Ustundag A, Duydu Y
Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Ankara University, Tandoğan, Ankara.
Biol Trace Elem Res. 2009 Apr;128(1):31-7. doi: 10.1007/s12011-008-8254-0. Epub 2008 Nov 1.
Numbers of studies have been carried out on the potential of lead genotoxicity. The mechanisms of lead genotoxicity are not fully known but partly attributed to the formation of highly reactive oxygen metabolites (ROM). However, lead ions have no ability to generate ROM. In this study, we have investigated the ability of lead and ALA to induce excision repairable DNA lesions by using cytosine arabinoside or cytokinesis block micronucleus (ARA-C/CBMN) assay. N-methyl-N-nitrosourea was used as a positive control which is a mutagen and known to induce excision repair. The results of the ARA-C/CBMN assay show that ALA exposures have significantly (p < 0.01) increased the ratio of excision repairable DNA lesions in peripheral blood lymphocytes; however, lead have not. Accordingly, accumulation of ALA should be considered as an effective partner of lead induced DNA damage in lead exposure.
已经开展了许多关于铅遗传毒性潜力的研究。铅遗传毒性的机制尚未完全明确，但部分归因于高活性氧代谢产物（ROM）的形成。然而，铅离子没有产生ROM的能力。在本研究中，我们通过使用阿糖胞苷或胞质分裂阻滞微核（ARA-C/CBMN）试验，研究了铅和ALA诱导可切除修复DNA损伤的能力。N-甲基-N-亚硝基脲用作阳性对照，它是一种诱变剂，已知可诱导切除修复。ARA-C/CBMN试验结果表明，接触ALA显著（p<0.01）增加了外周血淋巴细胞中可切除修复DNA损伤的比例；然而，铅并没有。因此，在铅暴露中，ALA的蓄积应被视为铅诱导DNA损伤的有效协同因素。
