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Impacto do fumo do cigarro passivo no proteoma humano: em busca de biomarcadores precoces de risco para a saúde
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Advisor(s)
Abstract(s)
Os não-fumadores expostos ao fumo do cigarro passivo ou, simplesmente fumo passivo (FP), apresentam um risco acrescido de desenvolver diversas doenças graves. No entanto, os mecanismos moleculares que explicam estes efeitos continuam pouco esclarecidos, o que reforça a necessidade de identificar biomarcadores capazes de avaliar o risco associado a esta exposição.
Neste estudo, analisámos o proteoma do epitélio nasal e do plasma de indivíduos não-fumadores saudáveis expostos ao FP no local de trabalho, num contexto ainda enquadrado pela Lei n.º 37/2007, utilizando uma abordagem proteómica ‘shotgun’ por espectrometria de massa.
No epitélio nasal, observámos um aumento de proteínas envolvidas em vias centrais do metabolismo energético, como a Gliceraldeído-3-fosfato desidrogenase (GAPDH) e a Triosefosfato isomerase (TPI1), sugerindo uma possível reprogramação metabólica induzida pela exposição. Identificámos também uma diminuição da tubulina beta-4B (TUBB4B), relacionada com a organização do citoesqueleto, e um aumento da proteína anti-apoptótica SERPINB3, apontando para alterações em processos de morte e sobrevivência celular.
No plasma, destacaram-se o aumento da Butirilcolinesterase (BChE) e a diminuição da Proteína de ligação à vitamina D (GC), ambas associadas à resposta a xenobióticos e a processos de lesão tecidular. Foram ainda detetadas alterações em proteínas reguladoras da inflamação sistémica, como C1R, C1QC, HRG e PROS1. A expressão diferencial de APOA4 e SERPINF2 sugere, adicionalmente, a ativação de mecanismos relacionados com risco aterotrombótico.
Em conjunto, estes resultados contribuem para aprofundar a compreensão das vias biológicas que ligam a exposição ao fumo passivo ao risco acrescido de cancro e de doenças cardiovasculares, e apresentam um conjunto promissor de potenciais biomarcadores para avaliação do risco associado à exposição ao FP.
Non-smokers exposed to secondhand smoke (SHS) have an increased risk of developing several serious diseases. However, the molecular mechanisms underlying these effects remain poorly understood, underscoring the need to identify biomarkers capable of assessing the risk associated wi th this exposure. In this study, we analysed the nasal epi thel ial and plasma proteomes of healthy non-smokers exposed to SHS in the workplace, in a context still regulated by Law No. 37/2007, using a shotgun proteomics approach by mass spectrometry. In the nasal epi thel ium, we obser ved an increase in proteins involved in key energy metabol ism pathways, such as Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) and Triosephosphate Isomerase (TPI1), suggesting a possible metabolic reprogramming induced by exposure. We also identified a decrease in beta-tubul in 4B (TUBB4B), related to cytoskeletal organisation, and an increase in the anti-apoptotic protein SERPINB3, indicating alterations in cell death and survival pathways. In plasma, we found an elevation of Butyrylcholinesterase (BChE) and a reduction of Vitamin D-binding Protein (GC), both linked to xenobiotic response and tissue injury processes. We also detected changes in regulators of systemic inflammation, such as C1R, C1QC, HRG, and PROS1. Additionally, the differential expression of APOA4 and SERPINF2 suggests activation of mechanisms related to atherothrombotic risk. Together, these findings deepen our understanding of the biological pathways linking secondhand smoke exposure to the increased risk of cancer and cardiovascular disease, and highlight a promising set of potential biomarkers for assessing SHS- related health risk.
Non-smokers exposed to secondhand smoke (SHS) have an increased risk of developing several serious diseases. However, the molecular mechanisms underlying these effects remain poorly understood, underscoring the need to identify biomarkers capable of assessing the risk associated wi th this exposure. In this study, we analysed the nasal epi thel ial and plasma proteomes of healthy non-smokers exposed to SHS in the workplace, in a context still regulated by Law No. 37/2007, using a shotgun proteomics approach by mass spectrometry. In the nasal epi thel ium, we obser ved an increase in proteins involved in key energy metabol ism pathways, such as Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) and Triosephosphate Isomerase (TPI1), suggesting a possible metabolic reprogramming induced by exposure. We also identified a decrease in beta-tubul in 4B (TUBB4B), related to cytoskeletal organisation, and an increase in the anti-apoptotic protein SERPINB3, indicating alterations in cell death and survival pathways. In plasma, we found an elevation of Butyrylcholinesterase (BChE) and a reduction of Vitamin D-binding Protein (GC), both linked to xenobiotic response and tissue injury processes. We also detected changes in regulators of systemic inflammation, such as C1R, C1QC, HRG, and PROS1. Additionally, the differential expression of APOA4 and SERPINF2 suggests activation of mechanisms related to atherothrombotic risk. Together, these findings deepen our understanding of the biological pathways linking secondhand smoke exposure to the increased risk of cancer and cardiovascular disease, and highlight a promising set of potential biomarkers for assessing SHS- related health risk.
Description
Keywords
Tabaco Fumo Ambiental do Tabaco Exposição Humana Biomarcadores Avaliação do Risco Genotoxicidade Ambiental Determinantes da Saúde e da Doença
Pedagogical Context
Citation
Boletim Epidemiológico Observações. 2025 maio-agosto;14(38): 71-75
Publisher
Instituto Nacional de Saúde Doutor Ricardo Jorge, IP