Holme J A, Søderlund J, Låg M, Brunborg G, Dybing E
Department of Environmental Medicine, National Institute of Public Health, Oslo 4, Norway.
Toxicol Appl Pharmacol. 1991 Aug;110(1):118-28. doi: 10.1016/0041-008x(91)90295-p.
The poly(ADP-ribosyl)transferase inhibitor, 3-aminobenzamide (3-ABA), reduced morphological evidence of 1,2-dibromo-3-chloropropane (DBCP)-induced DNA damage determined by alkaline elution. The DBCP plasma, kidney, and testis tissue doses determined between 1 and 8 hr after a single intraperitoneal injection were somewhat higher with than without 3-ABA pretreatment. Furthermore, the amount of DBCP metabolites covalently bound to macromolecules was reduced to about 20-30 percent of control, indicating that 3-ABA may have an effect on the formation/detoxication of reactive DBCP metabolites. Inhibitors of replicative DNA synthesis such as hydroxyurea or stimulation of DNA replication by nephrectomy did not affect the cytotoxicity, neither did inhibitors of DNA repair such as beta-cytosine arabinoside and beta-lapachone.
聚（ADP - 核糖基）转移酶抑制剂3 - 氨基苯甲酰胺（3 - ABA），通过碱性洗脱法降低了1,2 - 二溴 - 3 - 氯丙烷（DBCP）诱导的DNA损伤的形态学证据。单次腹腔注射后1至8小时测定的DBCP血浆、肾脏和睾丸组织剂量，在有3 - ABA预处理的情况下比没有预处理时略高。此外，与大分子共价结合的DBCP代谢物的量减少至对照的约20% - 30%，这表明3 - ABA可能对活性DBCP代谢物的形成/解毒有影响。诸如羟基脲等复制性DNA合成抑制剂或肾切除对DNA复制的刺激均不影响细胞毒性，DNA修复抑制剂如β - 阿糖胞苷和β - 拉帕醌也不影响。
