Oxidative muscular injury and its relevance to hyperthyroidism

Asayama, Kohtaro; Kato, Kiyohiko

doi:10.1016/0891-5849(90)90077-v

Cited by 137 publications

(82 citation statements)

References 114 publications

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“…It has been shown for more than ten years that exhaustive exercise increases levels of lipid peroxidation in skeletal muscle, this being generally thought to be related to the pathogenesis of exercise myopathy [1]. Previously we found that muscle atrophy induced by immobilization is also accompanied by oxidative stress; thiobarbituric acidreactive substance (TBARS) and oxidized glutathione (GSSG) were increased and total glutathione (GSH) was decreased in atrophied muscle [2].…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress during recovery from muscle atrophy

et al. 1993

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Single ankle joints of male Wistar rats (15-week-old) were immobilized in the extended position for 7 days and remobilized for 5 days after the immobilization period. Atrophic and contralateral soleus, typical slow red muscles, were collected and their levels of thiobarbituric acid-reactive substance (TBARS) and glutathione were measured. Five-day remobilization did not increase muscle weight significantly. However, there were significant increases in TBARS and oxidized glutathione in the recovering muscle, which strongly suggested that enhanced oxidative stress occurred during the recovery from disuse muscle atrophy. Vitamin E injection accelerated the recovery from atrophy, thus showing that oxidative stress slowed it down.

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Section: Introductionmentioning

confidence: 99%

Oxidative stress during recovery from muscle atrophy

et al. 1993

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“…One of the major effects of thyroid hormone is to increase mitochondrial respiration through changes in the number and activity of mitochondrial respiratory chain components (Roodyn et al 1965, Nishiki et al 1978. A hypermetabolic state due to hyperthyroidism has been shown to accelerate reactive oxygen metabolite production in the mitochondria and to induce changes in the antioxidant system of the tissues (Asayama & Kato 1990, Venditti et al 1997. Hypermetabolism induced by thyrotoxicosis is known to aggravate oxidant-mediated tissue injury.…”

Section: Introductionmentioning

confidence: 99%

Methimazole-induced hypothyroidism in rats ameliorates oxidative injury in experimental colitis

Isman¹,

Yeğen²,

Ali̇can³

2003

Journal of Endocrinology

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Depression of metabolism by hypothyroidism decreases oxidant production and thus protects tissues against oxidant damage. Moreover, it is well-known that abnormal gut motility is a common manifestation in hypo/ hyperthyroidism. In this study, we aimed to investigate the putative beneficial effects of methimazole on oxidative injury and dysmotility in a rat colitis model. Methimazole (0·04%) was administered in drinking water starting 15 days prior to induction of colitis. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (30 mg/ml; 0·8 ml) in ethanol. Six days after the induction of colitis, the fecal output was measured and used as an index for colonic motility. All rats were decapitated on the seventh day. The distal colon was weighed and the mucosal lesions were scored. Colonic lipid peroxidation (LP) and glutathione (GSH) measurements were performed. The macroscopic score, the colonic wet weight and LP values of the euthyroid colitis group were found to be higher than those of the control group (P<0·05-0·001). All these parameters were reduced in the methimazoletreated colitis group (P<0·01-0·001). The decrease in colonic GSH levels in the colitis group was completely abolished in the methimazole-treated colitis rats (P<0·01). Induction of colitis increased the average fecal output compared with the control group (P<0·05) and methimazole in the colitis group exaggerated the fecal output (P<0·001). In conclusion, methimazole reduces colonic oxidative injury probably due to hypometabolism, which is associated with a decrease in the production of reactive oxygen intermediates and an increase in the response of antioxidant systems.

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“…The previous biochemical studies carried out in animals by inducing hyperthyroidism show products of lipid peroxidation as indicators of oxidative stress in case of thyroid dysfunction, which are indirect markers of ROS generation (1,4,7,10,21). Moreover, in many cases, lipid peroxidation is a secondary phenomenon (25) and this does not therefore directly indicate an important role for oxidative stress in the disease concerned.…”

Section: Discussionmentioning

confidence: 99%

Flow‐cytometric analysis of reactive oxygen species in peripheral blood mononuclear cells of patients with thyroid dysfunction

Sarkar

Varshney

Chopra

et al. 2005

Cytometry Part B Clinical

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Background: Thyroid hormones are major regulators of energy metabolism and increased levels of the hormones (hyperthyroidism) results in an increase in the metabolic rate. Thyroid dysfunction causing alteration in hormone secretion leads to perturbations in the metabolic status. The hypermetabolic state may cause increased generation of reactive oxygen species (ROS), leading to oxidative stress in these patients. This study was carried out to verify our proposition by measuring the ROS in the terminally differentiated cells like the peripheral blood mononuclear cells of the patients.Methods: Flow-cytometric analysis of the ROS was carried out using 2 0 ,7 0 dichlorofluorescein diacetate in the isolated peripheral blood mononuclear cells of the subjects.Results: ROS generation was found to be 3-folds higher in hyperthyroids as compared with euthyroids and hypothyroids and this was not found to be gender specific.Conclusions: Hyperthyroidism results in ROS generation in patients, which can be detected flow cytometrically in the peripheral blood mononuclear cells. Hence, this could complement the other thyroid function tests facilitating the diagnosis and design of appropriate therapy. q 2005 International Society for Analytical Cytology

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Oxidative muscular injury and its relevance to hyperthyroidism

Cited by 137 publications

References 114 publications

Oxidative stress during recovery from muscle atrophy

Oxidative stress during recovery from muscle atrophy

Methimazole-induced hypothyroidism in rats ameliorates oxidative injury in experimental colitis

Flow‐cytometric analysis of reactive oxygen species in peripheral blood mononuclear cells of patients with thyroid dysfunction

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