{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T17:28:01Z","timestamp":1764782881681},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,2,4]],"date-time":"2005-02-04T00:00:00Z","timestamp":1107475200000},"content-version":"vor","delay-in-days":7461,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[1984,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>3\u2010Aminobenzamide (3\u2010AB), an inhibitor of poly(ADP\u2010ribosylation), is lethal to human fibroblasts with damaged DNA. Its cytotoxicity was determined relative to a number of factors including the types of lesions, the kinetics of repair, and the availability of alternative repair systems. A variety of alkylating agents, UV or gamma irradiation, or antimetabolites were used to create DNA lesions. 3\u2010AB enhanced lethality with monofunctional alkylating agents only. Within this class of compounds, methylmethanesulfonate (MMS) treatments made cells more sensitive to 3\u2010AB than did treatment with methylnitrosourea (MNU) or methylnitronitrosoguanidine (MNNG). 3\u2010AB interfered with a dynamic repair process lasting several days, since human fibroblasts remained sensitive to 3\u2010AB for 36\u201348 hours following MMS treatment. During this same interval, 3\u2010AB caused these cells to arrest in G<jats:sub>2<\/jats:sub> phase. Alkaline elution analysis also revealed that this slow repair was delayed further by 3\u2010AB. Human mutant cells defective in DNA repair differed in their responses to 3\u2010AB. Among mutants sensitive to monofunctional alkylating agents, ataxia telangiectasia cells were slightly more sensitive to 3\u2010AB than control cells, while Huntington's disease cells had a near\u2010normal response. Among UV\u2010sensitive strains, xeroderma pigmentosum variant (XPV) cells were more sensitive to 3\u2010AB after MMS than were XP complementation group A (A) cells, which responded normally. Greater lethality with 3\u2010AB could be dependent on inability of the mutant cells to repair damage by other processes.<\/jats:p>","DOI":"10.1002\/jcp.1041200312","type":"journal-article","created":{"date-parts":[[2005,2,26]],"date-time":"2005-02-26T14:16:18Z","timestamp":1109427378000},"page":"335-344","source":"Crossref","is-referenced-by-count":14,"title":["Factors modifying 3\u2010aminobenzamide cytotoxicity in normal and repair\u2010deficient human fibroblasts"],"prefix":"10.1002","volume":"120","author":[{"given":"Robert J.","family":"Boorstein","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arthur B.","family":"Pardee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,2,4]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"crossref","first-page":"10502","DOI":"10.1016\/S0021-9258(19)70491-8","article-title":"Poly (ADP\u2010ribose) synthesis in vitro programmed by damaged DNA. 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