Dobrakowski M, Pawlas N, Kasperczyk A, Kozłowska A, Olewińska E, Machoń-Grecka A, Kasperczyk S
1 Department of Biochemistry, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Poland.
2 Department of Chemical Hazards and Genetic Toxicology, Institute of Occupational Medicine and Environmental Health in Sosnowiec, Sosnowiec, Poland.
Hum Exp Toxicol. 2017 Jul;36(7):744-754. doi: 10.1177/0960327116665674. Epub 2016 Sep 5.
There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20-35 μg/dL (low exposure to lead (LE) group), a group with a PbB of 35-50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 μg/dL (high exposure to lead (HE) group). The control group consisted of 42 healthy males environmentally exposed to lead (PbB < 10 μg/dL). A comet assay was used to measure the DNA damage in leukocytes. We measured the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) as well as the concentration of malondialdehyde (MDA), and the value of the total antioxidant capacity. The level of PbB was significantly higher in the examined subgroups than in the control group. The percentage of DNA in the tail was significantly higher in the LE, ME, and HE subgroups than in the control group by 10% ( p = 0.001), 15% ( p < 0.001), and 20% ( p < 0.001), respectively. The activity of GR was significantly lower in the LE and ME subgroups than in the control group by 25% ( p = 0.007) and 17% ( p = 0.028), respectively. The activity of G6PD was significantly lower in the ME subgroup by 25% ( p = 0.022), whereas the activity of GST was significantly higher in the HE subgroup by 101% ( p = 0.001) than in the control group. Similarly, the activity of SOD was significantly higher in the LE and ME subgroups by 48% ( p = 0.026) and 34% ( p = 0.002), respectively. The concentration of MDA was significantly higher in the LE, ME, and HE subgroups than in the control group by 43% ( p = 0.016), 57% ( p < 0.001), and 108% ( p < 0.001), respectively. Occupational lead exposure induces DNA damage, including oxidative damage, in human leukocytes. The increase in DNA damage was accompanied by an elevated intensity of oxidative stress.
关于铅的遗传毒性研究结果存在许多差异。本研究的目的是探讨铅诱导的DNA损伤，包括氧化损伤，与人类白细胞中氧化应激强度参数和抗氧化防御系统的关系。研究对象为100名接触铅的男性工人。根据血铅（PbB）水平，他们被分为以下三个亚组：血铅水平为20 - 35μg/dL的一组（低铅暴露（LE）组），血铅水平为35 - 50μg/dL的一组（中等铅暴露（ME）组），以及血铅水平>50μg/dL的一组（高铅暴露（HE）组）。对照组由42名环境暴露于铅（PbB < 10μg/dL）的健康男性组成。采用彗星试验测量白细胞中的DNA损伤。我们测量了超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽还原酶（GR）、葡萄糖-6-磷酸脱氢酶（G6PD）和谷胱甘肽-S-转移酶（GST）的活性，以及丙二醛（MDA）的浓度和总抗氧化能力的值。所检查亚组的血铅水平显著高于对照组。LE、ME和HE亚组中尾部DNA的百分比分别比对照组显著高10%（p = 0.001）、15%（p < 0.001）和20%（p < 0.001）。LE和ME亚组中GR的活性分别比对照组显著低25%（p = 0.007）和17%（p = 0.028）。ME亚组中G6PD的活性显著低25%（p = 0.022），而HE亚组中GST的活性比对照组显著高101%（p = 0.001）。同样，LE和ME亚组中SOD的活性分别显著高48%（p = 0.026）和34%（p = 0.002）。LE、ME和HE亚组中MDA的浓度分别比对照组显著高43%（p = 0.016）、57%（p < 0.001）和108%（p < 0.001）。职业性铅暴露会诱导人类白细胞中的DNA损伤，包括氧化损伤。DNA损伤的增加伴随着氧化应激强度的升高。
