The Effect of Methimazole on the Oxidant and Antioxidant System in Patients With Hyperthyroidism

Ademoğlu, Evin; Gökkuşu, Cahide; Yarman, Sema; Azizlerli, H.

doi:10.1006/phrs.1998.0336

Cited by 33 publications

(28 citation statements)

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“…In agreement with the findings of others [8,35,36], we found serum vitamin E and plasma vitamin C levels were significantly reduced in hyperthyroid patients compared to control subjects. Vitamin E is a membrane antioxidant and takes part in conversion of superoxide radical and lipid peroxides to less toxic forms.…”

Section: Discussionsupporting

confidence: 82%

Effects of Propylthiouracil Treatment on Antioxidant Activities in Blood of Toxic Multinodular Goiter Patients

Özdem

Alicigüzel

Özdem³

et al. 2000

Pharmacology

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Erythrocyte, serum and plasma antioxidant activities and the effects of propylthiouracil (PTU) treatment on these activities were studied in patients with toxic multinodular goiter. The activities of the erythrocyte antioxidant enzymes (glucose-6-phosphate dehydrogenase, catalase, Cu/Zn-superoxide dismutase, selenium (Se)-dependent glutathione peroxidase and glutathione reductase) and the levels of erythrocyte Se, serum ceruloplasmin and plasma malondialdehyde were significantly higher while serum vitamin E, plasma vitamin C and plasma Se were lower in hyperthyroid patients. PTU treatment, not for 1 but for 3 months caused a partial reversal of antioxidant activities to euthyroid levels. It is suggested that alterations in blood antioxidant activities following PTU treatment might be due to the antioxidant and/or antithyroid effect of this drug.

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Section: Discussionsupporting

confidence: 82%

Effects of Propylthiouracil Treatment on Antioxidant Activities in Blood of Toxic Multinodular Goiter Patients

Özdem

Alicigüzel

Özdem³

et al. 2000

Pharmacology

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“…Vol. 63,2006 ≠ (11)(12)(13)(14)(15)(16) ≠ (12,14) ≠ (11,17) Ø (19) ≠ (15) ≠(45) (18)´ (19) Ø (35) Heart ≠ (14,18,(22)(23)(24) ≠ (14)´(44) ´ (24,34) Ø (32) EDL ´ (18,28) Soleus ≠ (18,25,28) Gastrocnemious ≠ (14,31) ≠ (14) White portion Ø (25) Hindlimb ≠ (33) Ø (33) Brain ≠ (20,21) ≠ (20) MLN ≠ (25) Thymus ≠ (25) Spleen ´ (25) Kidney ´ (32) Testis´ (27) Ø (27) ≠ (27) BAT ≠ (36) ´ (36) Blood ≠ (37)(38)…”

Section: Lipid Peroxidationunclassified

Thyroid hormone-induced oxidative stress

Venditti

Meo

2006

Cell. Mol. Life Sci.

336

230

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Hypermetabolic state in hyperthyroidism is associated with tissue oxidative injury. Available data indicate that hyperthyroid tissues exhibit an increased ROS and RNS production. The increased mitochondrial ROS generation is a side effect of the enhanced level of electron carriers, by which hyperthyroid tissues increase their metabolic capacity. Investigations of antioxidant defence system have returned controversial results. Moreover, other thyroid hormone-linked biochemical changes increase tissue susceptibility to oxidative challenge, which exacerbates the injury and dysfunction they suffer under stressful conditions. Mitochondria, as a primary target for oxidative stress, might account for hyperthyroidism linked tissue dysfunction. This is consistent with the inverse relationship found between functional recovery of ischemic hyperthyroid hearts and mitochondrial oxidative damage and respiration impairment. However, thyroid hormone-activated mitochondrial mechanisms provide protection against excessive tissue dysfunction, including increased expression of uncoupling proteins, proteolytic enzymes and transcriptional coactivator PGC-1, and stimulate opening of permeability transition pores.

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“…2A), the resident macrophages of the liver (29,39). In man, hyperthyroidism is characterized by significant changes in circulating parameters related to oxidative stress, including (i) higher levels of lipid peroxidation indicators (40)(41)(42)(43)(44)(45)(46)(47)(48)(49); (ii) enhancement in hydrogen peroxide and lipid hydroperoxide levels (49); and (iii) diminished levels of antioxidants such as a-tocopherol (41), coenzyme Q (44), ascorbic acid (41), and reduced thiols (42,46,50). These changes correlated with the enhancement in urinary lipid peroxidation products (40) and chemiluminescence response (51) and are either significantly reduced or normalized by thyrostatic therapy or antioxidant supplementation (40-46, 49, 50).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 99%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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The Effect of Methimazole on the Oxidant and Antioxidant System in Patients With Hyperthyroidism

Cited by 33 publications

References 0 publications

Effects of Propylthiouracil Treatment on Antioxidant Activities in Blood of Toxic Multinodular Goiter Patients

Effects of Propylthiouracil Treatment on Antioxidant Activities in Blood of Toxic Multinodular Goiter Patients

Thyroid hormone-induced oxidative stress

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

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