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

被引:0
|
作者
Neves, Sofia [1 ,2 ]
Pacheco, Solange [1 ]
Vaz, Fatima [1 ,2 ]
James, Peter [3 ]
Simoes, Tania [4 ]
Penque, Deborah [1 ,2 ]
机构
[1] Natl Inst Hlth Dr Ricardo Jorge, Human Genet Dept, Lab Prote, ISA IP, Lisbon, Portugal
[2] Univ Nova Lisboa, NOVA Med Sch FCM, Ctr Toxicogen & Human Hlth, ToxOm, Lisbon, Portugal
[3] Lund Univ, Dept Immunotechnol, Prot Technol Lab, Lund, Sweden
[4] Univ Cologne, CECAD Cologne Excellence Aging Res, Cologne, Germany
关键词
Cigarette smoke; Second-Hand Smoke; Protein network; Mass Spectrometry; Nasal epithelium; Proteomics; SQUAMOUS-CELL CARCINOMA; ATPASE ALPHA-1 SUBUNIT; TOBACCO-SMOKE; ANTIGEN; APOPTOSIS; FIBROSIS;
D O I
10.1016/j.etap.2024.104459
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
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. HIF1 alpha- 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.
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页数:14
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