Literature DB >> 10699758

Oxidative stress and gene regulation.

R G Allen1, M Tresini.   

Abstract

Reactive oxygen species are produced by all aerobic cells and are widely believed to play a pivotal role in aging as well as a number of degenerative diseases. The consequences of the generation of oxidants in cells does not appear to be limited to promotion of deleterious effects. Alterations in oxidative metabolism have long been known to occur during differentiation and development. Experimental perturbations in cellular redox state have been shown to exert a strong impact on these processes. The discovery of specific genes and pathways affected by oxidants led to the hypothesis that reactive oxygen species serve as subcellular messengers in gene regulatory and signal transduction pathways. Additionally, antioxidants can activate numerous genes and pathways. The burgeoning growth in the number of pathways shown to be dependent on oxidation or antioxidation has accelerated during the last decade. In the discussion presented here, we provide a tabular summary of many of the redox effects on gene expression and signaling pathways that are currently known to exist.

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Year:  2000        PMID: 10699758     DOI: 10.1016/s0891-5849(99)00242-7

Source DB:  PubMed          Journal:  Free Radic Biol Med        ISSN: 0891-5849            Impact factor:   7.376


  243 in total

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6.  Serum antioxidant capacity, biochemical profile and body composition of breast cancer survivors in a randomized Mediterranean dietary intervention study.

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Review 7.  The role of AP-1, NF-kappaB and ROS/NOS in skin carcinogenesis: the JB6 model is predictive.

Authors:  Arindam Dhar; Mathew R Young; Nancy H Colburn
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8.  Macrophage differentiation increases expression of the ascorbate transporter (SVCT2).

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9.  Evidence that reactive oxygen species do not mediate NF-kappaB activation.

Authors:  Makio Hayakawa; Hiroshi Miyashita; Isao Sakamoto; Masatoshi Kitagawa; Hirofumi Tanaka; Hideyo Yasuda; Michael Karin; Kiyomi Kikugawa
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10.  Succinate modulation of H2O2 release at NADH:ubiquinone oxidoreductase (Complex I) in brain mitochondria.

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