FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1998045763> ?p ?o ?g. }

• W1998045763 endingPage "417" @default.
• W1998045763 startingPage "405" @default.
• W1998045763 abstract "N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) and methyl methanesulfonate (MMS) are directly active alkylating agents that methylate cellular macromolecules by SN1 and SN2 mechanisms, respectively. These two chemicals produce similar types of alkylation products in DNA and a similar level of total alkylations on a molar basis, but strikingly different proportions of alkylations of ring oxygen atoms of purines and pyrimidines. Because of this attribute, they have been used in combination to attempt to determine which types of alkylation products are responsible for mutation, transformation, and toxicity. Studies have suggested that the mutation rates produced by these and similar chemicals in cells surviving toxicity correlate well with the number of methyl adducts at the O6 position of guanine, but that cytotoxicity (reduced colony-forming efficiency) does not correlate with any single adduct or with the total level of alkylation of DNA. In this study we have investigated the cytotoxic mechanisms of MNNG and MMS in synchronized 10T12 cells, using colony-forming ability as a measure of toxicity. Both MNNG and MMS cause dose-dependent reduction in the ability of 10T12 cells to produce colonies of more than 50 cells after 2 weeks in culture. MNNG is about 100-fold more toxic than MMS on a molar basis. As indicated by the inability of cells to exclude trypan blue, MMS kills a fraction of the population of treated 10T12 cells after a 30-min exposure; the fraction of cells that excludes trypan blue is correlated with dose of MMS and with colony-forming efficiency. Neither the fraction of cells that is permeable to trypan blue nor the relative colony-forming efficiency is affected by the phase of the cycle when 10T12 cells are treated with MMS. Furthermore, MMS toxicity for 10T12 cells is not potentiated by caffeine, MMS treatment does not delay progress of S phase, and cells that survive acute membrane toxicity complete the cell cycle without significant delay. In contrast, MNNG treatment produces toxicity that is maximal when 10T12 cells are exposed during the S phase and the effect of potentiated by caffeine. MNNG treatment delays DNA replication and this delay is reversed by caffeine. In sharp contrast to 10T12 cells treated with MMS. MNNG-treated cells are not made permeable to trypan blue, but are blocked in their ability to proliferate. These observations indicate that MNNG and MMS kill 10T12 cells by drastically different mechanisms, MNNG producing toxicity mainly by preventing chromosome replication and MMS producing toxicity mainly by damaging cell membranes." @default.
• W1998045763 created "2016-06-24" @default.
• W1998045763 creator A5008421134 @default.
• W1998045763 creator A5053336377 @default.
• W1998045763 date "1983-11-01" @default.
• W1998045763 modified "2023-09-28" @default.
• W1998045763 title "Cytotoxicity of monofunctional alkylating agents methyl methanesulfonate and methyl-N′-nitro-N-nitrosoguanidine have different mechanisms of toxicity for 10T12 cells" @default.
• W1998045763 cites W1003162216 @default.
• W1998045763 cites W1558355590 @default.
• W1998045763 cites W1591014292 @default.
• W1998045763 cites W1920518078 @default.
• W1998045763 cites W1935311510 @default.
• W1998045763 cites W1981036736 @default.
• W1998045763 cites W1981969682 @default.
• W1998045763 cites W1987701269 @default.
• W1998045763 cites W1989286824 @default.
• W1998045763 cites W1991283458 @default.
• W1998045763 cites W1997195405 @default.
• W1998045763 cites W2008306111 @default.
• W1998045763 cites W2043496776 @default.
• W1998045763 cites W2049320925 @default.
• W1998045763 cites W2054563608 @default.
• W1998045763 cites W2054629944 @default.
• W1998045763 cites W2075484487 @default.
• W1998045763 cites W2093885005 @default.
• W1998045763 cites W2259749878 @default.
• W1998045763 doi "https://doi.org/10.1016/0027-5107(83)90036-2" @default.
• W1998045763 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/6646150" @default.
• W1998045763 hasPublicationYear "1983" @default.
• W1998045763 type Work @default.
• W1998045763 sameAs 1998045763 @default.
• W1998045763 citedByCount "21" @default.
• W1998045763 countsByYear W19980457632012 @default.
• W1998045763 countsByYear W19980457632015 @default.
• W1998045763 countsByYear W19980457632017 @default.
• W1998045763 countsByYear W19980457632019 @default.
• W1998045763 countsByYear W19980457632023 @default.
• W1998045763 crossrefType "journal-article" @default.
• W1998045763 hasAuthorship W1998045763A5008421134 @default.
• W1998045763 hasAuthorship W1998045763A5053336377 @default.
• W1998045763 hasConcept C104317684 @default.
• W1998045763 hasConcept C109316439 @default.
• W1998045763 hasConcept C114246631 @default.
• W1998045763 hasConcept C143425029 @default.
• W1998045763 hasConcept C144024400 @default.
• W1998045763 hasConcept C1491633281 @default.
• W1998045763 hasConcept C149923435 @default.
• W1998045763 hasConcept C153911025 @default.
• W1998045763 hasConcept C161790260 @default.
• W1998045763 hasConcept C164361826 @default.
• W1998045763 hasConcept C178790620 @default.
• W1998045763 hasConcept C185592680 @default.
• W1998045763 hasConcept C202751555 @default.
• W1998045763 hasConcept C2776900477 @default.
• W1998045763 hasConcept C2778301229 @default.
• W1998045763 hasConcept C2778452553 @default.
• W1998045763 hasConcept C2779115727 @default.
• W1998045763 hasConcept C2780070996 @default.
• W1998045763 hasConcept C2780625556 @default.
• W1998045763 hasConcept C2908647359 @default.
• W1998045763 hasConcept C29730261 @default.
• W1998045763 hasConcept C501734568 @default.
• W1998045763 hasConcept C512185932 @default.
• W1998045763 hasConcept C552990157 @default.
• W1998045763 hasConcept C55493867 @default.
• W1998045763 hasConcept C86803240 @default.
• W1998045763 hasConceptScore W1998045763C104317684 @default.
• W1998045763 hasConceptScore W1998045763C109316439 @default.
• W1998045763 hasConceptScore W1998045763C114246631 @default.
• W1998045763 hasConceptScore W1998045763C143425029 @default.
• W1998045763 hasConceptScore W1998045763C144024400 @default.
• W1998045763 hasConceptScore W1998045763C1491633281 @default.
• W1998045763 hasConceptScore W1998045763C149923435 @default.
• W1998045763 hasConceptScore W1998045763C153911025 @default.
• W1998045763 hasConceptScore W1998045763C161790260 @default.
• W1998045763 hasConceptScore W1998045763C164361826 @default.
• W1998045763 hasConceptScore W1998045763C178790620 @default.
• W1998045763 hasConceptScore W1998045763C185592680 @default.
• W1998045763 hasConceptScore W1998045763C202751555 @default.
• W1998045763 hasConceptScore W1998045763C2776900477 @default.
• W1998045763 hasConceptScore W1998045763C2778301229 @default.
• W1998045763 hasConceptScore W1998045763C2778452553 @default.
• W1998045763 hasConceptScore W1998045763C2779115727 @default.
• W1998045763 hasConceptScore W1998045763C2780070996 @default.
• W1998045763 hasConceptScore W1998045763C2780625556 @default.
• W1998045763 hasConceptScore W1998045763C2908647359 @default.
• W1998045763 hasConceptScore W1998045763C29730261 @default.
• W1998045763 hasConceptScore W1998045763C501734568 @default.
• W1998045763 hasConceptScore W1998045763C512185932 @default.
• W1998045763 hasConceptScore W1998045763C552990157 @default.
• W1998045763 hasConceptScore W1998045763C55493867 @default.
• W1998045763 hasConceptScore W1998045763C86803240 @default.
• W1998045763 hasIssue "3" @default.
• W1998045763 hasLocation W19980457631 @default.
• W1998045763 hasLocation W19980457632 @default.
• W1998045763 hasOpenAccess W1998045763 @default.
• W1998045763 hasPrimaryLocation W19980457631 @default.
• W1998045763 hasRelatedWork W1968394537 @default.

• next