance, and liver histology, without increases in body weight, and these findings warrant further investigation.

TL;DR: Redox effects of protein disulfide isomerase (PDI), a thioredoxin superfamily oxidoreductase from the endoplasmic reticulum (ER), are discussed, suggesting a convergence between PDI and Nox family NADPH oxidases.

TL;DR: Treatment of human HepG2 cells with the anthocyanin C3G significantly reduced ROS levels induced by high glucose and has an effect of activating GSH synthesis through a novel antioxidant defense mechanism against excessive ROS production, contributing to the prevention of hyperglycemia-induced hepatic oxidative damage.

TL;DR: It is indicated that TMZ-induced ROS/ERK-mediated autophagy protected glioma cells from apoptosis, and the combination of resveratrol with TMZ could improve the efficacy of chemotherapy for brain tumors.

TL;DR: A new protocol to discretely measure specific H₂S pools using the monobromobimane method coupled with RP-HPLC, which allows very sensitive and accurate measurement of the three primary biological pools of H⁂S, including free, acid-labile, and bound sulfane sulfur, in various biological specimens.

TL;DR: This work reviews the stress signaling pathways elicited by electrophiles derived from unsaturated fatty acids, focusing on the Keap1-Nrf2 pathway, the heat shock response pathway (HSR), and the unfolded protein response pathways (UPR).

TL;DR: It is shown not only that mitochondrial dysfunction is a feature of cisplatin nephrotoxicity, but also that targeted delivery of superoxide dismutase mimetics to mitochondria largely prevents the renal effects of cisPlatin.

TL;DR: The studies suggest that Nox4, a member of the NADPH oxidase (Nox) family, is a source of reactive oxygen species (ROS) affecting cell migration and fibronectin expression, an EMT marker, in normal and metastatic breast epithelial cells.