FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016098250> ?p ?o ?g. }

• W2016098250 endingPage "143" @default.
• W2016098250 startingPage "131" @default.
• W2016098250 abstract "Attempts to establish the presence of oxidant stress and tissue damage in inflammatory bowel disease (IBD) have relied on determining the capacity of peripheral blood inflammatory cells to produce reactive oxygen species (ROS) and other indirect indices. These approaches have failed to address whether or not there are adequate chemical antioxidant defences to prevent oxidative injury in the inflamed mucosa. In this investigation we have determined the mucosal concentrations of reduced and total ascorbic acid and the redox status in paired non-inflamed and inflamed mucosa using colonic biopsies from IBD patients. In inflamed mucosa from Crohn's disease (CD) patients, reduced and total ascorbic acid content decreased by 35% (p = 0.014 and p = 0.009, respectively). In ulcerative colitis (UC) patients, mucosal total ascorbic acid content decreased by 73% (p = 0.069) and reduced ascorbic acid by 41% (p = 0.014). The proportion of total ascorbic acid present in its reduced form in histologically normal mucosa from CD patients was unusually low at approximately 30%. In the paired-inflamed mucosa from CD patients, the redox ratio was also approximately 30% despite the loss of 35% of total ascorbate. In UC patients, the ascorbate redox ratio in the non-inflamed mucosa was 23% which increased to 51% in paired inflamed mucosa. This increase reflected the loss (73%) of total ascorbate. Reduction of dehydroascorbic acid by GSH/NADPH dependent dehydroascorbic acid reductase decreased significantly (p = 0.046) in inflamed mucosa from UC patients, suggesting that the capacity of the inflamed mucosa to maintain the concentration of reduced ascorbic acid is also diminished. HPLC analysis of mucosal preparations for diketogulonic acid, the decomposition product of dehydroascorbic acid, did not account for the loss of total ascorbate in the inflamed mucosa suggesting that ascorbate equivalents underwent further decomposition reactions or were excreted to the colonic lumen. We conclude that the normal luminal environment is strongly oxidising in character and that oxidant stress derived from inflammatory cells contributes to the loss of 35-73% total and reduced ascorbate. In absolute terms, the overall loss of this antioxidant buffering capacity would decrease the capacity of the inflamed mucosa to prevent oxidative tissue damage and hinder recovery of the inflamed mucosa." @default.
• W2016098250 created "2016-06-24" @default.
• W2016098250 creator A5013206192 @default.
• W2016098250 creator A5066013141 @default.
• W2016098250 date "1995-01-01" @default.
• W2016098250 modified "2023-10-05" @default.
• W2016098250 title "Altered Ascorbic Acid Status in the Mucosa from Inflammatory Bowel Disease Patients" @default.
• W2016098250 cites W1506520614 @default.
• W2016098250 cites W1602033104 @default.
• W2016098250 cites W1670771883 @default.
• W2016098250 cites W1821299455 @default.
• W2016098250 cites W1920198420 @default.
• W2016098250 cites W1929815070 @default.
• W2016098250 cites W1962412749 @default.
• W2016098250 cites W1967225749 @default.
• W2016098250 cites W1986222438 @default.
• W2016098250 cites W1997731166 @default.
• W2016098250 cites W1998183746 @default.
• W2016098250 cites W2001078312 @default.
• W2016098250 cites W2002217241 @default.
• W2016098250 cites W2019349751 @default.
• W2016098250 cites W2024882740 @default.
• W2016098250 cites W2027416526 @default.
• W2016098250 cites W2081789577 @default.
• W2016098250 cites W2089772634 @default.
• W2016098250 cites W2089775737 @default.
• W2016098250 cites W2097322191 @default.
• W2016098250 cites W2099023343 @default.
• W2016098250 cites W2132103236 @default.
• W2016098250 cites W2136576257 @default.
• W2016098250 cites W2138094519 @default.
• W2016098250 cites W2202554561 @default.
• W2016098250 cites W2409388505 @default.
• W2016098250 cites W2462080623 @default.
• W2016098250 cites W2614442853 @default.
• W2016098250 doi "https://doi.org/10.3109/10715769509147535" @default.
• W2016098250 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7704184" @default.
• W2016098250 hasPublicationYear "1995" @default.
• W2016098250 type Work @default.
• W2016098250 sameAs 2016098250 @default.
• W2016098250 citedByCount "116" @default.
• W2016098250 countsByYear W20160982502012 @default.
• W2016098250 countsByYear W20160982502013 @default.
• W2016098250 countsByYear W20160982502014 @default.
• W2016098250 countsByYear W20160982502015 @default.
• W2016098250 countsByYear W20160982502016 @default.
• W2016098250 countsByYear W20160982502017 @default.
• W2016098250 countsByYear W20160982502018 @default.
• W2016098250 countsByYear W20160982502019 @default.
• W2016098250 countsByYear W20160982502020 @default.
• W2016098250 countsByYear W20160982502021 @default.
• W2016098250 countsByYear W20160982502022 @default.
• W2016098250 countsByYear W20160982502023 @default.
• W2016098250 crossrefType "journal-article" @default.
• W2016098250 hasAuthorship W2016098250A5013206192 @default.
• W2016098250 hasAuthorship W2016098250A5066013141 @default.
• W2016098250 hasConcept C126322002 @default.
• W2016098250 hasConcept C142724271 @default.
• W2016098250 hasConcept C185592680 @default.
• W2016098250 hasConcept C203014093 @default.
• W2016098250 hasConcept C2776151105 @default.
• W2016098250 hasConcept C2778004101 @default.
• W2016098250 hasConcept C2778260677 @default.
• W2016098250 hasConcept C2779134260 @default.
• W2016098250 hasConcept C2779211342 @default.
• W2016098250 hasConcept C2780479503 @default.
• W2016098250 hasConcept C2986274086 @default.
• W2016098250 hasConcept C3019368612 @default.
• W2016098250 hasConcept C31903555 @default.
• W2016098250 hasConcept C55493867 @default.
• W2016098250 hasConcept C71924100 @default.
• W2016098250 hasConceptScore W2016098250C126322002 @default.
• W2016098250 hasConceptScore W2016098250C142724271 @default.
• W2016098250 hasConceptScore W2016098250C185592680 @default.
• W2016098250 hasConceptScore W2016098250C203014093 @default.
• W2016098250 hasConceptScore W2016098250C2776151105 @default.
• W2016098250 hasConceptScore W2016098250C2778004101 @default.
• W2016098250 hasConceptScore W2016098250C2778260677 @default.
• W2016098250 hasConceptScore W2016098250C2779134260 @default.
• W2016098250 hasConceptScore W2016098250C2779211342 @default.
• W2016098250 hasConceptScore W2016098250C2780479503 @default.
• W2016098250 hasConceptScore W2016098250C2986274086 @default.
• W2016098250 hasConceptScore W2016098250C3019368612 @default.
• W2016098250 hasConceptScore W2016098250C31903555 @default.
• W2016098250 hasConceptScore W2016098250C55493867 @default.
• W2016098250 hasConceptScore W2016098250C71924100 @default.
• W2016098250 hasIssue "2" @default.
• W2016098250 hasLocation W20160982501 @default.
• W2016098250 hasLocation W20160982502 @default.
• W2016098250 hasOpenAccess W2016098250 @default.
• W2016098250 hasPrimaryLocation W20160982501 @default.
• W2016098250 hasRelatedWork W139548325 @default.
• W2016098250 hasRelatedWork W1524541850 @default.
• W2016098250 hasRelatedWork W156791464 @default.
• W2016098250 hasRelatedWork W2016098250 @default.
• W2016098250 hasRelatedWork W2041552608 @default.
• W2016098250 hasRelatedWork W2096007079 @default.
• W2016098250 hasRelatedWork W2376429181 @default.

• next