Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects

Menzies, Keir J.; Robinson, Brian H.; Hood, David A.

doi:10.1152/ajpcell.00415.2007

Cited by 47 publications

(24 citation statements)

References 53 publications

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“…As a consequence of TH stimulation, increasing levels of mitochondrial activities of bio-energetic enzymes can subsequently enhance ATP generation [42]. According to our results, phosphine poisoning caused a 50% decline in cellular ATP reserve.…”

Section: Accepted Manuscriptsupporting

confidence: 52%

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

et al. 2015

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Section: Accepted Manuscriptsupporting

confidence: 52%

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

et al. 2015

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“…Columbano et al (16) reported that T3 stimulated the proliferation of hepatocytes in rat models of liver regeneration. T3 could reduce cellular oxidative stress, which may help attenuate reactive oxygen species (ROS)-mediated damage, along with improving mitochondrial function and energy status in cells with mitochondrial DNA defects (17). The NADH dehydrogenase flavoprotein 2 gene located on 18p11.22 encodes a component of mitochondrial complex 1.…”

Section: Ohkubo Et Almentioning

confidence: 99%

Hypothyroidism and Levothyroxine-responsive Liver Dysfunction in a Patient with Ring Chromosome 18 Syndrome

Ohkubo¹,

Ihara²,

Ohga³

et al. 2012

Thyroid

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Background: Ring chromosome 18 [r(18)] is a rare constitutional chromosomal aberration syndrome, characterized by dysmorphic face, hypoactivity, short stature, and delayed development. Autoimmune thyroiditis and immunoglobulin (Ig) A deficiency are occasionally associated with chromosome-18 deletion syndromes. Summary: Here, we report a 2-year-old male child with r(18) syndrome and a selective IgA deficiency ( < 1.6 mg/ dL, reference range [rr]: 20-149), who developed hypothyroidism and liver dysfunction. Thyroid function tests (thyroid-stimulating hormone [TSH]: 1031 lIU/mL, rr 0.43-4.0; free triiodothyronine: 0.52 pg/mL, rr 2.37-4.65; free thyroxine: 0.11 ng/dL, rr 1.03-2.00) and positive thyroid antibodies (anti-TSH receptor 1.7 IU/L, cut-off index [coi]: < 1.0, antithyroid peroxidase 171 IU/mL, coi < 0.3, and antithyroglobulin 2.8 IU/mL, coi < 0.3) indicated autoimmune hypothyroidism. Elevated levels of aspartate aminotransferase (AST, 240 IU/L, rr 17-39) and alanine aminotransferase (ALT, 315 IU/L, rr 4-23), but negative antibodies against LKM and mitochondrial M2, suggested no autoimmune hepatitis. Transaminase levels became normalized after he was given levothyroxine therapy to achieve the euthyroid state, but they repeatedly became elevated when levothyroxine was inadvertently discontinued (peak AST = 409 IU/L; peak ALT = 390 IU/L). A maintenance dose of levothyroxine has effectively maintained the euthyroid state and normalized liver function tests despite no immunosuppressive therapy. Conclusions: The r(18) patient with autoimmune hypothyroidism and IgA deficiency suffered from idiopathic hepatitis. The liver dysfunction was associated with hypothyroidism that resolved with thyroid hormone treatment. While the former combination has been described, the latter has not. The reason for the development of hepatitis in association with hypothyroidism is unexplained. However, we postulate that it might be related, in ways that are not clear, to the deleted genes of r(18).

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“…Available data showed that T3 could reduce oxidative stress and weaken the damage mediated by reactive oxidative species (ROS). 9 Antioxidant treatment is regarded as a potential effective measure to attenuate the oxidative stress. Pyrrolidine dithiocarbamate (PDTC), a metal chelator and antioxidant, is a specific inhibitor of NF-kB.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant therapy improves non-thyroidal illness syndrome in uremic rats

Yang

2016

Renal Failure

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Background The roles of antioxidant therapy on non-thyroidal illness syndrome (NTIS) in uremic rats is still unclear. Materials and methods Twenty-four Sprague-Dawley (SD) rats were randomly divided into blank, 5/6 nephrectomy (Nx), pyrrolidine dithiocarbamate (PDTC, 10 mg/100 g), sodium bicarbonate (SB, 0.1 g/100 g), N-acetylcysteine (NAC, 80 mg/100 g) and thyroid hormones (TH, levothyroxine 2 mg/100 g) groups. The serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), advanced oxidation protein products (AOPP), interleukin (IL)-1b, free triiodothyronine (FT3), and thyroid stimulating hormone (TSH) were detected in the sixth week. The expressions of IL-1b and deiodinase type 1 (DIO1) were assessed by western blotting. The nuclear factor kappa B (NF-kB) inflammatory signal pathway was confirmed by electrophoretic mobility shift assay (EMSA). Results Compared with 5/6 Nx group, PDTC and NAC significantly reduced the levels (p50.01, respectively) of serum MDA, AOPP, TSH, and elevated levels of serum SOD (p50.01, respectively) and FT3 (p ¼ 0.016 and p50.01). Neither had significant effects on serum IL-1b content (p ¼ 0.612 and p ¼ 0.582). PDTC and NAC markedly decreased the protein expression of IL-1b (p50.01) and increased the protein expression of DIO1 (p50.01), respectively. Both had been considerably blunted NF-kB activity (p50.01). Conclusions In uremic rat model, PDTC and NAC can effectively improve oxidative stress level and NTIS. In terms of improving oxidative stress level, NAC is probably superior to PDTC.

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Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects

Abstract: Menzies KJ, Robinson BH, Hood DA. Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects.

Cited by 47 publications

References 53 publications

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

Hypothyroidism and Levothyroxine-responsive Liver Dysfunction in a Patient with Ring Chromosome 18 Syndrome

Antioxidant therapy improves non-thyroidal illness syndrome in uremic rats

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