FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000243579> ?p ?o ?g. }

• W2000243579 endingPage "53" @default.
• W2000243579 startingPage "42" @default.
• W2000243579 abstract "Acrylamide (ACR), a potent neurotoxin, can be produced during food processing at high temperature. This study examined the redox-dependent apoptotic and inflammatory responses of ACR in an immortalized mouse microglia cell line BV2. The exposure of BV2 cells to ACR reduced cell viability and induced apoptosis in a concentration-dependent manner. ACR impaired cell energy metabolism by decreasing mitochondrial respiration, anaerobic glycolysis, and lowering expression of the complex I, III, and IV subunits. Mitochondrial dysfunction was associated with a decrease of the mitochondrial membrane potential and the Bcl-2/Bax ratio, thus resulting in activation of the mitochondrion-driven apoptotic signaling. This was accompanied by (a) the modulation of redox-sensitive signaling, suppressed Akt activation and increased JNK and p38 activation, and (b) increased expression of NFκB and downstream inducible nitric oxide synthase (iNOS) and nitric oxide generation, thus supporting indirectly a proinflammatory effect of ACR. Nrf2 expression was also increased but not its translocation to the nucleus. Expectedly, the electrophilic attack of ACR on GSH resulted in substantial loss of GSH with a minor GSSG formation. These changes in the cell׳s redox status elicited by ACR resulted in increased H2O2 formation. The changes in mitochondrial functionality and complex subunit expression caused by ACR were reversed by N-acetyl-L-cysteine (NAC). Likewise, NAC restored the cell׳s redox status by increasing GSH levels with concomitant attenuation of H2O2 generation; these effects resulted in decreased apoptotic cell death and inflammatory responses. ACR-mediated mitochondrial dysfunction along with a more oxidized redox status seems to be critical events leading to activation of the intrinsic apoptotic pathway and inflammatory responses." @default.
• W2000243579 created "2016-06-24" @default.
• W2000243579 creator A5001881392 @default.
• W2000243579 creator A5012587937 @default.
• W2000243579 creator A5029551526 @default.
• W2000243579 creator A5033795683 @default.
• W2000243579 creator A5050251296 @default.
• W2000243579 creator A5056286763 @default.
• W2000243579 creator A5090864700 @default.
• W2000243579 date "2015-07-01" @default.
• W2000243579 modified "2023-10-16" @default.
• W2000243579 title "Acrylamide induces mitochondrial dysfunction and apoptosis in BV-2 microglial cells" @default.
• W2000243579 cites W152231878 @default.
• W2000243579 cites W1523151859 @default.
• W2000243579 cites W1942214720 @default.
• W2000243579 cites W1965199792 @default.
• W2000243579 cites W1965642982 @default.
• W2000243579 cites W1969966531 @default.
• W2000243579 cites W1975980701 @default.
• W2000243579 cites W1986517451 @default.
• W2000243579 cites W1987577991 @default.
• W2000243579 cites W1988631382 @default.
• W2000243579 cites W2000503562 @default.
• W2000243579 cites W2003803700 @default.
• W2000243579 cites W2004349171 @default.
• W2000243579 cites W2005398690 @default.
• W2000243579 cites W2006182237 @default.
• W2000243579 cites W2007419421 @default.
• W2000243579 cites W2007856857 @default.
• W2000243579 cites W2008271079 @default.
• W2000243579 cites W2008414965 @default.
• W2000243579 cites W2024007859 @default.
• W2000243579 cites W2024805816 @default.
• W2000243579 cites W2026141598 @default.
• W2000243579 cites W2028892046 @default.
• W2000243579 cites W2029388216 @default.
• W2000243579 cites W2031035081 @default.
• W2000243579 cites W2033966441 @default.
• W2000243579 cites W2034558145 @default.
• W2000243579 cites W2035147973 @default.
• W2000243579 cites W2035245129 @default.
• W2000243579 cites W2035692542 @default.
• W2000243579 cites W2038136644 @default.
• W2000243579 cites W2038683700 @default.
• W2000243579 cites W2044010527 @default.
• W2000243579 cites W2044105520 @default.
• W2000243579 cites W2044273377 @default.
• W2000243579 cites W2044571716 @default.
• W2000243579 cites W2044660587 @default.
• W2000243579 cites W2045079365 @default.
• W2000243579 cites W2052020575 @default.
• W2000243579 cites W2053554709 @default.
• W2000243579 cites W2055385665 @default.
• W2000243579 cites W2063953032 @default.
• W2000243579 cites W2064046464 @default.
• W2000243579 cites W2064380367 @default.
• W2000243579 cites W2066619250 @default.
• W2000243579 cites W2068287372 @default.
• W2000243579 cites W2073925710 @default.
• W2000243579 cites W2074661552 @default.
• W2000243579 cites W2075669866 @default.
• W2000243579 cites W2081994535 @default.
• W2000243579 cites W2089620470 @default.
• W2000243579 cites W2095315837 @default.
• W2000243579 cites W2101838335 @default.
• W2000243579 cites W2110683265 @default.
• W2000243579 cites W2111154757 @default.
• W2000243579 cites W2114918609 @default.
• W2000243579 cites W2123803574 @default.
• W2000243579 cites W2127621191 @default.
• W2000243579 cites W2130866079 @default.
• W2000243579 cites W2134183006 @default.
• W2000243579 cites W2134198441 @default.
• W2000243579 cites W2135472400 @default.
• W2000243579 cites W2151092369 @default.
• W2000243579 cites W2160738126 @default.
• W2000243579 cites W2160974829 @default.
• W2000243579 cites W2330842740 @default.
• W2000243579 cites W2948665150 @default.
• W2000243579 cites W3004118171 @default.
• W2000243579 cites W333643404 @default.
• W2000243579 doi "https://doi.org/10.1016/j.freeradbiomed.2015.03.013" @default.
• W2000243579 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25817051" @default.
• W2000243579 hasPublicationYear "2015" @default.
• W2000243579 type Work @default.
• W2000243579 sameAs 2000243579 @default.
• W2000243579 citedByCount "82" @default.
• W2000243579 countsByYear W20002435792016 @default.
• W2000243579 countsByYear W20002435792017 @default.
• W2000243579 countsByYear W20002435792018 @default.
• W2000243579 countsByYear W20002435792019 @default.
• W2000243579 countsByYear W20002435792020 @default.
• W2000243579 countsByYear W20002435792021 @default.
• W2000243579 countsByYear W20002435792022 @default.
• W2000243579 countsByYear W20002435792023 @default.
• W2000243579 crossrefType "journal-article" @default.
• W2000243579 hasAuthorship W2000243579A5001881392 @default.
• W2000243579 hasAuthorship W2000243579A5012587937 @default.

• next