Kurşuna maruz kalan bireylerde lenfosit DNA hasarının belirlenmesi

Mesleki olarak kursuna maruziyet bir cok saglik sorununa neden olabilir. Kursun bir cok enzimin aktivitesini engelleyebilir ve oksidatif strese neden olabilir, DNA tek zincir kiriklarinin, cift zincir kiriklarinin ve DNA-protein capraz baglarinin sikligini artirabilecegi gibi mikronuklei ve kromozomal aberasyon olusumuna ve DNA hasarina neden olabilir. Genetik hasardaki artis ise insanda kanser olusumuna neden olmaktadir. Bu calismada, kursuna mesleki olarak maruz kalmis bireylerde lenfosit DNA hasari ve kan kursun duzeyleri arasindaki baglanti arastirilmistir. Bu baglantiyi degerlendirebilmek icin kursuna maruz kalmis 61 iscinin lenfositlerindeki DNA hasari izlenmistir. DNA hasar duzeyleri uc komet parametresi (TI, TM ve DNAt)?ne gore degerlendirilmistir. Kan kursun duzeyleri ile TI, TM ve DNAt parametreleri arasinda istatistiksel olarak anlamli pozitif iliski bulunmustur (p<0.01). Sigara kullaniminin DNA hasarinda bagimsiz bir etkisinin oldugu belirlenmistir. DNA hasari parametreleri acisindan sigara kullanan ve kullanmayan bireyler arasinda anlamli bir fark gozlenmistir (p<0.05). Ayrica, sigara kullanan ve kullanmayan bireylerin kursun ve DNA hasari duzeyleri karsilastirildiginda, sigara kullanan bireylerdeki kursun ve DNA hasari duzeyinin sigara kullanmayan bireylere gore anlamli derecede yuksek oldugu bulunmustur (p<0.05). Komet yontemi ile yaptigimiz degerlendirmeye gore elde ettigimiz sonuclar kursuna maruziyetin periferal lenfositlerde tek zincir kiriklari olusturarak genotoksik etkiye neden oldugunu gostermistir.AbstractOccupational exposure to lead can cause many health problems. Lead can inhibit activity of many enzymes, cause oxidative stress, and increase the frequency of DNA single strand breaks, DNA double strand breaks and DNA-protein cross links. Lead can lead to micronuclei and chromosomal aberrations and cause DNA damage. Increased genetic damage causes cancer in humans. The aim of this study was to investigate the association between DNA damage and blood lead levels in individuals occupationally exposed to lead. To evaluate this association, 61 workers exposed to lead were monitored in terms of DNA damage in blood lymphocytes. The levels of DNA damage were measured according to three comet assay parameters, including tail intensity (TI), tail moment (TM) and DNA tail (DNAt). A statistically significant positive correlation was found between the lead levels and TI, TM and DNAt (p<0.01). Smoking had independent effects on DNA damage. Statistically significant difference was observed between smokers and non-smokers in regards to DNA damage parameters (p<0.05). In addition, when the lead and DNA damage levels of smokers and non-smokers were compared, the lead and DNA damage levels in smokers were found to be significantly higher than the levels observed in nonsmoking workers (p<0.05). Our results show that exposure to lead induces genotoxic effects in peripheral lymphocytes by forming single DNA breakages, as measured by comet assays.