FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2121559221> ?p ?o ?g. }

• W2121559221 endingPage "202" @default.
• W2121559221 startingPage "195" @default.
• W2121559221 abstract "Dacarbazine (DTIC) is a synthetic chemical antitumor agent which is used to treat malignant melanoma and Hodgkin’s disease. DTIC is a prodrug which is converted to an active form undergoing demethylation by liver enzymes. The active form prevents the progress of disease via alkylation of DNA strand. In the structure of this drug, the imidazole ring, a triazen chain and carboxamide group exist. Based on the literature, the ring and carboxamide group do not have a key role in antitumor activity of the drug. On the other hand, imidazole ring has a unique tautomerization which may participate in the mechanism of action of DTIC and carboxamide group may determine the rich guanine pieces in DNA strand. In order to investigate the mechanistic role of imidazole group and its known tautomerization in DTIC cytotoxicity, derivative of DTIC with a pyridine ring (3-(3,3-dimethyl-1triazenyl)pyridine, (compound I) instead of imidazole ring was synthesized. In the following, the cellular and molecular mechanism of cytotoxicity induced by DTIC and its pyridine derivative toward the isolated rat hepatocytes were studied and compared. Hepatocyte reactive oxygen species (ROS) generation was significantly increased by both DTIC and compound B before cytotoxicity ensued. In addition, DTIC and compound I induced lysosomal damage and hepatocyte protease activation. Endocytosis inhibitors, lysosomotropic agents or lysosomal protease inhibitors also prevented both DTIC and compound B induced hepatocytes cytotoxicity. Furthermore desferoxamine (a ferric chelator), antioxidants or ROS scavengers (catalase, mannitol or dimethylsulfoxide) prevented both DTIC and compound I cytotoxicity. It is concluded that H 2 O 2 reacts with lysosomal Fe 2+ to form hydroxyl radical which (Haber-Weiss reaction) causes lysosomal membrane disruption, proteases and other digestive enzymes release and finally the cell death." @default.
• W2121559221 created "2016-06-24" @default.
• W2121559221 creator A5008684643 @default.
• W2121559221 creator A5064230925 @default.
• W2121559221 creator A5076656415 @default.
• W2121559221 date "2006-10-01" @default.
• W2121559221 modified "2023-09-25" @default.
• W2121559221 title "Lysosomal Oxidative Stress Cytotoxicity Induced by Dacarbazine and It’s Pyridine Derivative in Hepatocytes" @default.
• W2121559221 cites W1566167018 @default.
• W2121559221 cites W1866456441 @default.
• W2121559221 cites W1971999069 @default.
• W2121559221 cites W1997927392 @default.
• W2121559221 cites W2005816149 @default.
• W2121559221 cites W2010451932 @default.
• W2121559221 cites W2011606516 @default.
• W2121559221 cites W2015796087 @default.
• W2121559221 cites W2029257301 @default.
• W2121559221 cites W2034551396 @default.
• W2121559221 cites W2034992929 @default.
• W2121559221 cites W2047558574 @default.
• W2121559221 cites W2072415705 @default.
• W2121559221 cites W2079676483 @default.
• W2121559221 cites W2090698021 @default.
• W2121559221 cites W2401094079 @default.
• W2121559221 cites W2414335587 @default.
• W2121559221 cites W2414704639 @default.
• W2121559221 cites W2114618598 @default.
• W2121559221 hasPublicationYear "2006" @default.
• W2121559221 type Work @default.
• W2121559221 sameAs 2121559221 @default.
• W2121559221 citedByCount "0" @default.
• W2121559221 crossrefType "journal-article" @default.
• W2121559221 hasAuthorship W2121559221A5008684643 @default.
• W2121559221 hasAuthorship W2121559221A5064230925 @default.
• W2121559221 hasAuthorship W2121559221A5076656415 @default.
• W2121559221 hasConcept C109316439 @default.
• W2121559221 hasConcept C185592680 @default.
• W2121559221 hasConcept C202751555 @default.
• W2121559221 hasConcept C2777658100 @default.
• W2121559221 hasConcept C2780964509 @default.
• W2121559221 hasConcept C502942594 @default.
• W2121559221 hasConcept C55493867 @default.
• W2121559221 hasConcept C71240020 @default.
• W2121559221 hasConcept C86803240 @default.
• W2121559221 hasConceptScore W2121559221C109316439 @default.
• W2121559221 hasConceptScore W2121559221C185592680 @default.
• W2121559221 hasConceptScore W2121559221C202751555 @default.
• W2121559221 hasConceptScore W2121559221C2777658100 @default.
• W2121559221 hasConceptScore W2121559221C2780964509 @default.
• W2121559221 hasConceptScore W2121559221C502942594 @default.
• W2121559221 hasConceptScore W2121559221C55493867 @default.
• W2121559221 hasConceptScore W2121559221C71240020 @default.
• W2121559221 hasConceptScore W2121559221C86803240 @default.
• W2121559221 hasIssue "4" @default.
• W2121559221 hasLocation W21215592211 @default.
• W2121559221 hasOpenAccess W2121559221 @default.
• W2121559221 hasPrimaryLocation W21215592211 @default.
• W2121559221 hasRelatedWork W1012645698 @default.
• W2121559221 hasRelatedWork W1523406979 @default.
• W2121559221 hasRelatedWork W1590154438 @default.
• W2121559221 hasRelatedWork W1879911442 @default.
• W2121559221 hasRelatedWork W1916361835 @default.
• W2121559221 hasRelatedWork W1978302262 @default.
• W2121559221 hasRelatedWork W1982526582 @default.
• W2121559221 hasRelatedWork W1987158405 @default.
• W2121559221 hasRelatedWork W2036254586 @default.
• W2121559221 hasRelatedWork W2076172982 @default.
• W2121559221 hasRelatedWork W2081098417 @default.
• W2121559221 hasRelatedWork W2081703161 @default.
• W2121559221 hasRelatedWork W2087058128 @default.
• W2121559221 hasRelatedWork W2094018033 @default.
• W2121559221 hasRelatedWork W2121563340 @default.
• W2121559221 hasRelatedWork W2223153011 @default.
• W2121559221 hasRelatedWork W2611429311 @default.
• W2121559221 hasRelatedWork W2925309190 @default.
• W2121559221 hasRelatedWork W3092252834 @default.
• W2121559221 hasRelatedWork W3017795043 @default.
• W2121559221 hasVolume "2" @default.
• W2121559221 isParatext "false" @default.
• W2121559221 isRetracted "false" @default.
• W2121559221 magId "2121559221" @default.
• W2121559221 workType "article" @default.