Percorrer por autor "Pacheco, Solange A."
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- Discriminative Protein Markers of Second-Hand Smoke Exposure Identified by Shotgun ProteomicsPublication . Neves, Sofia; Pacheco, Solange A.; Vaz, Fátima; Saraiva, Joana; James, Peter; Simões, Tânia; Penque, DeborahObjective: Chronic exposure to second-hand smoke (SHS) increases the risk of developing tobacco-related pathologies such as lung cancer and cardiovascular diseases. This study aimed to identify potential protein biomarkers for response and risk assessment of SHS exposure. Methods: A shotgun proteomics approach was employed to analyse protein expression profiles in nasal epithelium and plasma samples from healthy, non-smoking restaurant workers who were either exposed or not exposed to SHS in the workplace. A label-free quantification strategy was used to measure differential protein expression between the two groups. Logistic regression modelling was applied to identify the proteins that best discriminated exposed individuals from non-exposed controls, with the goal of establishing an expression profile indicative of SHS-related response. Results: In the nasal epithelium, SHS exposure was associated with modulation of proteins involved in HIF1α-regulated glycolytic pathways, xenobiotic metabolism, cell proliferation, and differentiation. In plasma, differentially expressed proteins were related to systemic inflammation and atherosclerosis. Among these, three plasma proteins—Histidine-rich glycoprotein (HRG), Vitamin D-binding protein (GC), and Leucine-rich alpha-2-glycoprotein (LRG1)—showed a significant discriminatory potential between SHS-exposed and non-exposed individuals. Conclusions: The identified proteins, particularly HRG, GC, and LRG1, are promising response biomarkers for SHS exposure. Their expression profiles may support the development of molecular tools for individual response assessment associated with environmental tobacco smoke.
- Effects of occupational exposure to tobacco smoke: is there a link between environmental exposure and disease?Publication . Pacheco, Solange A.; Torres, Vukosava M.; Louro, Henriqueta; Gomes, Filomena; Lopes, Carlos; Marçal, Nelson; Fragoso, Elsa; Martins, Carla; Oliveira, Cátia L.; Hagenfeldt, Manuela; Bugalho-Almeida, António; Penque, Deborah; Simões, TâniaIn a previous study, evidence was provided that indoor secondhand tobacco smoke (SHS) air pollution remains high in Lisbon restaurants where smoking is allowed, regardless of the protective measures used. The aim of this study was to determine in these locations the levels of polycyclic aromatic hydrocarbons (PAH) associated with the particulate phase of SHS (PPAH), a fraction that contains recognized carginogens, such as benzo[a]pyrene (BaP). Data showed that restaurant smoking areas might contain PPAH levels as high as 110 ng/m(3), a value significantly higher than that estimated for nonsmoking areas (30 ng/m(3)) or smoke-free restaurants (22 ng/m(3)). The effective exposure to SHS components in restaurant smoking rooms was confirmed as cotinine levels found in workers' urine. Considering that all workers exhibited normal lung function, eventual molecular changes in blood that might be associated with occupational exposure to SHS and SHS-associated PPAH were investigated by measurement of two oxidative markers, total antioxidant status (TAS) and 8-hydroxyguanosine (8-OHdG) in plasma and serum, respectively. SHS-exposed workers exhibited higher mean levels of serum 8-OHdG than nonexposed workers, regardless of smoking status. By using a proteomics approach based on 2D-DIGE-MS, it was possible to identify nine differentially expressed proteins in the plasma of SHS-exposed nonsmoker workers. Two acute-phase inflammation proteins, ceruloplasmin and inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4), were predominant. These two proteins presented a high number of isoforms modulated by SHS exposure with the high-molecular-weight (high-MW) isoforms decreased in abundance while low-MW isoforms were increased in abundance. Whether these expression profiles are due to (1) a specific proteolytic cleavage, (2) a change on protein stability, or (3) alterations on post-translational modification pattern of these proteins remains to be investigated. Considering that these events seem to precede the first symptoms of tobacco-related diseases, our findings might contribute to elucidation of early SHS-induced pathogenic mechanisms and constitute a useful tool for monitoring the effects of SHS on occupationally exposed individuals such as those working in the hospitality industry.
- Impacto do fumo do cigarro passivo no proteoma humano: em busca de biomarcadores precoces de risco para a saúdePublication . Neves, Sofia; Pacheco, Solange A.; Vaz, Fátima; Valentim-Coelho, Cristina; Saraiva, Joana; James, Peter; Simões, Tânia; Penque, DeborahOs 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.