Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos

Detalhes bibliográficos
Autor(a) principal: Giuberti, Karina
Data de Publicação: 2010
Tipo de documento: Tese
Idioma: por
Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
Texto Completo: http://repositorio.ufes.br/handle/10/5172
Resumo: Mercury is naturally present in earth's crust and it is inevitable, some degree of exposure during the whole life. It has been demonstrated a variety of pathological actions of mercury on the central nervous system, renal system and its association with increased cardiovascular risk. However, its toxic effects on the cardiovascular system under conditions of normotension and hypertension are not yet fully elucidated. In this study, Wistar and SHR rats (2.5 months old) were divided into four groups: control Wistar (Wistar CT) and control SHR (SHR CT) who received intramuscular injections of saline for 30 days or mercury (Hg Wistar) and (SHR Hg), which received 0.07 mg/kg/day HgCl2, the first dose was 4.6 mg/kg, reaching a final plasma concentration of about 29 ηM of mercury. At the end of treatment the following aspects were performed: assessment of weight, histological, hematological and biochemical profiles, measurements of hemodynamic parameters, angiotensin converting enzyme (ACE) activity and the production of malondealdeide (MDA) in the plasma of all animals. Chronic exposure to HgCl2 did not affect the weight and histological parameters when comparing Wistar CT vs Wistar Hg rats neither SHR CT compared to SHR Hg rats. In the hematological evaluation, the Wistar Hg rats showed a increased in platelet content (Wistar CT: 757 ± 55 vs Wistar Hg: 913 ± 20 103/µL) and neutrophils percentage (Wistar CT: 14 ± 5 vs Wistar Hg: 30 ± 4.3 %) and the percentage of lymphocytes decreased (Wistar CT: 83 ± 4.6 vs Wistar Hg: 68 ± 4.5 %), while in the SHR Hg, the percentage of neutrophils decreased (SHR CT: 45 ± 5.9 vs SHR Hg: 21.3 ± 4.8 %) and lymphocytes increased (SHR CT: 53 ± 6.5 vs SHR Hg: 76 ± 4.3 %). The glicemy values was increased in the Wistar Hg group (Wistar CT: 161.6 ± 12.3 vs Wistar Hg: 209 ± 15.4 mg/dL) meanwhile plasmatic globulin decreased (Wistar CT: 3.21 ± 0.09 vs Wistar Hg : 2.84 ± 0.1 g/dL). The systolic blood pressure, measured weekly by tail plethysmography, increased in rats in the fourth week of treatment (Wistar CT: 117 ± 3 vs Wistar Hg: 143 ± 5 mmHg). We also observed an increase in LV end-diastolic pressure of Wistar Hg rats (Wistar CT: 0.25 ± 0.4 vs Wistar Hg: 3.3 ± 0.5 mmHg). Treatment with Hg increased ACE activity in plasma (Wistar CT: 187.1 ± 16.2 vs Wistar Hg: 235.5 ± 14.2 ηmol/mL/min) and hearts of normotensive rats (Wistar CT: 3,4 ± 0.2 vs Wistar Hg: 4.1 ± 0.1 ηmol/mL/min/mg). In SHR Hg, ACE activity was increased in plasma (SHR CT: 113 ± 11.4 vs SHR Hg: 163 ± 15.8 ηmol/mL/min) and decreased in kidney (SHR CT: 80 ± 6.3 vs SHR Hg: 61.4 ± 2.8 ηmol/mL/min/mg), lung (SHR CT: 87.6 ± 2.2 vs SHR Hg: 75 ± 4 ηmol/mL/ min/mg), heart (SHR CT: 17.9 ± 1.1 vs SHR Hg: 14.8 ± 0.58 ηmol/mL/min/mg), brain (SHR CT: 40.3 ± 2.3 vs SHR Hg: 27.8 ± 1.8 ηmol/mL/min/mg) and aorta (SHR CT: 670 ± 16.3 vs SHR Hg: 535 ± 19.2 ηmol/mL/min/mg). The involvement of oxidative stress was assessed indirectly by measuring the production of MDA, which was found increased in the Wistar Hg rats in both plasma (Wistar CT: 0.93 ± 0.06 vs Wistar Hg: 1.28 ± 0.18 mM) and in heart (Wistar CT: 0.22 ± 0.01 vs Wistar Hg: 0.28 ± 0.01 mM) and decreased in the kidney (Wistar CT: 0.38 ± 0.03 vs Wistar Hg: 0.14 ± 0.01 mM). In SHR Hg rats, this production was increased in heart (SHR CT: 0.45 ± 0.02 vs SHR Hg: 0.55 ± 0.02 mM) and aorta (SHR CT: 0.96 ± 0.11 vs SHR Hg: 1.51 ± 0.14 mM) and decreased in the lungs (SHR CT: 0.21 ± 0.01 vs SHR Hg: 0.12 ± 0.01 mM), kidney (SHR CT: 0.96 ± 0.03 vs SHR Hg: 0.51 ± 0.01 mM) and brain (SHR CT: 0.54 ± 0.03 vs SHR Hg: 0.34 ± 0.01 mM). These results suggest that chronic exposure to mercury even at very low concentrations interferes with the activity of angiotensin converting enzyme and production of free radicals. Also it alters the levels of the blood glucose, platelet, immune, systolic blood pressure, and left ventricular end diastolic pressure. The results isolated or interconnected, can contribute to the understanding of various diseases related to contamination with metal. It can be conclude that such exposure represents a risk factor for developing of cardiovascular disease in normotensive animals (Wistar) and it may represents a aggregating factor of pre-existing risks to hypertensive rats (SHR).
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spelling Vassallo, Dalton ValentimSánchez, Mercedes SalaicesStefanon, IvanitaGiuberti, KarinaFuturo Neto, Henrique de AzevedoMassaroni, LeilaKalinin, Ana Lucia2016-08-29T15:37:58Z2016-07-112016-08-29T15:37:58Z2010-10-05Mercury is naturally present in earth's crust and it is inevitable, some degree of exposure during the whole life. It has been demonstrated a variety of pathological actions of mercury on the central nervous system, renal system and its association with increased cardiovascular risk. However, its toxic effects on the cardiovascular system under conditions of normotension and hypertension are not yet fully elucidated. In this study, Wistar and SHR rats (2.5 months old) were divided into four groups: control Wistar (Wistar CT) and control SHR (SHR CT) who received intramuscular injections of saline for 30 days or mercury (Hg Wistar) and (SHR Hg), which received 0.07 mg/kg/day HgCl2, the first dose was 4.6 mg/kg, reaching a final plasma concentration of about 29 ηM of mercury. At the end of treatment the following aspects were performed: assessment of weight, histological, hematological and biochemical profiles, measurements of hemodynamic parameters, angiotensin converting enzyme (ACE) activity and the production of malondealdeide (MDA) in the plasma of all animals. Chronic exposure to HgCl2 did not affect the weight and histological parameters when comparing Wistar CT vs Wistar Hg rats neither SHR CT compared to SHR Hg rats. In the hematological evaluation, the Wistar Hg rats showed a increased in platelet content (Wistar CT: 757 ± 55 vs Wistar Hg: 913 ± 20 103/µL) and neutrophils percentage (Wistar CT: 14 ± 5 vs Wistar Hg: 30 ± 4.3 %) and the percentage of lymphocytes decreased (Wistar CT: 83 ± 4.6 vs Wistar Hg: 68 ± 4.5 %), while in the SHR Hg, the percentage of neutrophils decreased (SHR CT: 45 ± 5.9 vs SHR Hg: 21.3 ± 4.8 %) and lymphocytes increased (SHR CT: 53 ± 6.5 vs SHR Hg: 76 ± 4.3 %). The glicemy values was increased in the Wistar Hg group (Wistar CT: 161.6 ± 12.3 vs Wistar Hg: 209 ± 15.4 mg/dL) meanwhile plasmatic globulin decreased (Wistar CT: 3.21 ± 0.09 vs Wistar Hg : 2.84 ± 0.1 g/dL). The systolic blood pressure, measured weekly by tail plethysmography, increased in rats in the fourth week of treatment (Wistar CT: 117 ± 3 vs Wistar Hg: 143 ± 5 mmHg). We also observed an increase in LV end-diastolic pressure of Wistar Hg rats (Wistar CT: 0.25 ± 0.4 vs Wistar Hg: 3.3 ± 0.5 mmHg). Treatment with Hg increased ACE activity in plasma (Wistar CT: 187.1 ± 16.2 vs Wistar Hg: 235.5 ± 14.2 ηmol/mL/min) and hearts of normotensive rats (Wistar CT: 3,4 ± 0.2 vs Wistar Hg: 4.1 ± 0.1 ηmol/mL/min/mg). In SHR Hg, ACE activity was increased in plasma (SHR CT: 113 ± 11.4 vs SHR Hg: 163 ± 15.8 ηmol/mL/min) and decreased in kidney (SHR CT: 80 ± 6.3 vs SHR Hg: 61.4 ± 2.8 ηmol/mL/min/mg), lung (SHR CT: 87.6 ± 2.2 vs SHR Hg: 75 ± 4 ηmol/mL/ min/mg), heart (SHR CT: 17.9 ± 1.1 vs SHR Hg: 14.8 ± 0.58 ηmol/mL/min/mg), brain (SHR CT: 40.3 ± 2.3 vs SHR Hg: 27.8 ± 1.8 ηmol/mL/min/mg) and aorta (SHR CT: 670 ± 16.3 vs SHR Hg: 535 ± 19.2 ηmol/mL/min/mg). The involvement of oxidative stress was assessed indirectly by measuring the production of MDA, which was found increased in the Wistar Hg rats in both plasma (Wistar CT: 0.93 ± 0.06 vs Wistar Hg: 1.28 ± 0.18 mM) and in heart (Wistar CT: 0.22 ± 0.01 vs Wistar Hg: 0.28 ± 0.01 mM) and decreased in the kidney (Wistar CT: 0.38 ± 0.03 vs Wistar Hg: 0.14 ± 0.01 mM). In SHR Hg rats, this production was increased in heart (SHR CT: 0.45 ± 0.02 vs SHR Hg: 0.55 ± 0.02 mM) and aorta (SHR CT: 0.96 ± 0.11 vs SHR Hg: 1.51 ± 0.14 mM) and decreased in the lungs (SHR CT: 0.21 ± 0.01 vs SHR Hg: 0.12 ± 0.01 mM), kidney (SHR CT: 0.96 ± 0.03 vs SHR Hg: 0.51 ± 0.01 mM) and brain (SHR CT: 0.54 ± 0.03 vs SHR Hg: 0.34 ± 0.01 mM). These results suggest that chronic exposure to mercury even at very low concentrations interferes with the activity of angiotensin converting enzyme and production of free radicals. Also it alters the levels of the blood glucose, platelet, immune, systolic blood pressure, and left ventricular end diastolic pressure. The results isolated or interconnected, can contribute to the understanding of various diseases related to contamination with metal. It can be conclude that such exposure represents a risk factor for developing of cardiovascular disease in normotensive animals (Wistar) and it may represents a aggregating factor of pre-existing risks to hypertensive rats (SHR).O mercúrio está naturalmente presente na crosta terrestre e é inevitável, algum grau de exposição dos seres vivos a ele. Tem sido investigada uma variedade de alterações induzidas pelo mercúrio sobre o sistema nervoso central, renal e a sua associação com o aumento de risco cardiovascular. Entretanto, seus efeitos tóxicos sobre o sistema cardiovascular, em condições de normotensão e hipertensão, ainda não estão totalmente elucidados. Neste estudo, ratos Wistar e SHR (2,5 meses de idade) foram divididos em quatro grupos: controle Wistar (Wistar CT) e controle SHR (SHR CT) que receberam injeções intramusculares de salina por 30 dias ou mercúrio (Wistar Hg) e (SHR Hg), que receberam diariamente 0,07 μg/Kg de HgCl2, sendo a primeira dose 4,6 μg/Kg, alcançando uma concentração plasmática final de cerca de 29 ηM de mercúrio. Ao término do tratamento, foram realizadas: a avaliação ponderal, histológica, hematológica, o perfil bioquímico, as medidas dos parâmetros hemodinâmicos, a atividade da ECA e a produção de MDA de todos os animais. A exposição crônica ao HgCl2 não alterou os parâmetros ponderais e histológicos quando comparados os grupos Wistar CT vs Wistar Hg e SHR CT vs SHR Hg. Na avaliação hematológica, os ratos Wistar Hg apresentaram aumento no conteúdo plaquetário (Wistar CT: 757 ± 55 vs Wistar Hg: 913 ± 20 103/μL) e da porcentagem de neutrófilos (Wistar CT: 14 ± 5 vs Wistar Hg: 30 ± 4,3 %) e o percentual de linfócitos diminuído (Wistar CT: 83 ± 4,6 vs Wistar Hg: 68 ± 4,5 %), enquanto os ratos SHR Hg, apresentaram o percentual de neutrófilos diminuído (SHR CT: 45 ± 5,9 vs SHR Hg: 21,3 ± 4,8 %) e o de linfócitos aumentado (SHR CT: 53 ± 6,5 vs SHR Hg: 76 ± 4,3). A glicemia do grupo Wistar Hg estava aumentada (Wistar CT: 161,6 ± 12,3 vs Wistar Hg: 209 ± 15,4 mg/dL) e de globulina diminuída (Wistar CT: 3,21 ± 0,09 vs Wistar Hg: 2,84 ± 0,1 g/dL). A pressão arterial sistólica, medida semanalmente por pletismografia de cauda, aumentou nos ratos Wistar na quarta semana de tratamento (Wistar CT: 117 ± 3 vs Wistar Hg: 143 ± 5 mmHg). Foi observado também, aumento na pressão diastólica final do VE dos ratos Wistar Hg (Wistar CT: 0,25 ± 0,4 vs Wistar Hg: 3,3 ± 0,5 mmHg). O tratamento com Hg aumentou a atividade da ECA no plasma (Wistar CT: 187,1 ± 16,2 vs Wistar Hg: 235,5 ± 14,2 ηmol/mL/min) e no coração dos ratos normotensos (Wistar CT: 3,4 ± 0,2 vs Wistar Hg: 4,1 ± 0,1 ηmol/mL/min/mg). Nos animais SHR Hg, a atividade da ECA estava aumentada no plasma (SHR CT: 113 ± 11,4 vs SHR Hg: 163 ± 15,8 ηmol/mL/min) e diminuída nos rins (SHR CT: 80 ± 6,3 vs SHR Hg: 61,4 ± 2,8 ηmol/mL/min/mg), pulmões (SHR CT: 87,6 ± 2,2 vs SHR Hg: 75 ± 4 ηmol/mL/min/mg), coração (SHR CT: 17,9 ± 1,1 vs SHR Hg: 14,8 ± 0,58 ηmol/mL/min/mg), cérebro (SHR CT: 40,3 ± 2,3 vs SHR Hg: 27,8 ± 1,8 ηmol/mL/min/mg) e aorta (SHR CT: 670 ± 16,3 vs SHR Hg: 535 ± 19,2 ηmol/mL/min/mg). A participação do estresse oxidativo foi avaliada de maneira indireta através da medida da produção de MDA, que se encontrou aumentada nos ratos Wistar Hg, tanto no plasma ( istar CT: 0,93 ± 0,06 vs Wistar Hg: 1,28 ± 0,18 mM) quanto no coração (Wistar CT: 0,22 ± 0,01 vs Wistar Hg: 0,28 ± 0,01 mM) e diminuída nos rins (Wistar CT: 0,38 ± 0,03 vs Wistar Hg: 0,14 ± 0,01 mM). Nos ratos SHR Hg, esta produção estava aumentada no coração (SHR CT: 0,45 ± 0,02 vs SHR Hg: 0,55 ± 0,02 mM) e na aorta (SHR CT: 0,96 ± 0,11 vs SHR Hg: 1,51 ± 0,14 mM) e diminuída nos pulmões (SHR CT: 0,21 ± 0,01 vs SHR Hg: 0,12 ± 0,01 mM), rins (SHR CT: 0,96 ± 0,03 vs SHR Hg: 0,51 ± 0,01 mM) e cérebro (SHR CT: 0,54 ± 0,03 vs SHR Hg: 0,34 ± 0,01 mM). Estes resultados sugerem, que a exposição crônica ao mercúrio mesmo em baixíssima concentração, interfere na atividade da enzima conversora de angiotensina e na produção de radicais livres. Também altera os valores glicêmicos, plaquetários, imunológicos, da pressão arterial sistólica e da pressão diastólica final do ventrículo esquerdo. Os resultados isolados ou interligados, podem contribuir para o entendimento das várias patologias relacionadas à contaminação com o metal. Podemos concluir que esta exposição representa um fator de risco para o esenvolvimento de doenças cardiovasculares nos animais normotensos (Wistar) e um fator agregante aos riscos pré-existentes nos animais hipertensos (SHR).TextGIUBERTI, Karina. Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos. 2010. Tese (Doutorado em Ciências Fisiológicas) - Universidade Federal do Espírito Santo, Centro de Ciências da Saúde, Vitória, 2010.http://repositorio.ufes.br/handle/10/5172porUniversidade Federal do Espírito SantoDoutorado em Ciências FisiológicasPrograma de Pós-Graduação em Ciências FisiológicasUFESBRCentro de Ciências da SaúdeECACloreto de mercúrioEstresse oxidativoPressão arterial sistólicaFisiologia612Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratosinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)instname:Universidade Federal do Espírito Santo (UFES)instacron:UFESORIGINALKarina-Gilberti-2010-trabalho.pdfapplication/pdf931452http://repositorio.ufes.br/bitstreams/3695560a-baf0-4c35-9516-a455ce593edc/download95425c28d1665b17d3f29ac197633d6dMD5110/51722024-07-16 17:10:02.999oai:repositorio.ufes.br:10/5172http://repositorio.ufes.brRepositório InstitucionalPUBhttp://repositorio.ufes.br/oai/requestopendoar:21082024-10-15T17:52:33.987721Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) - Universidade Federal do Espírito Santo (UFES)false
dc.title.none.fl_str_mv Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
title Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
spellingShingle Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
Giuberti, Karina
ECA
Cloreto de mercúrio
Estresse oxidativo
Pressão arterial sistólica
Fisiologia
612
title_short Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
title_full Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
title_fullStr Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
title_full_unstemmed Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
title_sort Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos
author Giuberti, Karina
author_facet Giuberti, Karina
author_role author
dc.contributor.advisor-co1.fl_str_mv Vassallo, Dalton Valentim
dc.contributor.advisor-co2.fl_str_mv Sánchez, Mercedes Salaices
dc.contributor.advisor1.fl_str_mv Stefanon, Ivanita
dc.contributor.author.fl_str_mv Giuberti, Karina
dc.contributor.referee1.fl_str_mv Futuro Neto, Henrique de Azevedo
dc.contributor.referee2.fl_str_mv Massaroni, Leila
dc.contributor.referee3.fl_str_mv Kalinin, Ana Lucia
contributor_str_mv Vassallo, Dalton Valentim
Sánchez, Mercedes Salaices
Stefanon, Ivanita
Futuro Neto, Henrique de Azevedo
Massaroni, Leila
Kalinin, Ana Lucia
dc.subject.por.fl_str_mv ECA
Cloreto de mercúrio
Estresse oxidativo
Pressão arterial sistólica
topic ECA
Cloreto de mercúrio
Estresse oxidativo
Pressão arterial sistólica
Fisiologia
612
dc.subject.cnpq.fl_str_mv Fisiologia
dc.subject.udc.none.fl_str_mv 612
description Mercury is naturally present in earth's crust and it is inevitable, some degree of exposure during the whole life. It has been demonstrated a variety of pathological actions of mercury on the central nervous system, renal system and its association with increased cardiovascular risk. However, its toxic effects on the cardiovascular system under conditions of normotension and hypertension are not yet fully elucidated. In this study, Wistar and SHR rats (2.5 months old) were divided into four groups: control Wistar (Wistar CT) and control SHR (SHR CT) who received intramuscular injections of saline for 30 days or mercury (Hg Wistar) and (SHR Hg), which received 0.07 mg/kg/day HgCl2, the first dose was 4.6 mg/kg, reaching a final plasma concentration of about 29 ηM of mercury. At the end of treatment the following aspects were performed: assessment of weight, histological, hematological and biochemical profiles, measurements of hemodynamic parameters, angiotensin converting enzyme (ACE) activity and the production of malondealdeide (MDA) in the plasma of all animals. Chronic exposure to HgCl2 did not affect the weight and histological parameters when comparing Wistar CT vs Wistar Hg rats neither SHR CT compared to SHR Hg rats. In the hematological evaluation, the Wistar Hg rats showed a increased in platelet content (Wistar CT: 757 ± 55 vs Wistar Hg: 913 ± 20 103/µL) and neutrophils percentage (Wistar CT: 14 ± 5 vs Wistar Hg: 30 ± 4.3 %) and the percentage of lymphocytes decreased (Wistar CT: 83 ± 4.6 vs Wistar Hg: 68 ± 4.5 %), while in the SHR Hg, the percentage of neutrophils decreased (SHR CT: 45 ± 5.9 vs SHR Hg: 21.3 ± 4.8 %) and lymphocytes increased (SHR CT: 53 ± 6.5 vs SHR Hg: 76 ± 4.3 %). The glicemy values was increased in the Wistar Hg group (Wistar CT: 161.6 ± 12.3 vs Wistar Hg: 209 ± 15.4 mg/dL) meanwhile plasmatic globulin decreased (Wistar CT: 3.21 ± 0.09 vs Wistar Hg : 2.84 ± 0.1 g/dL). The systolic blood pressure, measured weekly by tail plethysmography, increased in rats in the fourth week of treatment (Wistar CT: 117 ± 3 vs Wistar Hg: 143 ± 5 mmHg). We also observed an increase in LV end-diastolic pressure of Wistar Hg rats (Wistar CT: 0.25 ± 0.4 vs Wistar Hg: 3.3 ± 0.5 mmHg). Treatment with Hg increased ACE activity in plasma (Wistar CT: 187.1 ± 16.2 vs Wistar Hg: 235.5 ± 14.2 ηmol/mL/min) and hearts of normotensive rats (Wistar CT: 3,4 ± 0.2 vs Wistar Hg: 4.1 ± 0.1 ηmol/mL/min/mg). In SHR Hg, ACE activity was increased in plasma (SHR CT: 113 ± 11.4 vs SHR Hg: 163 ± 15.8 ηmol/mL/min) and decreased in kidney (SHR CT: 80 ± 6.3 vs SHR Hg: 61.4 ± 2.8 ηmol/mL/min/mg), lung (SHR CT: 87.6 ± 2.2 vs SHR Hg: 75 ± 4 ηmol/mL/ min/mg), heart (SHR CT: 17.9 ± 1.1 vs SHR Hg: 14.8 ± 0.58 ηmol/mL/min/mg), brain (SHR CT: 40.3 ± 2.3 vs SHR Hg: 27.8 ± 1.8 ηmol/mL/min/mg) and aorta (SHR CT: 670 ± 16.3 vs SHR Hg: 535 ± 19.2 ηmol/mL/min/mg). The involvement of oxidative stress was assessed indirectly by measuring the production of MDA, which was found increased in the Wistar Hg rats in both plasma (Wistar CT: 0.93 ± 0.06 vs Wistar Hg: 1.28 ± 0.18 mM) and in heart (Wistar CT: 0.22 ± 0.01 vs Wistar Hg: 0.28 ± 0.01 mM) and decreased in the kidney (Wistar CT: 0.38 ± 0.03 vs Wistar Hg: 0.14 ± 0.01 mM). In SHR Hg rats, this production was increased in heart (SHR CT: 0.45 ± 0.02 vs SHR Hg: 0.55 ± 0.02 mM) and aorta (SHR CT: 0.96 ± 0.11 vs SHR Hg: 1.51 ± 0.14 mM) and decreased in the lungs (SHR CT: 0.21 ± 0.01 vs SHR Hg: 0.12 ± 0.01 mM), kidney (SHR CT: 0.96 ± 0.03 vs SHR Hg: 0.51 ± 0.01 mM) and brain (SHR CT: 0.54 ± 0.03 vs SHR Hg: 0.34 ± 0.01 mM). These results suggest that chronic exposure to mercury even at very low concentrations interferes with the activity of angiotensin converting enzyme and production of free radicals. Also it alters the levels of the blood glucose, platelet, immune, systolic blood pressure, and left ventricular end diastolic pressure. The results isolated or interconnected, can contribute to the understanding of various diseases related to contamination with metal. It can be conclude that such exposure represents a risk factor for developing of cardiovascular disease in normotensive animals (Wistar) and it may represents a aggregating factor of pre-existing risks to hypertensive rats (SHR).
publishDate 2010
dc.date.issued.fl_str_mv 2010-10-05
dc.date.accessioned.fl_str_mv 2016-08-29T15:37:58Z
dc.date.available.fl_str_mv 2016-07-11
2016-08-29T15:37:58Z
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dc.identifier.citation.fl_str_mv GIUBERTI, Karina. Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos. 2010. Tese (Doutorado em Ciências Fisiológicas) - Universidade Federal do Espírito Santo, Centro de Ciências da Saúde, Vitória, 2010.
dc.identifier.uri.fl_str_mv http://repositorio.ufes.br/handle/10/5172
identifier_str_mv GIUBERTI, Karina. Efeitos da exposição crônica a baixas concentrações de cloreto de mercúrio (20 ηM) sobre o sistema cardiovascular de ratos. 2010. Tese (Doutorado em Ciências Fisiológicas) - Universidade Federal do Espírito Santo, Centro de Ciências da Saúde, Vitória, 2010.
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Doutorado em Ciências Fisiológicas
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dc.publisher.department.fl_str_mv Centro de Ciências da Saúde
publisher.none.fl_str_mv Universidade Federal do Espírito Santo
Doutorado em Ciências Fisiológicas
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