Antioxidants and methimazole in the treatment of Graves' disease: effect on urinary malondialdehyde levels

Guerra, Liliana N.; Molina, Marı́a del Carmen; Miler, Eliana A.; Moiguer, Silvia; Karner, Mirta; Burdman, J. A.

doi:10.1016/j.cccn.2004.08.020

Cited by 38 publications

(38 citation statements)

References 20 publications

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“…13 In previous reports, we have shown that hyperthyroid patients had higher malondialdehyde (MDA) content and superoxide dismutase (SOD) activity compared to euthyroid controls. 8, 14 We have reported that a combined treatment with methimazole and an antioxidant mixture (including vitamin C and vitamin E) improved the clinical manifestations of hyperthyroidism. 8 Even though we studied the effect of thyroid hormone in the oxidative metabolism of patients, we could not demonstrate that the hormone exerts a direct effect on oxidative metabolism by modifying some oxidative stress parameters.…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormone effect in human hepatocytes

et al. 2008

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We have already demonstrated that a combined treatment of methimazole and an antioxidant mixture improved the condition of hyperthyroid patients both biochemically and clinically. Elevated thyroid hormone levels might trigger signs and symptoms of hyperthyroidism through the increase of free radicals. To study the direct effect of thyroid hormone on cellular markers of oxidative stress, we carried out in vitro assays in which 0.1-20.0 nM T3 (6.5-1300.0 ng/dl) doses were added to culture media of the human hepatocyte cell line Hep G2 for 1-24 h. T3 increased malondialdehyde (MDA) and intracellular oxidized glutathione (GSSG) levels; SOD activity was also higher with hormone treatment, whereas catalase and glutathione peroxidase activities showed no variation at different T3 doses and during all experimental times. When ascorbic acid was added to the culture, the MDA level decreased and SOD activity was increased. With higher doses of T3 (e.g. 200 nM), cell death occurred (69% of apoptotic cells). The increase in SOD activity was not enough to overcome the effect of T3 since MDA and GSSG remained high during a 24-h experiment. We showed a beneficial effect of ascorbic acid when cells were exposed to a T3 dose of 20 nM, a higher level of hormone than that achieved in hyperthyroidism.

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Section: Introductionmentioning

confidence: 99%

Thyroid hormone effect in human hepatocytes

et al. 2008

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“…The majority of studies evaluating the effect of thyroid status in humans have been performed in hyperthyroid patients with GD, either under basal conditions or after restoration of euthyroidism with antithyroid drug (ATD) or radioiodine [14,15,16,17,18,19,20,21,22,23,24]. …”

Section: Thyroid Function and Oxidative Stressmentioning

confidence: 99%

Oxidative Stress in Graves Disease

Marcocci¹,

Leo²,

Altea³

2012

Eur Thyroid J

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Increased reactive oxygen species (ROS) generation and the consequent oxidative damage are involved in the development of several diseases, including autoimmune diseases. Graves’ disease is an autoimmune disorder characterized by hyperthyroidism and, less frequently, orbitopathy. Hyperthyroidism is characterized by increased oxidative stress. Untreated hyperthyroidism is associated with an increase of several parameters of oxidative stress and in most studies (but not all) by an increase of antioxidant defense enzymes. Restoration of euthyroidism with antithyroid drug is associated with a reversal of the biochemical abnormalities associated with oxidative stress. Animal and human studies suggest that increased ROS may directly contribute to some clinical manifestation of the disease, including orbitopathy. Antioxidants administered alone improve some clinical signs and symptoms of hyperthyroidism and, when associated with antithyroid drugs, induce a more rapid control of clinical manifestations and a faster achievement of euthyroidism. A large randomized clinical trial has shown that antioxidant supplementation (selenium) may also be beneficial for mild Graves’ orbitopathy.

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“…[10][11][12] More recently, there is growing evidence that oxidative stress plays an important role in the pathogenesis of Graves' disease. [13][14][15] Graves' disease is characterized by the overproduction of thyroid hormones, which can accelerate the basic metabolic rate and cellular oxidative metabolism by the induction of mitochondrial enzymes and causes ROS overproduction and an increase of oxidative stress. 16 Bednarek et al 17 reported that the increase in oxidative stress parameters, such as hydrogen peroxide, thiobarbituric acid-reactive substances, superoxide dismutase, and catalase in hyperthyroid patients can be normalized after euthyroidism achievement except those with infiltrative ophthalmopathy.…”

Section: Introductionmentioning

confidence: 99%