对汽车喷漆工人的基因毒性、氧化应激和免疫参数进行评估。
Evaluation of genotoxicity, oxidative stress and immune parameters of auto-paint workers.
发表日期:2023 Aug 23
作者:
Sultan Pınar Cetintepe, Merve Hazar, Izem Bilinmiş, Sevtap Aydin Dilsiz, Nursen Basaran
来源:
ENVIRONMENTAL RESEARCH
摘要:
汽车工业是一个非常广泛的领域,涵盖了发动机零件、车身、塑料制品的制造以及汽车的组装。由于需要使用许多腐蚀性和刺激性化学品,例如油漆、胶水、酸和碱,所以在生产的不同阶段存在化学风险。本研究的目的是研究土耳其安卡拉地区汽车喷漆工人的遗传毒性、氧化应激和免疫参数。通过碱性彗星实验评估了主要负责汽车喷漆工作的工人的DNA损伤情况,并对一些氧化应激和免疫生物标志物的水平进行了调查。与对照组相比,工人们的淋巴细胞DNA损伤增加,8-羟基-2'-脱氧鸟苷(8-OHdG)和丙二醛(MDA)水平增高,而谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GR)水平降低。研究组间在白细胞介素(IL)-1beta、IL-17、IL-23、Clara细胞分泌蛋白(CC16)、肿瘤坏死因子-alpha(TNF-alpha)、过氧化物酶(CAT)和超氧化物歧化酶(SOD)水平上没有显著差异。结果显示,汽车工业中的职业化学品暴露可能会导致工人因氧化应激而发生DNA损伤。版权所有 © 2023 Elsevier Inc. 发布
The automotive industry is a very wide area from the manufacturing of the pieces of the engine, the body, plastics to the assembly of the car. There is a chemical risk at different stages of production because of the requirement of the use of many corrosive and irritant chemicals such as paints, adhesives, acids, and bases. The aim of the study was to determine the genotoxicity, oxidative stress and immune parameters of automotive paint workers in Ankara, Türkiye. DNA damage of workers mainly responsible from the painting of the automotives were evaluated using the alkaline comet assay and the levels of some oxidative stress and immune biomarkers were also investigated. Increased lymphocyte DNA damage and also higher 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA) levels were observed while decreased glutathione (GSH), glutathione peroxidase (GPx), and glutathione reductase (GR) levels were found in the workers compared to their controls There were no significant differences between the study groups in the levels of interleukin (IL)- 1beta, IL-17, IL-23, Clara cell secretory protein (CC16), tumor necrosis factor-alpha (TNF-alpha), catalase (CAT), and superoxide dismutase (SOD). The results show that occupational exposure to chemicals in automotive industry may cause DNA damage in workers due to oxidative stress.Copyright © 2023. Published by Elsevier Inc.