Serum total antioxidant status and lipid peroxidation marker malondialdehyde levels in overt and subclinical hypothyroidism

Torun, Ayşe Nur; Kulaksızoğlu, Sevsen; Kulaksızoğlu, Mustafa; Pamuk, Barış Önder; Isbilen, Elif; Tütüncü, Neslihan Başçıl

doi:10.1111/j.1365-2265.2008.03348.x

Cited by 205 publications

(165 citation statements)

References 41 publications

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“…This also seems to be the first study to report the association between dysthyroidism-induced cardiometabolic disorders with cardiac redox status. Our observations were in consonance with the results of Torun et al 56 and Akinci et al 57 that documented a similar trend in the serum levels of MDA and catalase. Oxidative stress, which is characterized by an imbalance between free radicals and antioxidants in favour of radicals, participates in the pathogenesis of many diseases and their complications.…”

Section: Discussionsupporting

confidence: 82%

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

Ajayi¹,

Akhigbe²,

Ajayi³

2017

JCDR

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Background: It is a known fact that altered thyroid state is associated with cardiometabolic disturbances. Raised TNF-α and lipid peroxidation have also been reported to be involved in the pathogenesis of cardiometabolic disorders. Aim: The present study evaluates the effect of dysthyroidism on cardiac TNF-α and lipid peroxidation, and whether the effect is estradiol-dependent. Methods: Male white New Zealand rabbits were randomized into three groups; control, carbimazole-induced hypothyroidism, and levothyroxine-induced hyperthyroidism. Results: Dysthyroidism led to altered glucose metabolism and dyslipidaemia with elevated LDL, TNF-α, and MDA. There was also decreased HDL, GSH, catalase, and 17β-estradiol. Serum electrolytes and hemorheological variables were not significantly affected. Conclusion: These findings demonstrate that dysthyroidism-induced cardiometabolic disturbance is associated with elevated cardiac TNF-α and oxidative stress via an estradiol-dependent mechanism.

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Section: Discussionsupporting

confidence: 82%

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

Ajayi¹,

Akhigbe²,

Ajayi³

2017

JCDR

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“…This pro-oxidant condition has been shown both in experimental animals and in man, and it has been associated with cellular dysfunctions in several target tissues (5). An increase in oxidative stress has been observed also in hypothyroidism, even if subclinical, due to both an impaired antioxidant status and the altered lipid metabolism (37). Furthermore, GD is an inflammatory condition with the production of acute-phase proteins and several proinflammatory cytokines, including IL-12, IL-18, and TNF-α (7).…”

Section: © 2 0 1 1 E D I T R I C E K U R T I S F O R P E R S O N a mentioning

confidence: 99%

Decreased number of circulating endothelial progenitor cells in patients with Graves’ hyperthyroidism

Ciuceis

Pilu

Cappelli

et al. 2010

J Endocrinol Invest

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ABSTRACT. Objective: A relevant biological role of circulating endothelial progenitor cells (EPC) was recently demonstrated. EPC are generated in the bone marrow, and interact with damaged endothelium, restoring the integrity of the monolayer. Therefore, aim of the present study was to evaluate EPC in the blood of patients with untreated Graves' hyperthyroidism (GD), in whom an increased oxidative stress was observed. Design and methods: Twenty-three patients with untreated active GD and 18 matched normal controls (NC) were included in the study. Circulating EPC were isolated from peripheral blood. Mononuclear cells were cultured with endothelial basal medium supplemented with EGM SingleQuots, and were identified by positive double staining after 7 days in culture. Circulating levels of C reactive protein, total antioxidant power, interleukin ( INTRODUCTIONGraves' disease (GD) is a thyroid disorder caused by an antibody-mediated immune reaction against the receptor for TSH resulting in an abnormal chronic stimulation of the gland and consequent hyperthyroidism (1, 2). This, in turn, causes the clinical symptoms of hyperthyroidism. Indeed, thyroid hormones may exert multiple effects on the heart and vascular system, inducing an hyperkinetic status and the onset of isolated systolic hypertension (3, 4). Activation of the sympathetic and of the renin-angiotensin-aldosterone (RAS) systems may elicit a major role in inducing cardiovascular changes in GD (5). Moreover, in hyperthyroidism, an unbalance between oxidant and antioxidant substances has been identified, thus leading to enhanced generation of reactive oxygen species (ROS), able to induce vascular dysfunction and damage (6). This may be the consequence of both an activation of RAS system and of a stimulation of energy metabolism induced by thyroid hormones (5). In addition, chronic inflammation has been shown in active GD, as well as in autoimmune thyroid disorders, and production of acute-phase proteins and proinflammatory cytokines [such as interleukin (IL)-12, IL-18, and tumor necrosis factor-α (TNF-α)] (7). Hemodynamic and metabolic changes may lead to vascular injury, as suggested by an increase of markers of endothelial damage observed in GD (8-10). In the last years, endothelial progenitor cells (EPC) have been recognized to play important roles in post-natal neovascularization and vascular repair, and, therefore in maintaining endothelial integrity and function (11,12). EPC are generated from bone marrow and represent precursors which preserve stem cell features, able therefore to proliferate, migrate, and differentiate in mature endothelial cells (11,12). EPC number has been demonstrated to be correlated with the number of cardiovascular risk factors, with indices of endothelial dysfunction (13-15), and the incidence of cardiovascular events (16,17). However, no data are presently available about the EPC number in hyperthyroidism caused by GD. Therefore the aim of the present study is to investigate the presence of oxidative stress and inflammation ...

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“…(23)(24)51) Moulakakis et al (23) demonstraram que aortas de ratos com hipotireoidismo subclínico induzido apresentavam níveis de malondialdeído (produto final da peroxidação lipídica) e 8-oxoguanina-DNA (uma das bases modificadas no ácido desoxirribonucléico pela reação a espécies reativas de oxigênio) elevados em comparação a um grupo controle. Em humanos também já foi demonstrado que concentrações séricas de malondialdeído estavam significativamente aumentadas tanto em hipotireoideos subclínicos quanto clínicos.…”

Section: Potenciais Contribuições Do Exercício Físico Nas Disfunções unclassified

“…Em humanos também já foi demonstrado que concentrações séricas de malondialdeído estavam significativamente aumentadas tanto em hipotireoideos subclínicos quanto clínicos. (24) Embora estudos mostrem que o exercício físico é capaz de retardar a formação de radicais livres, aumentar a produção de antioxidantes endógenos e reduzir o estresse oxidativo nas doenças cardiovasculares como a hipertensão, diabetes e aterosclerose (52)(53) , dados analisando seus efeitos sobre o estresse oxidativo em sujeitos com hipotireoidismo não foram encontrados mediante os critérios adotados para a seleção dos manuscritos.…”

Section: Potenciais Contribuições Do Exercício Físico Nas Disfunções unclassified

Influência do exercício físico nas alterações cardiovasculares induzidas pelo hipotireoidismo

Souza¹,

Lima²,

Nóbrega³

et al. 2012

RBAFS

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ResumoO hipotireoidismo é uma disfunção da tireóide que não produz seus hormônios ou só o faz através de uma alta produção do hormônio tireoestimulante. Essa enfermidade está associada ao desenvolvimento de disfunções cardiovasculares diversas. Esta revisão traz à comunidade científica e aos profissionais da saúde, informações atualizadas sobre as repercussões cardiovasculares do hipotireoidismo, sua influência na capacidade para o exercício físico, e o potencial do exercício físico para minimizar ou restaurar estas disfunções. Um levantamento dos estudos publicados entre 1995 e 2011 foi conduzido na base de dados PubMed utilizando os descritores: physical exercise, blood pressure, cardiovascular, vascular endothelial, oxidative stress, autonomic nervous system, cardiac function, subclinical hypothyroidism e hypothyroidism. Foram considerados, os artigos que avaliaram a função cardiovascular de hipotireoideos subclínicos e clínicos, e a influência do exercício físico sobre as funções cardiovasculares afetadas nesta doença. Verificamos que a capacidade aeróbia de hipotireoideos subclínicos e clínicos está reduzida, e que a função endotelial, o estresse oxidativo e a função autonômica estão prejudicados nestes sujeitos. O exercício físico parece ser capaz de restaurar a função endotelial, apesar de não fazer o mesmo na disfunção autonômica. Não existem investigações associando o efeito do exercício físico na função cardíaca e no estresse oxidativo. Apesar de ser uma enfermidade tão prevalente quanto o diabetes, não existe uma recomendação para a prescrição de exercício físico para os hipotireoideos, tal como há para obesos, cardiopatas e diabéticos. Perspectivas sobre como avançar no conhecimento da prescrição do exercício físico são apresentadas. Palavras-chaveHipotireoidismo; Exercício físico; Sistema cardiovascular. Abstract Hypothyroidism is a disorder of the thyroid gland that does not produce its hormones or only does in response to a high production of thyroid-stimulating hormone. This disease is associated with the development of various cardiometabolic disorders. This review brings to the scientific community and health professionals, updated information about the cardiovascular effects of hypothyroidism, its influence on physical

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Serum total antioxidant status and lipid peroxidation marker malondialdehyde levels in overt and subclinical hypothyroidism

Abstract: These results suggest an increased oxidative stress in both hypothyroid and subclinical hypothyroidism states, which can be explained by both the insufficient increase in the antioxidant status and the altered lipid metabolism in these cases.

Cited by 205 publications

References 41 publications

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

Decreased number of circulating endothelial progenitor cells in patients with Graves’ hyperthyroidism

Influência do exercício físico nas alterações cardiovasculares induzidas pelo hipotireoidismo

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