17 research outputs found

    DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

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    Oxidative stress and lipid peroxidation (LPO) induced by inflammation, excess metal storage and excess caloric intake cause generalized DNA damage, producing genotoxic and mutagenic effects. The consequent deregulation of cell homeostasis is implicated in the pathogenesis of a number of malignancies and degenerative diseases. Reactive aldehydes produced by LPO, such as malondialdehyde, acrolein, crotonaldehyde and 4-hydroxy-2-nonenal, react with DNA bases, generating promutagenic exocyclic DNA adducts, which likely contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. However, reactive aldehydes, when added to tumor cells, can exert an anticancerous effect. They act, analogously to other chemotherapeutic drugs, by forming DNA adducts and, in this way, they drive the tumor cells toward apoptosis. The aldehyde-DNA adducts, which can be observed during inflammation, play an important role by inducing epigenetic changes which, in turn, can modulate the inflammatory process. The pathogenic role of the adducts formed by the products of LPO with biological macromolecules in the breaking of immunological tolerance to self antigens and in the development of autoimmunity has been supported by a wealth of evidence. The instrumental role of the adducts of reactive LPO products with self protein antigens in the sensitization of autoreactive cells to the respective unmodified proteins and in the intermolecular spreading of the autoimmune responses to aldehyde-modified and native DNA is well documented. In contrast, further investigation is required in order to establish whether the formation of adducts of LPO products with DNA might incite substantial immune responsivity and might be instrumental for the spreading of the immunological responses from aldehyde-modified DNA to native DNA and similarly modified, unmodified and/or structurally analogous self protein antigens, thus leading to autoimmunity

    DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

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    Stable Ischemic Heart Disease

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    Stable Ischemic Heart Disease

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    Stable Ischemic Heart Disease Stable Ischemic Heart Disease

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    Maximum rooting depth of vegetation types at the global scale

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    The depth at which plants are able to grow roots has important implications for the whole ecosystem hydrological balance, as well as for carbon and nutrient cycling. Here we summarize maximum rooting depth of species belonging to the major terrestrial biomes. We found 290 observations of maximum rooting depth in the literature which covered 255 woody and herbaceous species. Maximum rooting depth ranged from 0.3 m for some tundra species to 68 m for Boscia albitrunca in the central Kalahari; 196 species had roots at least 2 m deep, 50 species had roots at a depth of 5 m or more, and 22 species had roots as deep as 10 m or more. The average for the globe was 4.6 +0.5 m. Maximum root depth by biome was 2.0 m for boreal forest, 2.1 m for cropland, 9.5 m for desert, 5.2 m for sclerophyllous shrubland and forest, 3.9 m for temperate coniferous forest, 2.9 m for temperate deciduous forest, 2.6 m for temperate grassland, 3.7 m for tropical deciduous forest, 7.3 m for tropical evergreen forest, 15.0 m for tropical grassland/savanna, and 0.5 m for tundra. Grouping all species across biomes (except croplands) by three basic functional groups (trees, shrubs, and herbaceous plants), the average maximum rooting depth was 7.0 m for trees, 5.1 m for shrubs, and 2.6 m for herbaceous plants

    Maximum rooting depth of vegetation types at the global scale

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    Recent discovery and development of protein tyrosine phosphatase inhibitors

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