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• W2954335469 endingPage "179" @default.
• W2954335469 startingPage "165" @default.
• W2954335469 abstract "Monocytes and macrophages play a key role in the development of inflammation: under the action of lipopolysaccharides (LPS), absorbed from the intestine, monocytes and macrophages form reactive oxygen species (ROS) and cytokines, this leads to the development of oxidative stress, inflammation and/or apoptosis in all types of tissues. In the cells LPS induce an “internal” TLR4-mediated MAP-kinase inflammatory signaling pathway and cytokines through the superfamily of tumor necrosis factor receptor (TNFR) and the “death domain” (DD) initiate an “external” caspase apoptosis cascade or necrosis activation that causes necroptosis. Many of the proteins involved in intracellular signaling cascades (MYD88, ASK1, IKKa/b, NF-kB, AP-1) are redox-sensitive and their activity is regulated by antioxidants thioredoxin, glutaredoxin, nitroredoxin, and glutathione. Oxidation of these signaling proteins induced by ROS enhances the development of inflammation and apoptosis, and their reduction with antioxidants, on the contrary, stabilizes the signaling cascades speed, preventing the vicious circle of oxidative stress, inflammation and apoptosis that follows it. Antioxidant (AO) enzymes thioredoxin reductase (TRXR), glutaredoxin reductase (GLRXR), glutathione reductase (GR) are required for reduction of non-enzymatic antioxidants (thioredoxin, glutaredoxin, nitroredoxin, glutathione), and AO enzymes (SOD, catalase, GPX) are required for ROS deactivation. The key AO enzymes (TRXR and GPX) are selenium-dependent; therefore selenium deficiency leads to a decrease in the body's antioxidant defense, the development of oxidative stress, inflammation, and/or apoptosis in various cell types. Nrf2-Keap1 signaling pathway activated by selenium deficiency and/or oxidative stress is necessary to restore redox homeostasis in the cell. In addition, expression of some genes is changed with selenium deficiency. Consequently, growth and proliferation of cells, their movement, development, death, and survival, as well as the interaction between cells, the redox regulation of intracellular signaling cascades of inflammation and apoptosis, depend on the selenium status of the body. Prophylactic administration of selenium-containing preparations (natural and synthetic (organic and inorganic)) is able to normalize the activity of AO enzymes and the general status of the body. Organic selenium compounds have a high bioavailability and, depending on their concentration, can act both as selenium donors to prevent selenium deficiency and as antitumor drugs due to their toxicity and participation in the regulation of signaling pathways of apoptosis. Known selenorganic compounds diphenyldiselenide and ethaselen share similarity with the Russian organo selenium compound, diacetophenonylselenide (DAPS-25), which serves as a source of bioavailable selenium, exhibits a wide range of biological activity, including antioxidant activity, that governs cell redox balance, inflammation and apoptosis regulation." @default.
• W2954335469 created "2019-07-12" @default.
• W2954335469 creator A5000486291 @default.
• W2954335469 creator A5053008517 @default.
• W2954335469 creator A5084691584 @default.
• W2954335469 creator A5074145150 @default.
• W2954335469 date "2019-01-01" @default.
• W2954335469 modified "2023-10-12" @default.
• W2954335469 title "Selenium compounds in redox regulation of inflammation and apoptosis" @default.
• W2954335469 cites W1540651211 @default.
• W2954335469 cites W1587498818 @default.
• W2954335469 cites W1600951549 @default.
• W2954335469 cites W1842535138 @default.
• W2954335469 cites W1875631470 @default.
• W2954335469 cites W1957136694 @default.
• W2954335469 cites W1963916684 @default.
• W2954335469 cites W1966549549 @default.
• W2954335469 cites W1967265218 @default.
• W2954335469 cites W1967717285 @default.
• W2954335469 cites W1970942229 @default.
• W2954335469 cites W1971691443 @default.
• W2954335469 cites W1977706521 @default.
• W2954335469 cites W1978772332 @default.
• W2954335469 cites W1981852031 @default.
• W2954335469 cites W1994186505 @default.
• W2954335469 cites W1997183854 @default.
• W2954335469 cites W1997382890 @default.
• W2954335469 cites W1997634540 @default.
• W2954335469 cites W1998401344 @default.
• W2954335469 cites W1999070086 @default.
• W2954335469 cites W2001399393 @default.
• W2954335469 cites W2002015567 @default.
• W2954335469 cites W2003683297 @default.
• W2954335469 cites W2004724154 @default.
• W2954335469 cites W2014054401 @default.
• W2954335469 cites W2025578279 @default.
• W2954335469 cites W2028606943 @default.
• W2954335469 cites W2029334399 @default.
• W2954335469 cites W2029342214 @default.
• W2954335469 cites W2031950618 @default.
• W2954335469 cites W2033413855 @default.
• W2954335469 cites W2033978865 @default.
• W2954335469 cites W2038324446 @default.
• W2954335469 cites W2039198912 @default.
• W2954335469 cites W2045786144 @default.
• W2954335469 cites W2057453845 @default.
• W2954335469 cites W2064899853 @default.
• W2954335469 cites W2065546882 @default.
• W2954335469 cites W2067668889 @default.
• W2954335469 cites W2071468228 @default.
• W2954335469 cites W2073357660 @default.
• W2954335469 cites W2074006488 @default.
• W2954335469 cites W2075179001 @default.
• W2954335469 cites W2075882939 @default.
• W2954335469 cites W2076159984 @default.
• W2954335469 cites W2077219185 @default.
• W2954335469 cites W2077549620 @default.
• W2954335469 cites W2079425870 @default.
• W2954335469 cites W2081519457 @default.
• W2954335469 cites W2083882252 @default.
• W2954335469 cites W2084004698 @default.
• W2954335469 cites W2092210221 @default.
• W2954335469 cites W2093123316 @default.
• W2954335469 cites W2098303916 @default.
• W2954335469 cites W2100494125 @default.
• W2954335469 cites W2100957071 @default.
• W2954335469 cites W2104928760 @default.
• W2954335469 cites W2122341467 @default.
• W2954335469 cites W2125208859 @default.
• W2954335469 cites W2125865950 @default.
• W2954335469 cites W2128327754 @default.
• W2954335469 cites W2130719768 @default.
• W2954335469 cites W2131363279 @default.
• W2954335469 cites W2132403739 @default.
• W2954335469 cites W2134192973 @default.
• W2954335469 cites W2135057047 @default.
• W2954335469 cites W2137261693 @default.
• W2954335469 cites W2138271341 @default.
• W2954335469 cites W2141400467 @default.
• W2954335469 cites W2141802124 @default.
• W2954335469 cites W2145318799 @default.
• W2954335469 cites W2146558971 @default.
• W2954335469 cites W2149611550 @default.
• W2954335469 cites W2149668250 @default.
• W2954335469 cites W2158131507 @default.
• W2954335469 cites W2166800890 @default.
• W2954335469 cites W2178040734 @default.
• W2954335469 cites W2184577754 @default.
• W2954335469 cites W2191169263 @default.
• W2954335469 cites W2220596386 @default.
• W2954335469 cites W2230520707 @default.
• W2954335469 cites W2238745372 @default.
• W2954335469 cites W2329148881 @default.
• W2954335469 cites W2342333688 @default.
• W2954335469 cites W2407715304 @default.
• W2954335469 cites W2507521067 @default.
• W2954335469 cites W2520129402 @default.
• W2954335469 cites W2528155872 @default.

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