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1.
Int J Mol Sci ; 22(11)2021 Jun 02.
Artigo em Inglês | MEDLINE | ID: mdl-34199457

RESUMO

Polycyclic aromatic hydrocarbons (PAHs) are chemical compounds comprised of carbon and hydrogen molecules in a cyclic arrangement. PAHs are associated with risks to human health, especially carcinogenesis. One form of exposure to these compounds is through ingestion of contaminated food, which can occur during preparation and processing involving high temperatures (e.g., grilling, smoking, toasting, roasting, and frying) as well as through PAHs present in the soil, air, and water (i.e., environmental pollution). Differently from changes caused by microbiological characteristics and lipid oxidation, consumers cannot sensorially perceive PAH contamination in food products, thereby hindering their ability to reject these foods. Herein, the occurrence and biological effects of PAHs were comprehensively explored, as well as analytical methods to monitor their levels, legislations, and strategies to reduce their generation in food products. This review updates the current knowledge and addresses recent regulation changes concerning the widespread PAHs contamination in several types of food, often surpassing the concentration limits deemed acceptable by current legislations. Therefore, effective measures involving different food processing strategies are needed to prevent and reduce PAHs contamination, thereby decreasing human exposure and detrimental health effects. Furthermore, gaps in literature have been addressed to provide a basis for future studies.


Assuntos
Carcinogênese/efeitos dos fármacos , Poluição Ambiental/efeitos adversos , Alimentos/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Benzopirenos/efeitos adversos , Carcinogênese/genética , Carvão Vegetal/efeitos adversos , Culinária , Adutos de DNA/efeitos adversos , Análise de Alimentos , Manipulação de Alimentos , Humanos
2.
Mol Cell Biochem ; 474(1-2): 27-39, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32715408

RESUMO

Epidemiological studies have exhibited a strong correlation between exposure to air pollution and deaths due to vascular diseases such as atherosclerosis. Benzo-a-pyrene-1,6-quinone (BP-1,6-Q) is one of the components of air pollution. This study was to examine the role of GSH in BP-1,6-Q mediated cytotoxicity in human EA.hy96 endothelial cells and demonstrated that induction of cellular glutathione by a potent triterpenoid, CDDO-Im (1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole), protects cells against BP-1,6-Q induced protein and lipid damage. Incubation of EA.hy926 endothelial cells with BP-1,6-Q caused a significant increase in dose-dependent cytotoxicity as measured by LDH release assay and both apoptotic and necrotic cell deaths as measured by flow cytometric analysis. Incubation of EA.hy926 endothelial cells with BP-1,6-Q also caused a significant decrease in cellular GSH levels. The diminishment of cellular GSH by buthionine sulfoximine (BSO) potentiated BP-1,6-Q-induced toxicity significantly suggesting a critical involvement of GSH in BP-1,6-Q induced cellular toxicity. GSH-induction by CDDO-Im significantly protects cells against BP-1,6-Q induced protein and lipid damage as measured by protein carbonyl (PC) assay and thiobarbituric acid reactive substances (TBARS) assay, respectively. However, the co-treatment of cells with CDDO-Im and BSO reversed the cytoprotective effect of CDDO-Im on BP-1,6-Q-mediated lipid peroxidation and protein oxidation. These results suggest that induction of GSH by CDDO-Im might be the important cellular defense against BP-1,6-Q induced protein and lipid damage. These findings would contribute to better understand the action of BP-1,6-Q and may help to develop novel therapies to protect against BP-1,6-Q-induced atherogenesis.


Assuntos
Apoptose , Benzopirenos/efeitos adversos , Citoproteção , Endotélio Vascular/efeitos dos fármacos , Glutationa/metabolismo , Imidazóis/farmacologia , Ácido Oleanólico/análogos & derivados , Substâncias Protetoras/farmacologia , Células Cultivadas , Endotélio Vascular/metabolismo , Endotélio Vascular/patologia , Humanos , Peroxidação de Lipídeos , Necrose , Ácido Oleanólico/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
3.
Anal Chem ; 92(10): 7200-7208, 2020 05 19.
Artigo em Inglês | MEDLINE | ID: mdl-32233451

RESUMO

The health impact of environmental pollution involving an increase in human diseases has been subject to extensive study in recent decades. The methodology in biomimetic investigation of these pathophysiologic events is still in progress to uncover the gaps in knowledge associated with pollution and its influences on health. Herein, we describe a comprehensive evaluation of environmental pollutant-caused lung inflammation and injury using a microfluidic pulmonary alveolus platform with alveolar-capillary interfaces. We performed a microfluidic three-dimensional coculture with physiological microenvironment simulation at microscale control and demonstrated a reliable reconstruction of tissue layers including alveolar epithelium and microvascular endothelium with typical mechanical, structural, and junctional integrity, as well as viability. On-chip detection and analysis of pulmonary alveolus responses focusing on various inflammatory and injurious dynamics to the respective pollutant stimulations were achieved in the coculture-based microfluidic pulmonary alveolus model, in comparison with common on-chip monoculture and off-chip culture tools. We confirmed the synergistic effects of the epithelial and endothelial interfaces on the stimuli resistance and verified the importance of creating complex tissue microenvironments in vitro to explore pollution-involved human pathology. We believe the microfluidic approach presents great promise in environmental monitoring, drug discovery, and tissue engineering.


Assuntos
Benzopirenos/efeitos adversos , Poluentes Ambientais/efeitos adversos , Técnicas Analíticas Microfluídicas , Nicotina/efeitos adversos , Pneumonia/induzido quimicamente , Alvéolos Pulmonares/efeitos dos fármacos , Benzopirenos/química , Células Cultivadas , Técnicas de Cocultura , Citocinas/análise , Citocinas/metabolismo , Poluentes Ambientais/química , Humanos , Microscopia Confocal , Estrutura Molecular , Nicotina/química , Pneumonia/metabolismo , Pneumonia/patologia , Alvéolos Pulmonares/metabolismo , Alvéolos Pulmonares/patologia , Espécies Reativas de Oxigênio/metabolismo
4.
Asian Pac J Cancer Prev ; 21(2): 295-300, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-32102502

RESUMO

OBJECTIVE: Silica and Benzo(a)pyrene are listed as carcinogens. This study aims to explore Cyclin D1, CDK4 and difference of cell cycle adjusted by MAPK signal transduction pathway in silica and B(a)P-induced malignant transformation of human embryonic lung fibroblasts. METHODS: Activity of the subfamily (ERK, p38 and JNK) of mitogen-activated protein kinase (MAPK), cyclin D1 and CDK4 (cyclin dependent kinase) were evaluated using Human embryonic lung fibroblast (HELF) purchased from the cell room, basic research institute, Chinese Academy of Medical Sciences. The expression of cyclin D1 and CDK4 (cyclin dependent kinase) were measured in silica and B(a)P induced malignant using Western blot (WB) assay. RESULT: P-ERK and P-JNK expression increased significantly (P<0.01), while CDK4 and P-p38 expression decreased (P<0.01, P<0.05) in silica-induced malignant transformation cells compared with the control group. P-ERK, P-JNK and Cyclin D1 expression increased (P<0.01, P<0.01, P<0.05) in B(a)P-induced group compared with the control group. P-ERK and P-JNK expression decreased (P<0.01), while P-p38, Cyclin D1 and CDK4 expression increased (P<0.05, P<0.05, P<0.01) in B(a)P-induced group compared with the silica-induced group. CONCLUSION: MAPK and cyclin D1/CDK4 activation expressed differently in human embryo lung fibroblasts malignant transformation induced by silica and benzopyrene.


Assuntos
Benzopirenos/efeitos adversos , Transformação Celular Neoplásica/patologia , Ciclina D1/metabolismo , Quinase 4 Dependente de Ciclina/metabolismo , Fibroblastos/patologia , Pulmão/patologia , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Dióxido de Silício/efeitos adversos , Ciclo Celular , Transformação Celular Neoplásica/efeitos dos fármacos , Transformação Celular Neoplásica/metabolismo , Células Cultivadas , Ciclina D1/genética , Quinase 4 Dependente de Ciclina/genética , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Humanos , Pulmão/efeitos dos fármacos , Pulmão/embriologia , Pulmão/metabolismo , Proteínas Quinases Ativadas por Mitógeno/genética , Transdução de Sinais
5.
Int J Mol Sci ; 20(3)2019 Jan 26.
Artigo em Inglês | MEDLINE | ID: mdl-30691106

RESUMO

Pollution-induced skin damage results in oxidative stress; cellular toxicity; inflammation; and, ultimately, premature skin aging. Previous studies suggest that the activation of autophagy can protect oxidation-induced cellular damage and aging-like changes in skin. In order to develop new anti-pollution ingredients, this study screened various kinds of natural extracts to measure their autophagy activation efficacy in cultured dermal fibroblast. The stimulation of autophagy flux by the selected extracts was further confirmed both by the expression of proteins associated with the autophagy signals and by electron microscope. Crepidiastrum denticulatum (CD) extract treated cells showed the highest autophagic vacuole formation in the non-cytotoxic range. The phosphorylation of adenosine monophosphate kinase (AMPK), but not the inhibition of mammalian target of rapamycin (mTOR), was observed by CD-extract treatment. Its anti-pollution effects were further evaluated with model compounds, benzo[a]pyrene (BaP) and cadmium chloride (CdCl2), and a CD extract treatment resulted in both the protection of cytotoxicity and a reduction of proinflammatory cytokines. These results suggest that the autophagy activators can be a new protection regimen for anti-pollution. Therefore, CD extract can be used for anti-inflammatory and anti-pollution cosmetic ingredients.


Assuntos
Asteraceae/química , Poluentes Ambientais/efeitos adversos , Células Epidérmicas/citologia , Extratos Vegetais/farmacologia , Proteínas Quinases Ativadas por AMP/metabolismo , Autofagia , Benzopirenos/efeitos adversos , Cloreto de Cádmio/efeitos adversos , Células Cultivadas , Citocinas/metabolismo , Células Epidérmicas/efeitos dos fármacos , Células Epidérmicas/metabolismo , Fibroblastos/citologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Microscopia Eletrônica de Transmissão , Estresse Oxidativo/efeitos dos fármacos , Fosforilação , Extratos Vegetais/química , Serina-Treonina Quinases TOR/metabolismo
6.
Lymphat Res Biol ; 15(4): 317-323, 2017 12.
Artigo em Inglês | MEDLINE | ID: mdl-29087786

RESUMO

INTRODUCTION: Benzopyrones are plant-derived chemicals which have an evidenced degree of clinical efficacy in lymphedema management indicated in past trials. Unfortunately, in some of these cases idiosyncratic hepatotoxicity have been documented in a minority of patients. This review aims to tackle the problem of benzopyrone (particularly coumarin) toxicity by considering their metabolic pathways and identifying relevant alleles needed to take a targeted pharmacogenetic approach in its future use. METHODS AND RESULTS: The nontoxic 7-hydroxylation and the toxic heterocyclic "ring-splitting" epoxidation pathways are the two main detoxification pathways in the hepatometabolism of coumarin, the former catalyzed by CYP2A6 and the latter by possibly CYP1A and CYP2E. Acetaldehyde dehydrogenase (ALDH) clears toxic aldehyde intermediates. CYP2A6 polymorphism screening methods, including genotyping, by real-time polymerase chain reaction and chromatography-mass spectroscopy functional metabolite assays; efficiency of these techniques are continually improving. ALDH polymorphisms have also been implicated, with clinically viable screening tests, rapid genotyping, and sensitive questionnaires already available for ALDH2*1/ALDH2*2. Dysfunctional polymorphisms of the above genes and others are significantly more prevalent in Eastern Asian populations, uncommon in Caucasian populations. The role of other enzymes/genes in the pathway is yet to be clarified. CONCLUSION: Although screening techniques are becoming increasingly clinically feasible, uncertainty remains on the link between the genotype, metabolic phenotype, and the exact gene products involved. These must be elucidated further before a targeted pharmacogenomic approach is fully viable. In the meantime, treatment should be avoided in those with vulnerable familial and ethnic descents if used.


Assuntos
Benzopirenos/efeitos adversos , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/genética , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/prevenção & controle , Regulação Enzimológica da Expressão Gênica , Linfedema/tratamento farmacológico , Linfedema/genética , Farmacogenética , Variantes Farmacogenômicos , Aldeído-Desidrogenase Mitocondrial/genética , Aldeído-Desidrogenase Mitocondrial/metabolismo , Benzopirenos/uso terapêutico , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Cumarínicos/metabolismo , Citocromo P-450 CYP2A6/genética , Humanos , Inativação Metabólica/genética , Linfedema/metabolismo , Resultado do Tratamento
7.
J Toxicol Sci ; 40(3): 365-73, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-25971159

RESUMO

Toxic and harmful factors co-exist in the environment; these factors often interact to induce combined toxicity, which is the main focus of toxicological research. Furthermore, a large number of studies have shown that aluminum (Al) and benzo[a]pyrene (BaP) are neurotoxic and target the central nervous system to cause neuronal apoptosis. Because we are exposed to both Al and BaP in the air, water, food, and even medicine, the combined effects of these agents in humans must be examined. The present study examines the ability of Al and BaP co-exposure to intensify neuronal apoptosis. The primary neurons of newborn rats were cultured for 5 days, and cells from the same batch that were growing well were selected and assigned to the blank control group, the solvent control group (DMSO+S9+maltol), BaP groups (10, 40 µmol/L), Al (mal)3 groups (50, 100, 400 µmol/L) and co-exposure groups with different combinations of BaP and Al (mal)3. The cell viabilities indicated that 10 µM BaP or 50 µM Al (mal)3 was mildly toxic, and we selected 10 µM BaP+50 µM Al (mal)3 for subsequent co-exposure experiments. The morphological characteristics of cell apoptosis were much more obvious in the co-exposure group than in the Al-exposed cells or the BaP-exposed cells, as observed with a transmission electron microscope and a fluorescence inverted microscope. The apoptotic rates and caspase-3 activity quantitatively significantly differed between the co-exposure and Al-exposure groups, while the BaP-exposure group did not significantly differ from the control group. These results indicate that Al and BaP co-exposure exert synergistic effects on neuronal cell apoptosis.


Assuntos
Compostos de Alumínio/efeitos adversos , Apoptose/efeitos dos fármacos , Benzopirenos/efeitos adversos , Poluentes Ambientais/efeitos adversos , Neurônios/efeitos dos fármacos , Neurônios/patologia , Animais , Caspase 3/metabolismo , Células Cultivadas , Sinergismo Farmacológico , Microscopia Eletrônica de Transmissão , Microscopia de Fluorescência , Neurônios/enzimologia , Neurônios/ultraestrutura , Ratos Sprague-Dawley
8.
PLoS One ; 9(7): e102570, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25032692

RESUMO

Biomathematical modeling has become an important tool to assess xenobiotic exposure in humans. In the present study, we have used a human physiologically-based pharmacokinetic (PBPK) model and an simple compartmental toxicokinetic model of benzo(a)pyrene (BaP) kinetics and its 3-hydroxybenzo(a)pyrene (3-OHBaP) metabolite to reproduce the time-course of this biomarker of exposure in the urine of industrially exposed workers and in turn predict the most plausible exposure scenarios. The models were constructed from in vivo experimental data in rats and then extrapolated from animals to humans after assessing and adjusting the most sensitive model parameters as well as species specific physiological parameters. Repeated urinary voids from workers exposed to polycyclic aromatic hydrocarbons (PAHs) have been collected over the course of a typical workweek and during subsequent days off work; urinary concentrations of 3-OHBaP were then determined. Based on the information obtained for each worker (BaP air concentration, daily shift hours, tasks, protective equipment), the time courses of 3-OHBaP in the urine of the different workers have been simulated using the PBPK and toxicokinetic models, considering the various possible exposure routes, oral, dermal and inhalation. Both models were equally able to closely reproduce the observed time course of 3-OHBaP in the urine of workers and predicted similar exposure scenarios. Simulations of various scenarios suggest that the workers under study were exposed mainly by the dermal route. Comparison of measured air concentration levels of BaP with simulated values needed to obtain a good approximation of observed time course further pointed out that inhalation was not the main route of exposure for most of the studied workers. Both kinetic models appear as a useful tool to interpret biomonitoring data of PAH exposure on the basis of 3-OHBaP levels.


Assuntos
Benzo(a)pireno/farmacocinética , Benzopirenos/farmacocinética , Exposição Ocupacional/análise , Hidrocarbonetos Policíclicos Aromáticos/farmacocinética , Hidrocarbonetos Policíclicos Aromáticos/urina , Animais , Benzo(a)pireno/efeitos adversos , Benzopirenos/efeitos adversos , Monitoramento Ambiental , Humanos , Modelos Teóricos , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Ratos
9.
J Toxicol Sci ; 38(4): 629-42, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23892563

RESUMO

Deltamethrin, a pyrethroid insecticide, used extensively for pest control has been reported to cause adverse health effects including carcinogenic/toxic effects in animals but the underlying mechanism remains elusive. In the present study, we investigated the effect of deltamethrin after short exposure on early protein expression changes involved in neoplastic transformation in mouse skin, validated the results in human keratinocyte HaCaT cells and thereby explore the possible underlying mechanism. Deltamethrin (4 mg/kg b.wt) and benzo[a]pyrene (B[a]P, 0.05 mg/kg b.wt) were topically applied on Swiss albino mice, respectively. The comparative protein expression profiles with vehicle control were generated by 2-dimensional gel electrophoresis (2-DE) and mass spectrometry. 2-DE maps of deltamethrin and B[a]P treated mouse skin showed 20 and 24 significant (2 fold change, p < 0.05) differentially expressed protein spots, against vehicle controls. However, comparison between them showed relatively similar expression level of 20 spots. Among them, 5 proteins (carbonic anhydrase III, peroxiredoxin-2, calcyclin, superoxide dismutase [Cu-Zn], ubiquitin) are of particular significance as these are involved in cancer-related key processes. Deregulation of these was confirmed at protein and mRNA levels by immunoblotting and RT-PCR in mouse skin and HaCaT cells. Therefore, we conclude that these preliminarily identified proteins might be responsible for the neoplastic transformation of mouse skin epidermal cells and HaCaT cells by deltamethrin. This study proposes complementary mechanism where inhibition of proteasome activator protein (PA200) is responsible for accumulation of ubiquitinated-calcyclin, regulates deltamethrin-induced neoplastic changes in mouse skin and HaCaT cells.


Assuntos
Transformação Celular Neoplásica/induzido quimicamente , Transformação Celular Neoplásica/genética , Epiderme/patologia , Inseticidas/efeitos adversos , Nitrilas/efeitos adversos , Proteoma/metabolismo , Piretrinas/efeitos adversos , Administração Tópica , Animais , Benzopirenos/administração & dosagem , Benzopirenos/efeitos adversos , Eletroforese em Gel Bidimensional , Células Epidérmicas , Epiderme/metabolismo , Humanos , Inseticidas/administração & dosagem , Masculino , Espectrometria de Massas , Camundongos , Nitrilas/administração & dosagem , Proteínas Nucleares/antagonistas & inibidores , Proteínas Nucleares/fisiologia , Piretrinas/administração & dosagem
11.
Invest Ophthalmol Vis Sci ; 49(11): 5111-7, 2008 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-18586875

RESUMO

PURPOSE: To better understand the cellular and molecular basis for the epidemiologic association between cigarette smoke and age-related macular degeneration (AMD), the authors examined the effects of Benzo(e)Pyrene (B(e)P), a toxic element in cigarette smoke, on human retinal pigment epithelial cells (ARPE-19). METHODS: ARPE-19 cells were cultured in Dulbecco modified Eagle medium containing 10% fetal bovine serum. Cells were treated for 24 hours with 1000 microM, 400 microM, 200 microM, and 100 microM B(e)P. Cell viability was determined by a trypan blue dye-exclusion assay. Activities of caspase-3/7, caspase-8, caspase-9, and caspase-12 were measured by a fluorescence image scanner, and DNA laddering was evaluated by electrophoresis on 3% agarose gel. RESULTS: The mean percentage of cell viabilities of ARPE-19 cells was decreased in a dose-dependent manner after exposure to B(e)P at the higher concentrations of 1000 microM (20.0 +/- 0.4; P < 0.001), 400 microM (35.6 +/- 6.4; P < 0.001), and 200 microM (58.7 +/- 2.3; P < 0.001) but not at 100 microM (95.9 +/- 0.7; P > 0.05) compared with the equivalent dimethyl sulfoxide (DMSO)-treated control cultures. There were significant increases in caspase-3/7, -8, -9, and -12 activities compared with the DMSO-treated controls (P < 0.001). DNA laddering revealed bands at 200-bp intervals. CONCLUSIONS: These results show that B(e)P is a toxicant to human retinal pigment epithelial cells in vitro. It causes cell death and induces apoptosis by the involvement of multiple caspase pathways.


Assuntos
Benzopirenos/efeitos adversos , Fragmentação do DNA , Epitélio Pigmentado Ocular/efeitos dos fármacos , Poluição por Fumaça de Tabaco/análise , Apoptose , Caspases/metabolismo , Sobrevivência Celular , Células Cultivadas , DNA/efeitos dos fármacos , Eletroforese em Gel de Ágar , Humanos , Degeneração Macular/etiologia , Degeneração Macular/genética , Degeneração Macular/patologia , Epitélio Pigmentado Ocular/patologia , Fatores de Risco
12.
Gig Sanit ; (3): 6-8, 2008.
Artigo em Russo | MEDLINE | ID: mdl-18590139

RESUMO

The content of benzpyrene was studied in the ambient air of the mixed, residential, and industrial zones of Tashkent. There was no excess of the maximum allowable concentrations (MAC) of this substance in the ambient air of mixed and residential zones. There were 1.5-2-fold excesses in the MAC of benzpyrene in the places where apartment houses were contiguous with industrial enterprises and highways and 2.5-3-fold excesses in the ambient air of an industrial zone.


Assuntos
Benzopirenos/efeitos adversos , Poluição Ambiental/estatística & dados numéricos , Urbanização , Área Programática de Saúde , Humanos , Uzbequistão/epidemiologia
16.
Gig Sanit ; (2): 27-8, 2002.
Artigo em Russo | MEDLINE | ID: mdl-12077976

RESUMO

The researchers of the Republican Cancer Research Center of the Ministry of Health of the Republic of Uzbekistan have been monitoring the levels of the carcinogenic agent benz(a)pyrene (B(a)P) in the emissions by thermoelectric plants. Measuring has indicated that the effluent levels of B(a)P are related to the type of fuel put in the boilers and to the parameters of their use. The burning of gas in the furnaces results in air emissions of B(a)P at concentrations of as high as 50 ng/m3 and that of coal does as high as 300 ng/m3. Addition of fuel oil to coal or gas burning elevates the levels of B(a)P up to 450 and 180 ng/m3, respectively. Greater oxygen feed in the furnaces of boilers and their use at the maximum capacities (loads) cause a decrease in B(a)P in the waste gases. Recommendations on the optimum regimens of exploitation factors are given to lower environmental B(a)P levels, which must in turn reduce the incidence of cancer diseases.


Assuntos
Benzopirenos/efeitos adversos , Poluentes Ambientais/efeitos adversos , Centrais Elétricas/instrumentação , Emissões de Veículos/efeitos adversos , Humanos
19.
Rev. med. Tucumán ; 7(2): 91-101, abr.-jun. 2001. tab, graf
Artigo em Espanhol | BINACIS | ID: bin-8038

RESUMO

Se realizó un estudio en la ciudad capital de Tucumán, para establecer los niveles de contaminación del aire causados por la quema de neumáticos en la vía pública. Para ello se utilizaron dispositivos de toma de muestras y métodos analíticos normalizados para determinar los valores de concentración alcanzados por los contaminantes. Al seleccionar las sustancias investigadas en el aire se tuvo en cuenta la composición del caucho, los aditivos utilizados en la fabricación de gomas y los residuos gaseosos que se emiten durante una combustión incompleta de materiales orgánicos de elevado peso molecular. Se determinó el radio de influencia de la polución causada por estos episodios, el impacto ambiental y los posibles efectos adversos que pueden producirse a corto y largo plazo sobre la salud de las personas expuestas. Los resultados y las conclusiones del presente trabajo constituyen un precedente técnico para que las autoridades sanitarias puedan adoptar decisiones de carácter reglamentario y legal, para proceder en el caso de propagarse esta mala práctica. También permite ilustrar a la comunidad médica sobre los riesgos de aparición de ciertas enfermedades o el agravamiento de otras por la presencia de sustancias extrañas en el aire. Los resultados ambientales obtenidos en los focos emisores de humos fueron comparados con zonas de contaminación urbana normal y con un sitio de referencia, seleccionando para este último el sector central del parque de mayor extensión que posee la ciudad capital. Además de la polución atmosférica se pudo detectar la presencia de sustancias potencialmente peligrosas en las superficies de algunos alimentos expuestos al aire en los domicilios afectados. (AU)


Assuntos
Humanos , Poluição Ambiental/efeitos adversos , Poluição Ambiental/análise , Poluição Ambiental/prevenção & controle , Combustão , Fumaça/efeitos adversos , Alcatrão/efeitos adversos , Exposição Ambiental/efeitos adversos , Benzopirenos/efeitos adversos , Carcinógenos , Qualidade da Água , Medição de Risco/métodos , Contaminação de Alimentos
20.
J Natl Cancer Inst ; 92(10): 803-11, 2000 May 17.
Artigo em Inglês | MEDLINE | ID: mdl-10814675

RESUMO

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in combustion products of organic matter, including cigarette smoke. Metabolically activated diol epoxides of these compounds, including benzo[a]pyrene diol epoxide (B[a]PDE), have been suggested as causative agents in the development of lung cancer. We previously mapped the distribution of B[a]PDE adducts within the p53 tumor suppressor gene (also known as TP53), which is mutated in 60% of human lung cancers, and found that B[a]PDE adducts preferentially form at lung cancer mutational hotspots (codons 154, 157, 158, 245, 248, and 273). Other PAHs may be important in lung cancer as well. METHODS: Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells. RESULTS: CDE exposure produced only low levels of adducts. Exposure of cells to the other activated PAHs resulted in DNA damage patterns similar to those previously observed with B[a]PDE but with some distinct differences. 5-MCDE, 6-MCDE, B[g]CDE, and B[c]PDE efficiently induced adducts at guanines within codons 154, 156, 157, 158, and 159 of exon 5, codons 237, 245 and 248 of exon 7, and codon 273 of exon 8, but the relative levels of adducts at each site varied for each compound. B[g]CDE, B[c]PDE, and 5-MCDE induced damage at codon 158 more selectively than 6-MCDE or B[a]PDE. The sites most strongly involved in PAH adduct formation were also the sites of highest mutation frequency (codons 157, 158, 245, 248, and 273). CONCLUSION: The data suggest that PAHs contribute to the mutational spectrum in human lung cancer.


Assuntos
Brônquios/efeitos dos fármacos , Carcinógenos/efeitos adversos , Neoplasias Pulmonares/induzido quimicamente , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Sequência de Bases , Benzopirenos/efeitos adversos , Brônquios/metabolismo , Células Cultivadas , Crisenos/efeitos adversos , Códon , Adutos de DNA , Células Epiteliais/efeitos dos fármacos , Compostos de Epóxi/efeitos adversos , Genes p53 , Mutação , Fenantrenos/efeitos adversos
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