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- W2980920340 abstract "Autophagy is a highly conserved evolutionary survival or defence process that enables cells and organisms to survive periods of environmental stress by breaking down cellular organelles and macromolecules in autolysosomes to provide a supply of nutrients for cell maintenance. However, autophagy is also a part of normal cellular physiology that facilitates the turnover of cellular constituents under normal conditions: it can be readily augmented by mild environmental stress; but becomes dysfunctional with severe oxidative stress leading to cellular pathology. The molluscan hepatopancreas or digestive gland provides a versatile and environmentally relevant model to investigate lysosomal autophagy and stress-induced dysfunctional autophagy. This latter process has been implicated in many animal and human disease conditions, including degenerative and neurodegenerative diseases, as well as obesity related conditions. Many environmental pollutants have also been found to induce dysfunctional autophagy in molluscan hepatopancreatic digestive cells, and in this study, the marine blue mussel Mytilus galloprovincialis was exposed for 7 days to: 0.1 μM, 1 μM and 10 μM concentrations of fluoranthene and phenanthrene (PAHs); chlorpyrifos and malathion (organophosphorus compounds); atrazine (triazine herbicide); copper (transition metal) and dodecylbenzene sulphonic acid (LAS, surfactant). The marine snail or periwinkle, Littorina littorea, was also exposed to phenanthrene, chlorpyrifos and copper. Indices of oxidative stress, cell injury and dysfunctional autophagy were measured (i.e., lysosomal membrane stability, protein carbonyls, lipofuscin, and lysosomal accumulation of lipid or lipidosis). Evidence of oxidative stress, based on the elevation of lipofuscin and protein carbonyls, was found for all compounds tested; with chlorpyrifos being the most toxic to both species. Dysfunctional autophagy was induced by all of the compounds tested in both species, except for atrazine in mussels. This failure of normal autophagy was consistently associated with oxidative stress. Autophagic dysfunction is an important emerging feature in the aetiology of many disease conditions in animals and humans; and an explanatory conceptual mechanistic model has been developed for dysregulation of autophagy in response to oxidative stress." @default.
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- W2980920340 date "2019-12-01" @default.
- W2980920340 modified "2023-09-26" @default.
- W2980920340 title "Oxidative stress, lysosomal damage and dysfunctional autophagy in molluscan hepatopancreas (digestive gland) induced by chemical contaminants" @default.
- W2980920340 cites W1849052996 @default.
- W2980920340 cites W1927588525 @default.
- W2980920340 cites W1964552652 @default.
- W2980920340 cites W1967761442 @default.
- W2980920340 cites W1969113162 @default.
- W2980920340 cites W1969778144 @default.
- W2980920340 cites W1969873492 @default.
- W2980920340 cites W1972958434 @default.
- W2980920340 cites W1976815903 @default.
- W2980920340 cites W1977234647 @default.
- W2980920340 cites W1978119256 @default.
- W2980920340 cites W1981759914 @default.
- W2980920340 cites W1988550307 @default.
- W2980920340 cites W1996099327 @default.
- W2980920340 cites W1996183004 @default.
- W2980920340 cites W2001043627 @default.
- W2980920340 cites W2003122384 @default.
- W2980920340 cites W2008676944 @default.
- W2980920340 cites W2010232230 @default.
- W2980920340 cites W2011265703 @default.
- W2980920340 cites W2014070897 @default.
- W2980920340 cites W2014579900 @default.
- W2980920340 cites W2021345418 @default.
- W2980920340 cites W2022611274 @default.
- W2980920340 cites W2029265163 @default.
- W2980920340 cites W2033794627 @default.
- W2980920340 cites W2037627674 @default.
- W2980920340 cites W2038192950 @default.
- W2980920340 cites W2042037305 @default.
- W2980920340 cites W2042626652 @default.
- W2980920340 cites W2043151177 @default.
- W2980920340 cites W2043291430 @default.
- W2980920340 cites W2048020111 @default.
- W2980920340 cites W2050996541 @default.
- W2980920340 cites W2051091502 @default.
- W2980920340 cites W2058816754 @default.
- W2980920340 cites W2061044463 @default.
- W2980920340 cites W2061511771 @default.
- W2980920340 cites W2063403801 @default.
- W2980920340 cites W2067921487 @default.
- W2980920340 cites W2070407085 @default.
- W2980920340 cites W2075214208 @default.
- W2980920340 cites W2080630604 @default.
- W2980920340 cites W2084021451 @default.
- W2980920340 cites W2093818907 @default.
- W2980920340 cites W2095665447 @default.
- W2980920340 cites W2120595804 @default.
- W2980920340 cites W2127063807 @default.
- W2980920340 cites W2129664378 @default.
- W2980920340 cites W2136462514 @default.
- W2980920340 cites W2137713421 @default.
- W2980920340 cites W2140664473 @default.
- W2980920340 cites W2155664391 @default.
- W2980920340 cites W2170328046 @default.
- W2980920340 cites W2171152857 @default.
- W2980920340 cites W2216034599 @default.
- W2980920340 cites W2238467432 @default.
- W2980920340 cites W2257637313 @default.
- W2980920340 cites W2318467540 @default.
- W2980920340 cites W2406904044 @default.
- W2980920340 cites W2468138910 @default.
- W2980920340 cites W2524951371 @default.
- W2980920340 cites W2573914334 @default.
- W2980920340 cites W2597529135 @default.
- W2980920340 cites W2606461931 @default.
- W2980920340 cites W2610514067 @default.
- W2980920340 cites W2752326209 @default.
- W2980920340 cites W2761329528 @default.
- W2980920340 cites W2780178667 @default.
- W2980920340 cites W2790809759 @default.
- W2980920340 cites W2803679037 @default.
- W2980920340 cites W4231756003 @default.
- W2980920340 doi "https://doi.org/10.1016/j.marenvres.2019.104825" @default.
- W2980920340 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31668363" @default.
- W2980920340 hasPublicationYear "2019" @default.
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