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1.
Life Sci ; 251: 117644, 2020 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-32259604

RESUMO

AIMS: Electronic cigarette (ECIG) has been used as an alternative to tobacco smoking as it lacks the majority of toxicants found in tobacco smoke. However, the effect of ECIG aerosol inhalation on cardiac health are not well studied. The present study aimed to compare the effects of ECIGs with that of combustible tobacco cigarette (T-Cigs) and waterpipe (WP) smoke on cardiac biomarkers of oxidative stress, inflammation, and fibrosis. MAIN METHODS: Rats were randomized into control (fresh air, n = 12), ECIG aerosol (n = 12), T-Cig smoke (n = 15), or WP (n = 13) smoke conditions in which they were exposed 1 h/daily, 6 day/week for 4 weeks. Cardiac biomarkers of oxidative stress, inflammation, and remodeling were assessed. KEY FINDINGS: Relative to control, significant increase in heart to body weight ratio was observed in all exposed groups. Cardiac endothelin-1 and myeloperoxidase were increased for ECIG and T-Cig. Cardiac nitrite and TBARS were increased in all exposed groups, but activity of superoxide dismutase was increased for ECIG and T-Cig only while glutathione levels increased for ECIG only. No changes were observed for cardiac C-reactive protein and catalase activity. Cardiac fibrosis was observed in all exposed groups coupled with an increase in the transforming growth factor beta protein that was significant for ECIG only. SIGNIFICANCE: ECIG aerosol may promote cardiac alterations in similar manner to tobacco smoke by promoting myocardial oxidative stress and inflammation leading to fibrosis. With regard to cardiac health, exposure to ECIG aerosol and combustible T-Cig smoke may lead to similar adverse outcomes.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Inflamação/etiologia , Miocárdio/patologia , Fumaça/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Aerossóis , Animais , Fumar Cigarros/efeitos adversos , Fibrose/etiologia , Inflamação/patologia , Masculino , Estresse Oxidativo , Distribuição Aleatória , Ratos , Ratos Wistar , Vaping/efeitos adversos , Fumar Cachimbo de Água/efeitos adversos
3.
Am J Dent ; 33(2): 83-88, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32259413

RESUMO

PURPOSE: To evaluate the effect of cigarette smoke (CS) on color, roughness and gloss of bulk-fill resin composites. METHODS: Resin discs (10 x 2 mm) were made for resin composites (n= 10) : Filtek Z250XT (control), Filtek One Bulk Fill (FOBF), Tetric N-Ceram Bulk-Fill (TBF) and Aura Bulk-Fill (ABF). The color ( ΔL*, Δa*, Δb*, ΔE and ΔE00), roughness (Ra) and gloss analyses were performed at the baseline and after CS exposure (10 packs of cigarettes - Marlboro Red). The data were analyzed with repeated measures ANOVA and Tukey's test for Ra and gloss; and one-way ANOVA and Tukey's test for ΔL*, Δa*, Δb*, ΔE and ΔE00 ( α= 0.05). RESULTS: For ΔL*, all groups presented reduced luminosity and all bulk-fill resin composites differed statistically from the control (P< 0.05). ABF presented greater variation of ΔL*, differing statistically from all resin composites (P< 0.05). For ΔE and ΔE00, all bulk-fill resin composites showed greater staining, differing statistically from the control, which presented lower values. For Ra, after CS, only ABF presented a decrease, differing statistically from baseline (P< 0.05). After CS smoke, all groups presented gloss increase, statistically different from the baseline (P< 0.05), and when compared among resin composites, no difference was found. CLINICAL SIGNIFICANCE: Bulk-fill resin composites are more prone to staining by cigarette smoke when compared to the conventional microhybrid resin composites.


Assuntos
Resinas Compostas , Fumaça , Cor , Teste de Materiais , Fumar , Propriedades de Superfície , Viscosidade
4.
Med Sci Monit ; 26: e920793, 2020 Mar 23.
Artigo em Inglês | MEDLINE | ID: mdl-32201430

RESUMO

BACKGROUND Chronic obstructive pulmonary disease (COPD), a general airway disease, is featured by progressive and chronic immunoreaction in the lung. Increasing evidences have showed that cigarette smoking is the main reason in the COPD progression, and human pulmonary microvascular endothelial cell (HPMEC) apoptosis often be observed in COPD, while its pathogenesis is not yet fully described. Upregulation of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was observed in COPD patients, but the specific mechanism of lncRNA MEG3 in COPD remains unknown. The objective of this research was to explore the role of lncRNA MEG3 in cigarette smoke extract (CSE)-induced HPMECs. MATERIAL AND METHODS HPMECs were induced by a series of concentrations of CSE (0%, 0.1%, 1%, and 10%). Then cell apoptosis was analyzed by flow cytometry. Cell apoptosis related proteins were tested using western blot assay. Finally, we applied knockdown and over-expression system to explore the lncRNA MEG3 functions in CSE-induced HPMECs. RESULTS Our results indicated that various concentrations of CSE (0%, 0.1%, 1%, and 10%) significantly promoted cell apoptosis, augmented caspase-3 activity, upregulated Bax expression, decreased Bcl-2 expression, and enhanced lncRNA MEG3 level in HPMECs. LncRNA MEG3-plasmid transfection resulted in the upregulation of lncRNA MEG3, more apoptotic HPMECs, and higher caspase-3 activity. While lncRNA MEG3 knockdown presented the opposite effects. Further investigation suggested that all the effects of CSE treatment on HPMECs were markedly reversed by lncRNA MEG3-shRNA (short hairpin RNA). CONCLUSIONS Our study illustrated a protective effect of lncRNA MEG3-shRNA on CSE-induced HPMECs, indicting lncRNA MEG3 can be a new therapeutic approach for COPD treatment.


Assuntos
Doença Pulmonar Obstrutiva Crônica/metabolismo , RNA Longo não Codificante , Transdução de Sinais/fisiologia , Tabaco/efeitos adversos , Apoptose/fisiologia , Células Cultivadas , Células Endoteliais/metabolismo , Regulação da Expressão Gênica , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Fumaça/efeitos adversos
5.
Cell Physiol Biochem ; 54(2): 230-251, 2020 Mar 11.
Artigo em Inglês | MEDLINE | ID: mdl-32153152

RESUMO

BACKGROUND/AIMS: Adverse effects of cigarette smoke on health are widely known. Heating rather than combusting tobacco is one of strategies to reduce the formation of toxicants. The sensitive nature of mitochondrial dynamics makes the mitochondria an early indicator of cellular stress. For this reason, we studied the morphology and dynamics of the mitochondrial network in human bronchial epithelial cells (BEAS-2B) exposed to total particulate matter (TPM) generated from 3R4F reference cigarette smoke and from aerosol from a new candidate modified risk tobacco product, the Tobacco Heating System (THS 2.2). METHODS: Cells were subjected to short (1 week) and chronic (12 weeks) exposure to a low (7.5 µg/mL) concentration of 3R4F TPM and low (7.5 µg/mL), medium (37.5 µg/mL), and high (150 µg/mL) concentrations of TPM from THS 2.2. Confocal microscopy was applied to assess cellular and mitochondrial morphology. Cytosolic Ca2+ levels, mitochondrial membrane potential and mitochondrial mass were measured with appropriate fluorescent probes on laser scanning cytometer. The levels of proteins regulating mitochondrial dynamics and biogenesis were determined by Western blot. RESULTS: In BEAS-2B cells exposed for one week to the low concentration of 3R4F TPM and the high concentration of THS 2.2 TPM we observed clear changes in cell morphology, mitochondrial network fragmentation, altered levels of mitochondrial fusion and fission proteins and decreased biogenesis markers. Also cellular proliferation was slowed down. Upon chronic exposure (12 weeks) many parameters were affected in the opposite way comparing to short exposure. We observed strong increase of NRF2 protein level, reorganization of mitochondrial network and activation of the mitochondrial biogenesis process. CONCLUSION: Comparison of the effects of TPMs from 3R4F and from THS 2.2 revealed, that similar extent of alterations in mitochondrial dynamics and biogenesis is observed at 7.5 µg/mL of 3R4F TPM and 150 µg/mL of THS 2.2 TPM. 7 days exposure to the investigated components of cigarette smoke evoke mitochondrial stress, while upon chronic, 12 weeks exposure the hallmarks of cellular adaptation to the stressor were visible. The results also suggest that mitochondrial stress signaling is involved in the process of cellular adaptation under conditions of chronic stress caused by 3R4F and high concentration of THS 2.2.


Assuntos
Aerossóis/química , Mitocôndrias/metabolismo , Dinâmica Mitocondrial/efeitos dos fármacos , Material Particulado/toxicidade , Cálcio/metabolismo , Linhagem Celular , Corantes Fluorescentes/química , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Microscopia Confocal , Mitocôndrias/efeitos dos fármacos , Material Particulado/química , Fumaça/efeitos adversos , Fatores de Tempo , Produtos do Tabaco/análise
6.
Chemosphere ; 244: 125537, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32050337

RESUMO

Understanding exposure to air pollution during extreme events such as fire emergencies is critical for assessing their potential health impacts. However, air pollution emergencies often affect places without a network of air quality monitoring and characterising exposure retrospectively is methodologically challenging due to the complex behaviour of smoke and other air pollutants. Here we test the potential of roof cavity (attic) dust to act as a robust household-level exposure proxy, using a major air pollution event associated with a coal mine fire in the Latrobe Valley, Australia, as an illustrative study. To assess the relationship between roof cavity dust composition and mine fire exposure, we analysed the elemental and polycyclic aromatic hydrocarbon composition of roof cavity dust (<150µm) from 39 homes along a gradient of exposure to the mine fire plume. These homes were grouped into 12 zones along this exposure gradient: eight zones across Morwell, where mine fire impacts were greatest, and four in other Latrobe Valley towns at increasing distance from the fire. We identified two elements-barium and magnesium-as 'chemical markers' that show a clear and theoretically grounded relationship with the brown coal mine fire plume exposure. This relationship is robust to the influence of plausible confounders and contrasts with other, non-mine fire related elements, which showed distinct and varied distributional patterns. We conclude that targeted components of roof cavity dust can be a useful empirical marker of household exposure to severe air pollution events and their use could support epidemiological studies by providing spatially-resolved exposure estimates post-event.


Assuntos
Poluição do Ar em Ambientes Fechados/estatística & dados numéricos , Poeira/análise , Exposição por Inalação/estatística & dados numéricos , Poluentes Atmosféricos/análise , Austrália , Cidades , Carvão Mineral/análise , Monitoramento Ambiental , Humanos , Mineração , Hidrocarbonetos Policíclicos Aromáticos/análise , Estudos Retrospectivos , Fumaça/análise
7.
PLoS One ; 15(2): e0228919, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32040536

RESUMO

Cigarette smoking and tuberculosis are a significant cause of death worldwide. Several epidemiological studies have demonstrated cigarette smoking is a risk factor for tuberculosis. Electronic cigarettes have recently appeared as a healthier alternative to conventional smoking, although their impact in tuberculosis is not well understood. The aim of this study was to explore the effect of electronic cigarettes in phagocytosis of Mycobacterium tuberculosis and cytokines production. In vitro infection was carried out by exposing THP-1 macrophages to four electronic vapor extracts and the intracellular burden of M. tuberculosis was determined. The percentage of infection was evaluated by confocal microscopy and the cytokine production by Luminex. A reduction of intracellular M. tuberculosis burden in THP-1 macrophages was found after its exposure to electronic vapor extract; the same trend was observed by confocal microscopy when Mycobacterium bovis BCG-GFP strain was used. Electronic cigarettes stimulate a pro-inflammatory cytokine response. We conclude that electronic cigarettes impair the phagocytic function and the cytokine response to M. tuberculosis.


Assuntos
Citocinas/biossíntese , Sistemas Eletrônicos de Liberação de Nicotina , Mycobacterium tuberculosis/patogenicidade , Fagocitose , Fumar/efeitos adversos , Sobrevivência Celular , Humanos , Imunidade Inata , Mediadores da Inflamação/metabolismo , Macrófagos/imunologia , Macrófagos/microbiologia , Macrófagos/patologia , Mycobacterium tuberculosis/crescimento & desenvolvimento , Mycobacterium tuberculosis/imunologia , Fumaça/efeitos adversos , Células THP-1
8.
PLoS One ; 15(2): e0229256, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32084204

RESUMO

Cigarette smoke (CS) contains multiple gaseous and particulate materials that can cause lung inflammation, and smoking is the major cause of chronic obstructive pulmonary disease (COPD). We sought to determine the mechanisms of how CS triggers lung inflammation. Nur77, a nuclear hormone receptor belonging to the immediate-early response gene family, controls inflammatory responses, mainly by suppressing the NF-κB signaling pathway. Because it is unknown if Nur77's anti-inflammatory role modulates COPD, we assessed if and how Nur77 expression and activity are altered in CS-induced airway inflammation. In lung tissues and bronchial epithelial cells from COPD patients, we found Nur77 was downregulated. In a murine model of CS-induced airway inflammation, CS promoted lung inflammation and also reduced Nur77 activity in wild type (WT) mice, whereas lungs of Nur77-deficient mice showed exaggerated CS-induced inflammatory responses. Our findings in in vitro studies of human airway epithelial cells complemented those in vivo data in mice, together showing that CS induced threonine-phosphorylation of Nur77, which is known to interfere with its anti-inflammatory functions. In summary, our findings point to Nur77 as an important regulator of CS-induced inflammatory responses and support the potential benefits of Nur77 activation for COPD treatment.


Assuntos
Regulação para Baixo/efeitos dos fármacos , Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética , Doença Pulmonar Obstrutiva Crônica/genética , Fumaça/efeitos adversos , Tabaco/química , Animais , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Humanos , Inflamação/genética , Pulmão/patologia , Camundongos , Fosforilação/efeitos dos fármacos , Doença Pulmonar Obstrutiva Crônica/patologia , Treonina/metabolismo
9.
Nature ; 578(7794): 224-226, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-32042085
10.
Adv Exp Med Biol ; 1225: 53-69, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32030647

RESUMO

Tobacco smoke is a multicomponent mixture of chemical, organic, and inorganic compounds, as well as additive substances and radioactive materials. Many studies have proved the carcinogenicity of various of these compounds through the induction of DNA adducts, mutational potential, epigenetic changes, gene fusions, and chromosomal events. The tumor microenvironment plays an important role in malignant tumor formation and progression through the regulation of expression of key molecules which mediate the recruitment of immune cells to the tumor site and subsequently regulate tumor growth and metastasis. In this chapter, we discuss the effects of inhaled tobacco smoke in the tumor microenvironment of the respiratory tract. The mechanisms underlying these effects as well as their link with tumor progression are analyzed.


Assuntos
Neoplasias Pulmonares/patologia , Fumaça/efeitos adversos , Tabaco , Microambiente Tumoral/efeitos dos fármacos , Progressão da Doença , Humanos , Tabaco/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos
11.
Arterioscler Thromb Vasc Biol ; 40(2): 335-349, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31941383

RESUMO

OBJECTIVE: Cardiovascular disease is a major public health problem. Among cardiovascular disease's risk factors, tobacco smoking is considered the single most preventable cause of death, with thrombosis being the main mechanism of cardiovascular disease mortality in smokers. While tobacco smoking has been on the decline, the use of waterpipes/hookah has been rising, mainly due to the perception that they are less harmful than regular cigarettes. Strikingly, there are few studies on the negative effects of waterpipes on the cardiovascular system, and none regarding their direct contribution to thrombus formation. Approach and Results: We used a waterpipe whole-body exposure protocol that mimics real-life human exposure scenarios and investigated its effects, relative to clean air, on platelet function, hemostasis, and thrombogenesis. We found that waterpipe smoke (WPS)-exposed mice exhibited both shortened thrombus occlusion and bleeding times. Further, our results show that platelets from WPS-exposed mice are hyperactive, with enhanced agonist-induced aggregation, dense and α-granule secretion, αIIbß3 integrin activation, phosphatidylserine expression, and platelet spreading, when compared with clean air-exposed platelets. Finally, at the molecular level, it was found that Akt (protein kinase B) and ERK (extracellular signal-regulated kinases) phosphorylation are enhanced in the WPS and in nicotine-treated platelets. CONCLUSIONS: Our findings demonstrate that WPS exposure directly modulates hemostasis and increases the risk of thrombosis and that this is mediated, in part, via a state of platelet hyperactivity. The negative health impact of WPS/hookah, therefore, should not be underestimated. Moreover, this study should also help in raising public awareness of the toxic effects of waterpipe/hookah.


Assuntos
Plaquetas/efeitos dos fármacos , Artérias Carótidas/efeitos dos fármacos , Ativação Plaquetária/fisiologia , Cachimbos de Água , Fumar/efeitos adversos , Trombose/metabolismo , Animais , Plaquetas/metabolismo , Artérias Carótidas/patologia , Cotinina/toxicidade , Modelos Animais de Doenças , Citometria de Fluxo , Seguimentos , Immunoblotting , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Nicotina/toxicidade , Contagem de Plaquetas , Fumaça/efeitos adversos , Trombose/induzido quimicamente , Fatores de Tempo
12.
Am J Physiol Heart Circ Physiol ; 318(3): H604-H631, 2020 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-31975625

RESUMO

Smoking cigarettes is harmful to the cardiovascular system. Considerable attention has been paid to the reduced harm potential of alternative nicotine-containing inhalable products such as e-cigarettes. We investigated the effects of E-vapor aerosols or cigarette smoke (CS) on atherosclerosis progression, cardiovascular function, and molecular changes in the heart and aorta of female apolipoprotein E-deficient (ApoE-/-) mice. The mice were exposed to aerosols from three different E-vapor formulations: 1) carrier (propylene glycol and vegetable glycerol), 2) base (carrier and nicotine), or 3) test (base and flavor) or to CS from 3R4F reference cigarettes for up to 6 mo. Concentrations of CS and base or test aerosols were matched at 35 µg nicotine/L. Exposure to CS, compared with sham-exposed fresh air controls, accelerated atherosclerotic plaque formation, whereas no such effect was seen for any of the three E-vapor aerosols. Molecular changes indicated disease mechanisms related to oxidative stress and inflammation in general, plus changes in calcium regulation, and altered cytoskeletal organization and microtubule dynamics in the left ventricle. While ejection fraction, fractional shortening, cardiac output, and isovolumic contraction time remained unchanged following E-vapor aerosols exposure, the nicotine-containing base and test aerosols caused an increase in isovolumic relaxation time similar to CS. A nicotine-related increase in pulse wave velocity and arterial stiffness was also observed, but it was significantly lower for base and test aerosols than for CS. These results demonstrate that in comparison with CS, E-vapor aerosols induce substantially lower biological responses associated with smoking-related cardiovascular diseases.NEW & NOTEWORTHY Analysis of key urinary oxidative stress markers and proinflammatory cytokines showed an absence of oxidative stress and inflammation in the animals exposed to E-vapor aerosols. Conversely, animals exposed to conventional cigarette smoke had high urinary levels of these markers. When compared with conventional cigarette smoke, E-vapor aerosols induced smaller atherosclerotic plaque surface area and volume. Systolic and diastolic cardiac function, as well as endothelial function, were further significantly less affected by electronic cigarette aerosols than conventional cigarette smoke. Molecular analysis demonstrated that E-vapor aerosols induce significantly smaller transcriptomic dysregulation in the heart and aorta compared with conventional cigarette smoke.


Assuntos
Aerossóis/toxicidade , Aterosclerose/etiologia , Doenças Cardiovasculares/etiologia , Vapor do Cigarro Eletrônico/toxicidade , Coração/efeitos dos fármacos , Fumaça/efeitos adversos , Animais , Apolipoproteínas E/genética , Aterosclerose/metabolismo , Aterosclerose/patologia , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/patologia , Progressão da Doença , Feminino , Exposição por Inalação , Camundongos , Camundongos Knockout , Miocárdio/metabolismo , Miocárdio/patologia , Estresse Oxidativo/efeitos dos fármacos
13.
Am J Physiol Heart Circ Physiol ; 318(3): H508-H518, 2020 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-31975626

RESUMO

Cigarette smoking is a major risk factor for aortic aneurysm and dissection; however, no causative link between smoking and these aortic disorders has been proven. In the present study, we investigated the mechanism by which cigarette smoke affects vascular wall cells and found that cigarette smoke extract (CSE) induced a novel form of regulated cell death termed ferroptosis in vascular smooth muscle cells (VSMCs). CSE markedly induced cell death in A7r5 cells and primary rat VSMCs, but not in endothelial cells, which was completely inhibited by specific ferroptosis inhibitors [ferrostatin-1 (Fer-1) and Liproxstatin-1] and an iron chelator (deferoxamine). CSE-induced VSMC death was partially inhibited by a GSH precursor (N-acetyl cysteine) and an NADPH oxidase inhibitor [diphenyleneiodonium chloride (DPI)], but not by inhibitors of pan-caspases (Z-VAD), caspase-1 (Z-YVAD), or necroptosis (necrostatin-1). CSE also upregulated IL-1ß, IL-6, TNF-α, matrix metalloproteinase (MMP)-2, MMP-9, and TIMP-1 (tissue inhibitor of metalloproteinase)in A7r5 cells, which was inhibited by Fer-1. Furthermore, CSE induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. VSMC ferroptosis was induced by acrolein and methyl vinyl ketone, major constituents of CSE. Furthermore, CSE caused medial VSMC loss in ex vivo aortas. Electron microscopy analysis showed mitochondrial damage and fragmentation in medial VSMCs of CSE-treated aortas. All of these manifestations were partially restored by Fer-1. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death and suggest that ferroptosis is a potential therapeutic target for preventing aortic aneurysm and dissection.NEW & NOTEWORTHY Cigarette smoke extract (CSE)-induced cell death in rat vascular smooth muscle cells (VSMCs) was completely inhibited by specific ferroptosis inhibitors and an iron chelator. CSE also induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. CSE caused medial VSMC loss in ex vivo aortas. These findings demonstrate that ferroptosis is responsible for CSE-induced VSMC death.


Assuntos
Ferroptose/efeitos dos fármacos , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Fumaça , Animais , Morte Celular/efeitos dos fármacos , Linhagem Celular , Cicloexilaminas/farmacologia , Desferroxamina/farmacologia , Células Endoteliais/efeitos dos fármacos , Células Endoteliais/metabolismo , Masculino , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Miócitos de Músculo Liso/efeitos dos fármacos , NADPH Oxidases/metabolismo , Fenilenodiaminas/farmacologia , Quinoxalinas/farmacologia , Ratos , Ratos Sprague-Dawley , Sideróforos/farmacologia , Compostos de Espiro/farmacologia , Inibidor Tecidual de Metaloproteinase-1/metabolismo
14.
PLoS One ; 15(1): e0227508, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31935242

RESUMO

Herein, the concentrations of food toxicants, polycyclic aromatic hydrocarbons (PAHs) and heterocyclic aromatic amines (HAAs), in salmon fillets smoke flavored with different smoking wood chips (oak, apple, bourbon soaked oak, cherry and hickory) and barbecuing were determined. Benzo[a]anthracene (up to 0.24 ng/g) and chrysene (0.22 ng/g) were determined in the raw salmon fillets. While ∑PAH8 (benzo[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, dibenzo[a,h]anthracene, benzo[g,h,i]perylene, indeno[1,2,3-cd]pyrene) in the raw samples ranged between 0.44 and 0.46 ng/g, smoke flavoring increased the amount of ∑PAH8 and the amount varied between 0.47 and 0.73 ng/g. Salmon smoked flavored with bourbon soaked oak, cherry and hickory wood chips and barbecued showed significantly (P <0.05) lower contents of ∑PAH4 (benzo[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[a]pyrene) and ∑PAH8 compared to non-smoke flavored barbecued samples. Additionally, smoke flavoring with apple, bourbon soaked oak, and cherry wood chips significantly (P <0.05) reduced the total HAA contents in barbecued salmon. A remarkable result was that the bourbon-soaked oak and cherry wood chips had inhibitory effects on both PAH and HAA contents. In sum, barbecued non-smoke flavored and smoke flavored salmon with different wood chips could be considered safe from the perspective of the detected amounts of PAHs and HAAs in salmon fillets.


Assuntos
Aminas/análise , Aromatizantes/análise , Compostos Heterocíclicos/química , Hidrocarbonetos Policíclicos Aromáticos/análise , Alimentos Marinhos/análise , Animais , Benzo(a)pireno/análise , Cromatografia Líquida de Alta Pressão , Crisenos/análise , Fluorenos/análise , Limite de Detecção , Salmão , Fumaça , Madeira/química
15.
Chemosphere ; 243: 125379, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31995866

RESUMO

Semi-volatile organic compounds (SVOCs) of polycyclic aromatic hydrocarbons (PAHs) and organo-chlorinated pesticides (OCPs) were sampled (24 h, Hi-Vol XAD-2) in dry and wet season, and separately analyzed for particulate and gaseous phases. To reveal the influence of rice straw open burning (RSOB), SVOC levels and profiles were comparatively analyzed between two areas, rice plantation area (KL) with intensive RSOB activities and remote national park (KY), and with fresh RSOB smoke. PAHs were significantly higher in KL than KY in both seasons. PAHs levels in KL during burning season were ∼10 times above the wet season indicating RSOB influence. In KY, however, PAHs levels in wet season were 2 times above dry season suggesting impacts of local emission transport. OCPs levels were not statistically different between 2 seasons and between 2 sites in each season. RSOB smoke contained 5880 ng/m3 of 14 PAHs and 13.5 ng/m3 of 16 OCPs which were respectively 14 and 7 times above those in KL during burning period. The 4-ring compounds, most remarkably fluoranthene, and 5-ring (BbF and BaP) were dominant PAHs species in RSOB smoke. Similarity in PAH profiles and diagnostic ratios between KL dry season and RSOB smoke suggested its strong influence on the local air quality. Elevated OCPs levels in RSOB smoke may be associated with re-emission of the compounds accumulated in the paddy soil during the burning. RSOB in Southeast Asia has a serious implication on exposure to the toxic air pollutants hence should be eliminated with priority.


Assuntos
Agricultura/métodos , Poluentes Atmosféricos/análise , Oryza , Caules de Planta , Compostos Orgânicos Voláteis/análise , Poluição do Ar , Monitoramento Ambiental , Fluorenos , Hidrocarbonetos Clorados/análise , Praguicidas/análise , Hidrocarbonetos Policíclicos Aromáticos/análise , Estações do Ano , Fumaça , Solo , Tailândia
17.
Arch Oral Biol ; 111: 104646, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31896026

RESUMO

OBJECTIVE: This study aimed to investigate the effects of cigarette smoke (extract) on autophagy and apoptosis in oral mucosa epithelial cells. METHODS: The effects of cigarette smoke extract (CSE) on autophagy and apoptosis in oral epithelial cells were studied in vivo and in vitro. Leuk-1 cells were administered cigarette smoke extract or chloroquine (CQ) and rapamycin (RAPA) at different concentrations. Immunoblotting, immunofluorescence, Western blotting and flow cytometry were used to detect autophagy-related protein and apoptosis levels, screen the optimal concentration and stimulation time, and verify the effect of CSE stimulation on autophagy and apoptosis in leuk-1 cells. Meanwhile, autophagy expression in epithelial cells from the local oral tissues of mice who had smoked for 5 months was detected. RESULTS: Under CS stimulation, LC3-II and Beclin-1, the key proteins of leuk-1 autophagy, were upregulated in a concentration- and time-dependent manner. In addition, CS significantly upregulated the expression of Cleaved caspase-3 (C-casp3), a protein involved in apoptosis. However, under stimulation with CQ, autophagy in leuk-1 cells was inhibited and the level of C-casp3 and the apoptosis rate were increased. The autophagy activator RAPA significantly reduced the level of C-casp3 and apoptosis rate in leuk-1 cells. CONCLUSION: The results of this study indicate that CS can simultaneously activate autophagy and apoptosis in mouse and human oral epithelial cells, that autophagy inhibition can aggravate the CSE-triggered apoptosis of oral epithelial cells, and that autophagy induction can inhibit the CSE-triggered apoptosis of oral epithelial cells. Autophagy is suggested to play a protective role in the CSE-induced apoptosis of oral epithelial cells. Further studies are needed to explore the concrete mechanisms underlying the regulatory effects of CS-induced apoptosis and to gain in-depth insight into the complex interactions between apoptosis and autophagy.


Assuntos
Autofagia , Mucosa Bucal , Animais , Apoptose , Células Epiteliais , Humanos , Camundongos , Fumaça , Fumar , Tabaco
18.
Toxicol Lett ; 322: 20-31, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-31923465

RESUMO

Particulate matter (PM) from combustion processes has been associated with oxidative stress to DNA, whereas effects related to telomere dysfunction are less investigated. We collected air-borne PM from a passenger cabin of a diesel-propelled train and at a training facility for smoke diving exercises. Effects on oxidative stress biomarkers, genotoxicity measured by the comet assay and telomere length in PM-exposed A549 cells were compared with the genotoxicity and telomere length in peripheral blood mononuclear cells (PBMCs) from human volunteers exposed to the same aerosol source. Although elevated levels of DNA strand breaks and oxidatively damaged DNA in terms of Fpg-sensitive sites were observed in PBMCs from exposed humans, the PM collected at same locations did not cause genotoxicity in the comet assay in A549 cells. Nevertheless, A549 cells displayed telomere length shortening after four weeks exposure to PM. This is in line with slightly shorter telomere length in PBMCs from exposed humans, although it was not statistically significant. In conclusion, the results indicate that genotoxic potency measured by the comet assay of PM in A549 cells may not predict genotoxicity in exposed humans, whereas telomere length measurements may be a novel indicator of genotoxic stress in cell cultures and humans.


Assuntos
Dano ao DNA , Exposição por Inalação/efeitos adversos , Material Particulado/toxicidade , Fumaça/efeitos adversos , Homeostase do Telômero/efeitos dos fármacos , Emissões de Veículos/toxicidade , Células A549 , Poluentes Ocupacionais do Ar/toxicidade , Sobrevivência Celular/efeitos dos fármacos , Bombeiros , Humanos , Exposição por Inalação/análise , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/patologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Tamanho da Partícula , Homeostase do Telômero/genética
19.
Zhongguo Zhen Jiu ; 40(1): 49-53, 2020 Jan 12.
Artigo em Chinês | MEDLINE | ID: mdl-31930899

RESUMO

OBJECTIVE: To explore the epidemiologic characteristics of acupuncturists who are sensitive to stimulation of moxa smoke, which could provide further direction for safety protection of exerting moxibustion and to further verify the feasibility of internet survey. METHODS: A self-made questionnaire regarding body response to moxa smoke was established, which was used to conduct a face-to-face survey among acupuncturists who had performed long-term moxibustion. The Logistic regression model was used to analyze the factors affecting the stimulation response of acupuncturists and the epidemiological characteristics of acupuncturists was obtained. RESULTS: A total of 733 valid data was obtained. The multivariate Logistic regression analysis showed that the history of chronic respiratory disease was the main risk factor of stimulus response including cough, phlegm in the throat, asthma, dyspnea, shortness of breath and nasal dryness after exposure to moxa smoke (P<0.05, P<0.01). The risk of stimulus response such as cough, tearing and nasal dryness was higher in women than in men (P<0.05, P<0.01). The risk of dry eyes and eyes pain in smokers was higher than those in non-smokers (P<0.05). The risk of shortness of breath in those who were exposed to second-hand smoke was higher than those who were not exposed to second-hand smoke (P<0.05). The analysis of index trend line showed that the results of internet survey were similar to those of face-to-face survey. CONCLUSION: The stimulus response of acupuncturist after long-term exposure to moxa smoke is related to the history of chronic respiratory disease, being female, smoking or exposure of second-hand smoke, therefore more attention should be paid to those populations. In addition, the internet survey can be used for the epidemiological investigation of safety of moxa smoke.


Assuntos
Moxibustão , Fumaça , Tosse , Feminino , Humanos , Masculino , Muco , Inquéritos e Questionários
20.
Fitoterapia ; 140: 104434, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31760067

RESUMO

Fritillaria cirrhosa bulbus is a Chinese folk herb famous for its antitussive, expectorant, anti-asthma and anti-inflammatory properties, and is widely used to treat respiratory diseases. However, the impacts of F. cirrhosa bulbus on oxidative stress are still unkown. In the present study, we investigated the potential effect and mechanism of six isosteroid alkaloids with different chemical structures from F. cirrhosa bulbus on protection against cigarette smoke-induced oxidative stress in RAW264.7 macrophages. The results showed that six isosteroid alkaloids reduced reactive oxygen species (ROS) production, elevated glutathione (GSH) level and promoted heme oxygenase (HO-1) expression, which is in association with induction of NF-E2-related factor 2 (Nrf2) nuclear translocation and up-regulation of Nrf2 expression. Among these alkaloids, verticinone, verticine, imperialine-3-ß-D-glucoside, delavine and peimisine exhibited more potent effect against CSE-induced oxidative stress than that of imperialine. These findings for the first time demonstrated that F. cirrhosa bulbus may play a protective role in cellular oxidative stress by activating Nrf2-mediated antioxidant pathway. Furthermore, the differences in antioxidant effects of these alkaloids were compared, as well as the corresponding structure-activity relationships were preliminarily elucidated. This suggested that F. cirrhosa bulbus might be a promising therapeutic treatment for the prevent of oxidative stress-related diseases.


Assuntos
Alcaloides/farmacologia , Fritillaria/química , Estresse Oxidativo/efeitos dos fármacos , Fumaça/efeitos adversos , Alcaloides/isolamento & purificação , Animais , Glutationa/metabolismo , Heme Oxigenase-1/metabolismo , Proteínas de Membrana/metabolismo , Camundongos , Estrutura Molecular , Fator 2 Relacionado a NF-E2/metabolismo , Compostos Fitoquímicos/isolamento & purificação , Compostos Fitoquímicos/farmacologia , Raízes de Plantas/química , Plantas Medicinais/química , Células RAW 264.7 , Espécies Reativas de Oxigênio/metabolismo , Relação Estrutura-Atividade , Produtos do Tabaco
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