Thyroid hormone-induced oxidative stress

Abstract

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.

Regulation of oxidative stress and lipid peroxidation in PTU induced mice, treated with Pyrroloquinoline quinone (PQQ)

“…These observations corroborate with the earlier reports, where free radical scavenging property of PQQ has been highlighted (Misra et al, 2004;Shrivastava et al, 2010).With other two concentrations of PQQ (1 and 5 mg /kg) also, LPO was inhibited in the tissues of all the studied organs, with a significant elevation in SOD and CAT. Some workers suggest that hypothyroidism protects tissues against accelerated lipid peroxidation, although the data concerning oxidation / antioxidation in hypothyroidism are incomplete and contradictory (Isman et al, 2003;Venditti and Di Meo, 2006). In fact, Dariyerli et al, (2004) did not find any change in the content of malondialdehyde in rats with thiamizoleinduced hypothyroidism.…”

“…Further, thyroid dysfunction is postulated to be closely related to ROS formation, which might account for thyroid hormone-induced tissue damage. It is also known that thyroid dysfunction increases LPO reactions and ROS (Venditti and Di-Meo, 2006;Messarah et al, 2010). LPO is an autocatalytic mechanism leading to oxidative destruction of cellular membranes (Asayama and Kato, 1990 Jena et al 2012), it was thought that the compound may ameliorate hypothyroidism induced oxidative damage also.Because of this presumption and keeping in mind the unavailability of scientific literature on the role of PQQ in the regulation of thyroid dysfunctions, the present study was undertaken to evaluate the role of PQQ, if any , in ameliorating 6-n-propyl-2-thiouracil (PTU) induced oxidative damage in different organs.…”

Dose-Dependent Protective Effect of L-Carnitine on Oxidative Stress in the Livers of Hyperthyroid Rats

“…Earlier experimental and clinical studies have shown that hyperthyroidism caused both an elevation in the production of free oxygen radicals and an abnormal oxidative status of the organism [4,22]. Rybus-Kalinowska et al [3] reported that the pre-treatment levels of plasma MDA, which was used as an oxidative stress biomarker, were significantly higher in women with hyperthyroidism and that antithyroid therapy led to the normalization of the plasma MDA levels.…”

Oxidative Stress and Antioxidant Status in Hypo- and Hyperthyroidism

“…In examining antioxidant changes found in hyperthyroid tissues, it needs to be underscored that although thyroid hormone can directly control levels of enzymes with antioxidant activity or regulate scavenger content, antioxidant depletion could not be the cause, but the consequence of the oxidative stress. The effects of thyroid hormone on antioxidant status have been extensively investigated in rat tissues, while a few data concerning other species are available [159].…”