Occupational second-hand smoke exposure: A comparative shotgun proteomics study on nasal epithelia from healthy restaurant workers

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Sofia Neves , Solange Pacheco , Fátima Vaz , Peter James , Tânia Simões , Deborah Penque
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引用次数: 0

Abstract

Non-smokers exposed to second-hand smoke (SHS) present risk of developing tobacco smoke-associated pathologies. To investigate the airway molecular response to SHS exposure that could be used in health risk assessment, comparative shotgun proteomics was performed on nasal epithelium from a group of healthy restaurant workers, non-smokers (never and former) exposed and not exposed to SHS in the workplace. HIF1α-glycolytic targets (GAPDH, TPI) and proteins related to xenobiotic metabolism, cell proliferation and differentiation leading to cancer (ADH1C, TUBB4B, EEF2) showed significant modulation in non-smokers exposed. In never smokers exposed, enrichment of glutathione metabolism pathway and EEF2-regulating protein synthesis in genotoxic response were increased, while in former smokers exposed, proteins (LYZ, ATP1A1, SERPINB3) associated with tissue damage/regeneration, apoptosis inhibition and inflammation that may lead to asthma, COPD or cancer, were upregulated. The identified proteins are potential response and susceptibility/risk biomarkers for SHS exposure.

职业性二手烟暴露:对健康餐馆员工鼻腔上皮细胞的散弹枪蛋白质组学比较研究。
接触二手烟(SHS)的非吸烟者有可能患上烟草烟雾相关病症。为了研究气道分子对暴露于 SHS 的反应,以用于健康风险评估,我们对一组健康的餐厅工作人员、暴露于和未暴露于工作场所 SHS 的非吸烟者(从不吸烟和曾经吸烟)的鼻腔上皮细胞进行了霰弹枪蛋白质组学比较研究。在非吸烟者中,HIF1α-糖酵解靶标(GAPDH、TPI)和与异生物代谢、导致癌症的细胞增殖和分化有关的蛋白质(ADH1C、TUBB4B、EEF2)发生了显著变化。在从未接触过烟草的人中,谷胱甘肽代谢途径和 EEF2 调节基因毒性反应中的蛋白质合成的富集增加了,而在接触过烟草的人中,与组织损伤/再生、细胞凋亡抑制和炎症有关的蛋白质(LYZ、ATP1A1、SERPINB3)上调了,这可能会导致哮喘、慢性阻塞性肺病或癌症。这些已确定的蛋白质是暴露于 SHS 的潜在反应和易感性/风险生物标志物。
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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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