We are analyzing https://link.springer.com/article/10.1007/s00204-008-0304-z.

Title:
Intracellular redox status and oxidative stress: implications for cell proliferation, apoptosis, and carcinogenesis | Archives of Toxicology
Description:
Oxidative stress can be defined as the imbalance between cellular oxidant species production and antioxidant capability. Reactive oxygen species (ROS) are involved in a variety of different cellular processes ranging from apoptosis and necrosis to cell proliferation and carcinogenesis. In fact, molecular events, such as induction of cell proliferation, decreased apoptosis, and oxidative DNA damage have been proposed to be critically involved in carcinogenesis. Carcinogenicity and aging are characterized by a set of complex endpoints, which appear as a series of molecular reactions. ROS can modify many intracellular signaling pathways including protein phosphatases, protein kinases, and transcription factors, suggesting that the majority of the effects of ROS are through their actions on signaling pathways rather than via non-specific damage of macromolecules; however, exact mechanisms by which redox status induces cells to proliferate or to die, and how oxidative stress can lead to processes evoking tumor formation are still under investigation.
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Keywords {🔍}

google, scholar, pubmed, cas, cell, apoptosis, cells, cancer, oxidative, protein, biol, stress, carcinogenesis, kinase, redox, res, human, proliferation, chem, death, glutamine, reactive, signal, species, ros, growth, expression, activation, article, oxygen, damage, toxicol, pathway, dna, glutathione, biochem, physiol, matés, signaling, pathways, effects, factor, role, pharmacol, mitochondrial, molecular, mechanisms, induces, free, epithelial,

Topics {✒️}

n-acetyl-l-cysteine nadph c-jun nh2-terminal kinase rho/rok/pkc-delta pathway activation n-acetyl cysteine month download article/chapter heat shock-induced apoptosis c-myc determines sensitivity wild-type p53 protein tumor promoter-induced alterations glutathione s-transferase pi glutathione-s-transferase polymorphisms human glutaminyl-trna synthetase dmba-induced breast cancer d-serine exposure resulted redox-sensitive signalling cascades hyperoxia-induced lung damage es-cell-derived cardiomyogenesis peroxisome proliferator-induced hepatocarcinogenesis stress-induced cell death cell cycle-related events ultraviolet b-induced apoptosis anchorage-dependent cell growth chk1-dependent g2 checkpoint impaired e-cadherin expression lymphoblastoid cell line ask1-map kinase pathway fas-mediated cell death dose-response-mediated mechanisms arsenic-induced bladder cancer sp2/0-ag14 hybridoma cells intestinal epithelial cells oxidative stress-induced cancer 8-dihydroxy-4-methylcoumarin induces apoptosis p53-null cancer cells busulfan-induced senescence protein kinase cdelta alpha-lipoic acid mek/erk signalling glutamine-dependent antiapoptotic interaction cyclin-dependent kinase inhibitors cellular processes ranging ros-independent mitochondrial pathway c-myc oncoprotein hypoxia/reoxygenation trigger cd95 glutathione s-transferase neuronal caspase-independent apoptosis glucose-regulated protein 94 fas-mediated apoptosome formation erk promotes tumorigenesis apoptosis-related proteins

Questions {❓}

Ramsey MR, Sharpless NE (2006) ROS as a tumour suppressor?
Shmueli A, Oren M (2007) Mdm2: p53’s lifesaver?
Wodarz D, Komarova N (2007) Can loss of apoptosis protect against cancer?

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