Polimorfismo no gene de metilenetetrahidrofolato redutase não está relacionado com o risco de doença cerebrovascular isquêmica em uma população brasileira

OBJETIVO: Os dados são conflitantes em relação a risco de acidente cerebrovascular associado a polimorfismo do gene 5,10-metilenetetrahidrofolato redutase C677T, o qual predispõe a hiperhomocisteinemia. Um estudo de meta-análise sugere que o genotipo 5,10-metilenetetrahidrofolato redutase 677TT poderia ter uma pequena influência em determinar susceptibilidade a acidente cerebrovascular. MÉTODOS: Analisamos este polimorfismo em indivíduos brasileiros com acidente cerebrovascular isquêmico, baseando-se em um estudo de caso-controle. RESULTADOS: Comparamos os genótipos 5,10-metilenetetrahidrofolato redutase em grupos de indivíduos com acidente cerebrovascular isquêmico (n=127) e controle normal (n=126), e encontramos Odds Ratio de 1,97 (IC 95% 0,84 - 4,64) em uma análise multivariada, na qual os resultados foram ajustados a características clínicas basais dos indivíduos estudados. DISCUSSÃO: Nossos estudos indicam que o genótipo 5,10-metilenetetrahidrofolato redutase C677T não é um fator de risco para acidente cerebrovascular isquêmico entre indivíduos brasileiros.PURPOSE: Data are conflicting concerning the risk for ischemic stroke associated with a common polymorphism in the gene encoding 5,10-methylenetetrahydrofolate reductase C677T, which predisposes carriers to hyperhomocysteinemia. A meta-analysis study suggested that the 5,10-methylenetetrahydrofolate reductase 677TT genotype might have a small influence in determining susceptibility to ischemic stroke. METHODS: We analyzed the 5,10-methylenetetrahydrofolate reductase 677TT genotype polymorphism in Brazilian subjects with ischemic stroke, using a case-control design. RESULTS: We compared 5,10-methylenetetrahydrofolate reductase genotypes in groups of subjects presenting ischemic stroke (n = 127) and normal control (n = 126) and found an odds ratio of 1.97 (95% CI, 0.84-4.64) in a multivariate analysis in which results were adjusted to baseline clinical characteristics of study participants. CONCLUSION: We found that the homozygous 5,10-methylenetetrahydrofolate reductase C677T genotype was not a risk factor for ischemic stroke in these Brazilian subjects

NEONATAL JAUNDICE AND PHOTOTHERAPY: THE CONTRIBUTION OF NURSES TO THE EFFECTIVENESS OF

Resumo: A Icterícia Neonatal é um dos episódios mais comuns em uma UTI, assim os objetivos desta pesquisa são: identificar as dificuldades encontradas pelo enfermeiro na utilização da fototerapia em Rns com icterícia neonatal e descrever os cuidados dos enfermeiros aos Rns com icterícia, minimizando as dificuldades evidenciadas, de modo a contribuir para a melhoria da eficácia da fototerapia. Pesquisa exploratória, descritiva, bibliográfica na BVS (LILACS e BDENF) e qualitativa. Após a coleta de dados foi realizada uma leitura exploratória, seletiva, crítica e análise temática.  Categorias emergentes: Dificuldades encontradas pelos enfermeiros na utilização da fototerapia e os cuidados do enfermeiro para eficácia da fototerapia em Rns com icterícia. Concluímos que se faz necessário a implementação de uma rotina hospitalar na qual deve conter todas as ações necessárias a serem cumpridas em um Rn ictérico, visando um melhor cuidado do enfermeiro e reduzindo a dificuldade de implementação para um tratamento de qualidade.Descritores: Icterícia Neonatal, Cuidados de Enfermagem e Fototerapia

Air Pollution’s Impact on Cardiac Remodeling in an Experimental Model of Chagas Cardiomyopathy

BackgroundChagas disease is characterized by intense myocardial fibrosis stimulated by the exacerbated production of inflammatory cytokines, oxidative stress, and apoptosis. Air pollution is a serious public health problem and also follows this same path. Therefore, air pollution might amplify the inflammatory response of Chagas disease and increase myocardial fibrosis.MethodsWe studied groups of Trypanosoma cruzi infected Sirius hamsters (Chagas=CH and Chagas exposed to pollution=CH+P) and 2 control groups (control healthy animals=CT and control exposed to pollution=CT+P). We evaluated acute phase (60 days post infection) and chronic phase (10 months). Echocardiograms were performed to assess left ventricular systolic and diastolic diameter, in addition to ejection fraction. Interstitial collagen was measured by morphometry in picrosirius red staining tissue. The evaluation of inflammation was performed by gene and protein expression of cytokines IL10, IFN-γ, and TNF; oxidative stress was quantified by gene expression of NOX1, MnSOD, and iNOS and by analysis of reactive oxygen species; and apoptosis was performed by gene expression of BCL2 and Capsase3, in addition to TUNEL analysis.ResultsChagas groups had increased collagen deposition mainly in the acute phase, but air pollution did not increase this deposition. Also, Chagas groups had lower ejection fraction in the acute phase (p = 0.002) and again air pollution did not worsen ventricular function or dilation. The analysis of the inflammation and oxidative stress pathways were also not amplified by air pollution. Apoptosis analysis showed increased expression of BCL2 and Caspase3 genes in chagasic groups in the acute phase, with a marginal p of 0.054 in BCL2 expression among infected groups, and TUNEL technique showed amplified of apoptotic cells by pollution among infected groups.ConclusionsA possible modulation of the apoptotic pathway was observed, inferring interference from air pollution in this pathway. However, it was not enough to promote a greater collagen deposition, or worsening ventricular function or dilation caused by air pollution in this model of Chagas cardiomyopathy

COVID-Inconfidentes - SARS-CoV-2 seroprevalence in two Brazilian urban areas during the pandemic first wave: study protocol and initial results

Background: A population study is an important tool that can be used to understand the actual epidemiological scenario of the Covid-19 in different territories, identify its magnitude, understand its transmission dynamics, and its demographic, geographical, and social distribution. Objective: The aim of this study was to determine the prevalence and dynamics of SARS-CoV-2 infection in the population of two Brazilian cities during the pandemic first wave and subsequent socioeconomic and health effects. Materials & methods: This paper described the methodological procedures adopted and the prevalence of the SARS-CoV-2 infection in the population. A household survey was conducted between October and December 2020, in two historic cities of Brazil's mining region. Anti-SARS-CoV-2 antibody was detected using the Wondfo® rapid test. The face-to-face interview consisted of administration of a questionnaire containing registration data, sociodemographic and economic variables, living habits, general health condition, mental health, sleep habits, and eating and nutrition. Results: We evaluated 1,762 residents, of which 764 (43.4%) were in Mariana and 998 (56.6%) in Ouro Preto. For both cities, 51.9% of the interviewees were female, with a predominance of the age range 35 to 59 years old (47.2%). The prevalence of the SARS-CoV-2 infection was 5.5% in all cities, 6.2% in Ouro Preto, and 4.7% in Mariana. The prevalence was similar between cities (P>0.05). Conclusion: The study was effective in verifying the seroprevalence of infection by the virus and its findings will enable further analyses of the health conditions of the population related to social isolation and the risk of infection with SARS-CoV-2

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5–7 vast areas of the tropics remain understudied.8–11 In the American tropics, Amazonia stands out as the world’s most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13–15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazon’s biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region’s vulnerability to environmental change. 15%–18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

Polymorphisms of EGF e EGFR genes in diffusely infiltrative astrocytomas

INTRODUÇÃO: Os astrocitomas difusamente infiltrativos são os tumores mais freqüentes de Sistema Nervoso Central (SNC) com uma taxa de 5-7 novos casos por 100.000 pessoas ano. São tumores altamente invasivos e estão associados com alterações de alguns genes como EGF (fator de crescimento epidérmico) e o EGFR (receptor do fator de crescimento epidérmico), que podem criar um aumento da atividade mitogênica, acarretando aumento de proliferação e maturação celular, apoptose, angiogênese e metástase. O nível de expressão destes genes pode ser influenciado por alterações genéticas, como a presença de polimorfismos. Uma mudança única de base (SNP) pode alterar a expressão gênica e, sendo assim, estar associada ao aumento do risco de desenvolver astrocitomas. Nesse trabalho, foram analisados 2 SNPs na região não traduzida (c.-191C>A e c.-216G>T) e um SNP no exon 16 (c.2073A>T) do gene EGFR, e um outro SNP na região não traduzida no gene EGF (c.61A>G). Os SNPs foram associados a expressão gênica do EGFR e a sobrevida dos pacientes. MÈTODOS: Foi realizado um estudo caso-controle com 193 casos de astrocitomas difusamente infiltrativos e 200 controles por amplificação por PCR seguido de digestão enzimática. Os produtos digeridos das amostras foram analisados por eletroforese em gel de agarose e poliacrilamida e corados com brometo de etídeo. A expressão gênica foi realizada após extração de RNA do tecido tumoral seguida de transcrição reversa e PCR em tempo real. Testes de qui-quadrado, odds ratio (OR), intervalo de confiança 95% (IC95%), t de Student e curvas de Kaplan-Meier foram realizados para análises estatística. RESULTADOS: A análise das freqüências dos genótipos dos polimorfismos mostrou uma diferença na distribuição entre casos e controles para o polimorfismo c.2073A>T. Pacientes com o genótipo TT apresentou um menor risco para astrocitoma quando comparados com o genótipo AA (OR=0,51, IC95%=0,29-0,99). Nenhuma correlação foi encontrada para os outros polimorfismos analisados. Também não foi encontrada correlação entre os genótipos dos polimorfismos e os níveis de expressão de EGFR e a sobrevida dos pacientes. CONCLUSÃO: Nosso trabalho mostrou haver um possível fator de proteção quando o paciente é portador do genótipo TT, o que pode levar a uma diminuição do risco de desenvolver o tumor. Pacientes com genótipo TT do polimorfismo c.2073A>T do gene EGFR apresentam um menor risco para astrocitomas difusamente infiltrativos do que os com o genótipo AA.INTRODUCTION: Diffusely infiltrative astrocytomas are the most frequent tumors of the Central Nervous System (CNS) with a rate of 5-7 new cases in 100,000 individuals per year. They are highly invasive, and they are associated to alterations in some genes as EGF (epidermal growth factor) and EGFR (epidermal growth factor receptor), which may increase mitogenic activity, leading to increase of proliferation, cellular maturation, apoptosis, angiogenesis, and metastasis. Genetic alterations, as presence of polymorphisms of single nucleotide change (SNP) could influence their expression level, and thus could be associated to increased risk in developing astrocytomas. In the present study, two SNP of non-coding region (c.-191C>A and c.-216G>T) and one SNP in exon 16 (c.2073A>T) of EGFR, and another SNP of non-coding region of EGF (c.61A>G) were analyzed. The SNPs were associated to EGFR expression level and to survival time. METHOD: a case-control study of 193 of diffusely infiltrative astrocytomas and 200 controls was carried out, with PCR amplification and enzymatic digestion, which products were analyzed in agarose gel or polyacrylamide gel electrophoresis stained by ethidium bromide. EGFR expression level was studied by real time PCR after RNA extraction followed by reverse transcription of tumor tissues compared to epileptic non-neoplastic brain tissues. Stastistical analysis were performed by chi-square, odds ratio (OR), 95% confidence interval (95% CI), Student-t test and Kaplan Meier. RESULTS: The polymorphic genotype frequency was different between case and controls for the polymorphism c.2073A>T. Patients with TT genotype presented lower risk to develop astrocytoma when compared to genotype AA (OR=0.51, CI95%=0.29- 0.99). No other correlation was observed for the remaining studied polymorphisms. There was neither correlation between the polymorphic genotypes and the EGFR expression levels nor with survival time. CONCLUSION: The present study showed a possible protection factor in developing astrocytomas for the patients harboring the genotype TT of c.2073A>T polymorphism of EFGR, thus the patients presenting TT genotype have lower risk to develop diffusely infiltrative astrocytoma than patients presenting the genotype AA

Influence of air pollution on myocardial remodeling in Chagas disease in experimental model

A doença de Chagas é uma importante causa de miocardiopatia e insuficiência cardíaca no Brasil. Promove disfunção miocárdica caracterizada por intensa fibrose a qual está diretamente relacionada a uma complexa cascata de eventos como inflamação, estresse oxidativo e apoptose. Da mesma forma, a poluição atmosférica leva a ativação dessas mesmas vias, intensificando as respostas do organismo frente a essa agressão. Nossa hipótese é que a poluição poderia amplificar o estresse oxidativo e a inflamação, levando a maior perda de cardiomiócitos com consequente aumento da fibrose miocárdica na miocardiopatia chagásica. Nosso objetivo foi avaliar o papel da poluição do ar no remodelamento ventricular na doença de Chagas experimental. Foram utilizados 100 hamster sírio fêmeas, divididos em 4 grupos (controle Ct, controle com Poluição Ct+P, Infectado Ch e Infectado com Poluição Ch+P). Os animais foram infectados com 105 formas tripomastigotas do Trypanosoma cruzi e expostos à poluição por inalação de material particulado, produzido pela queima do diesel. A fração do volume de colágeno intersticial do ventrículo esquerdo (FVCI-VE) e do ventrículo direito (FVCI-VD) foi determinada em cortes histológicos, corados com picrosirius red. A análise anatômica e funcional foi realizada por ecocardiograma. A avaliação da inflamação foi realizada por análise da expressão gênica, utilizando a técnica de RT-PCR em tempo real e análise proteica por ELISA (IL-10, TNF- e INF-). O estresse oxidativo também foi avaliado por expressão gênica (Nox1, Nox4, MnSOD e iNOS), avaliação da glutationa total, peroxidação lipídica e produção de ROS. Avaliamos a apoptose por expressão gênica (BCL2 e CASP3) e pelo método de TUNEL. Os resultados foram avaliados em 3 fases: aguda, crônica e casuística total. O acúmulo do colágeno intersticial foi maior nos grupos chagásicos em relação aos controles (VE e VD: p<0,05) na casuística total. Nas fases aguda e crônica observamos maior deposição de colágeno no VE do grupo Ch+P comparado ao Ct (p=0,044 e p=0,018, respectivamente). Não houve interferência da poluição nos grupos infectados. Na análise da geometria do coração na fase crônica mostrou maior diâmetro diastólico (DDVE) e sistólico (DSVE) do ventrículo esquerdo no grupo ChxCt+P (p < 0,05 e p < 0,05, respectivamente). Já a fase aguda mostrou maior dilatação do VE no grupo Ch (DDVE: Ch x Ct p=0,003 e Ch x Ct + P p = 0,013; e DSVE: Ch x Ct p < 0,05 e Ch x Ct+P p<0,05). Mais uma vez a poluição do ar não interferiu nessa variável. Os parâmetros da função sistólica do VE, como fração de ejeção (FE) e fração de encurtamento (D), não apresentaram piora na fase crônica (p=0,09 em ambos). Já na fase aguda observamos alteração desses parâmetros no grupo Ch comparado aos controles (FE: Ch x Ct e Ch x Ct+P p < 0,01 e D: Ch x Ct e Ch x Ct+P p < 0,05). Os parâmetros de função diastólica, tempo de desaceleração (TD p = 0,11) e tempo de relaxamento isovolumétrico (TRIV p=0,80), na fase crônica, não apresentaram alteração. Já a variável da relação E/A apresentou-se menor no grupo Ch (p=0,003). Na fase aguda, observou-se maior significância no grupo Ch+P em relação ao grupo Ct no parâmetro da relação E/A e TD (p < 0,05 e p < 0,01) e TRIV foi significativamente maior no Ch+P grupo comparado aos demais grupos (p=0,0006). Não houve diferenças na análise de fase aguda e crônica quanto ao índice de performance miocárdica. A avaliação da inflamação pela expressão gênica (IL-10, TNF- e INF-) foi maior nos grupos chagásicos, tanto na casuística total como na fase aguda. A expressão proteica dessas mesmas citocinas foi maior nos grupos chagásicos apenas na fase aguda. Não houve amplificação da expressão gênica e proteica influenciada pela poluição. A avaliação do estresse oxidativo pela expressão gênica (Nox1, MnSOD e iNOS) foi maior nos grupos chagásicos em comparação aos controles, tanto na fase aguda como na casuística total. A fase crônica não apresentou alterações significativas em nenhum desses genes. A avaliação da glutationa total bem como a peroxidação lipídica não apresentaram diferenças significantes. A análise da produção de ROS apresentou diferenças quando comparado o grupo Ch+P aos grupos controles na fase aguda e na casuística total (aguda: Ch+P x Ct p<0,01 e Ch+P x Ct+P p<0,05; total: Ch+P x Ct p<0,01 e Ch+P x Ct+P p < 0,01) e na fase crônica observamos diferenças entre os grupos chagásicos comparado ao Ct (Ch x Ct p=0,037e Ch+P x Ct p=0,028). Em nenhuma análise de avaliação do estresse oxidativo houve interferência da poluição no grupo infectado. Na análise da apoptose pela expressão gênica observamos que os grupos infectados apresentaram maior expressão do gene BCL2 e CASP3 tanto na fase aguda como na casuística total, sendo significante na comparação entre os grupos. Nessas 2 fases o grupo Ch+P apresentou maior expressão que o grupo Ch, com p marginal de 0,064 (total) e 0,054 (aguda) na análise de BCL2. A técnica do TUNEL apresentou maior quantidade de células apoptóticas no grupo Ch+P tanto nas fases total como na aguda, sendo que nessa última obtivemos 2x mais células apoptóticas entre Ch+P x Ch, sugerindo modulação da apoptose pela poluição. A curva de sobrevida demonstra alta mortalidade 62% dos animais infectados (Ch e Ch+P) nos primeiros 38 dias após infecção. Concluímos que a poluição do ar não aumentou a deposição de colágeno, não piorou a dilatação ou função ventricular, não apresentou alteração das vias da inflamação e do estresse oxidativo, e nem sequer aumentou a mortalidade nesse modelo de miocardiopatia chagásica. Houve possível modulação da via apoptótica pela poluição que, entretanto, não aumentou a fibrose miocárdica nos animais infectados.Chagas disease is a major cause of cardiomyopathy and heart failure in Brazil. It promotes myocardial dysfunction that is characterized by fibrosis and which is directly related to a complex cascade of pathways, such as inflammation, oxidative stress and apoptosis. As well air pollution leads to intense activation of these pathways, intensifying the response against this aggression. Our hypothesis is that pollution could amplify oxidative stress and inflammation, leading to greater loss of cardiomyocytes with an increased myocardial fibrosis in Chagas cardiomyopathy. Therefore, our objective was to evaluate the role of air pollution in ventricular remodeling in experimental Chagas disease. One hundred female sirius hamsters were divided into four groups (control Ct, control with Pollution Ct+P, Infected Ch and Infected + Pollution Ch+P). The animals were infected with the injection of 105 trypomastigote forms of Trypanosoma cruzi. The animals were exposed to the inhalation of particulate matter, produced by burning of the diesel fuel. The interstitial collagen volume fraction of left ventricle (ICVF-LV) and right ventricle (ICVF-RV) was analyzed in histological sections stained with Picrosirius red. The anatomical and functional analysis was performed by echocardiogram. The evaluation of the inflammation was done by gene expression analysis using real-time RT-PCR and protein by ELISA (IL-10, TNF- and INF-). Oxidative stress also was evaluated by gene expression using the real-time RT-PCR (Nox1, Nox4, MnSOD and iNOS), total glutathione, lipid peroxidation and ROS production. We evaluated apoptosis by gene expression (BCL2 and CASP3) and by TUNEL. The results were evaluated in 3 phases: acute, chronic and total case series. The accumulation of interstitial collagen was higher in the chagasic groups (LV and RV: p<0.05) in the total series. In the acute and chronic phases, we observed greater collagen deposition in the LV of the Ch+P group compared to the Ct (p=0.044 and p=0.018, respectively). There was no interference of pollution in the infected groups. In the analysis of heart geometry in the chronic phase, it showed a larger LV diastolic (LVDD) and systolic (LVSD) diameter in the Ch x Ct+P group (p<0.05 and p<0.05, respectively). The acute phase showed greater LV dilation in the Ch group (LVDD: Ch x Ct p=0.003 and Ch x Ct+P p=0.013; and LVSD: Ch x Ct p<0.05 and Ch x Ct + P p<0.05). Again, air pollution did not affect this variable. The parameters of LV systolic function, such as ejection fraction (EF) and shortening fraction (D), no worsening of this function was observed in the chronic phase (p=0.09 in both). In the acute phase, we observed a decrease of this parameters in the Ch group compared to the controls (EF: Ch x Ct and Ch x Ct+P p<0.01 and D: Ch x Ct and Ch x Ct+P p<0.05). The diastolic function parameters, as deceleration time (DT p=0.11) and isovolumetric relaxation time (IRT p=0.80), in the chronic phase, no statistical significance was observed, however, E/A ratio was lower in the Ch group (p=0.003). In the acute phase, we observed higher values in the Ch+P compared to the Ct regarding E/A ratio and DT (p<0.05 and p<0.01), and IRT was significantly higher in Ch+P compared to the other groups (p=0.0006). There were no differences in the analysis of acute and chronic phase regarding the myocardial performance index. The evaluation of inflammation by gene expression (IL-10, TNF- and INF-) it was higher in chagasic groups, both in the total series and in the acute phase. The protein expression of these same cytokines was higher in the chagasic groups only in the acute phase, whereas in the chronic phase and in the total series there was no significance. There was no amplification of gene and protein expression influenced by pollution. The evaluation of oxidative stress by gene expression (Nox1, MnSOD and iNOS) was higher in chagasic groups compared to controls, both in the acute phase and in the total series. The chronic phase did not show significant changes in any of these analyzed genes. The evaluation of total glutathione as well as lipid peroxidation did not show significant differences. The ROS production analysis showed differences when comparing the Ch+P group to the control groups in the acute phase and in the total series (acute: Ch+P x Ct p<0.01 and Ch+P x Ct+P p<0.05; total: Ch+P x Ct p<0.01 and Ch+P x Ct+P p<0.01) and in the chronic phase we observed differences between the chagasic groups compared to Ct (Ch x Ct p=0.037 e Ch+P x Ct p=0.028). None analysis of oxidative stress showed interference of pollution in the infected group. In the analysis of apoptosis by gene expression, we observed that the infected groups showed greater expression of the BCL2 and CASP3 gene both in the acute phase and in the total series. In these 2 phases, the Ch+P group showed greater expression than the Ch group, with marginal p of 0.064 (total) and 0.054 (acute) in the analysis of BCL2. The TUNEL technique observed a greater number of apoptotic cells in the Ch+P group both in the total and in the acute phases, with 2x more apoptotic cells between Ch+P x Ch, suggesting modulation of apoptosis by pollution. The survival curve shows high mortality as 62% of infected animals (Ch and Ch+P) in the first 38 days after infection. We concluded that air pollution did not increase collagen deposition, did not worsen ventricular dilation or function, did not show changes in inflammation and oxidative stress pathways, and did not even increase mortality in this model of chagasic cardiomyopathy. There was possible modulation of the apoptotic pathway by pollution, which, however, did not increase myocardial fibrosis in infected animal