Effect of thyroid state on lipid peroxidation, antioxidant defences, and susceptibility to oxidative stress in rat tissues

Abstract

The effects of altered thyroid states on lipid peroxidation, antioxidant capacity, and susceptibility to oxidative stress of rat tissues were examined. Hypothyroidism was induced by administering methimazole in drinking water for 15 days. Hyperthyroidism was elicited by a 10-day treatment of hypothyroid rats with tri-iodothyronine (10 micrograms/100 g body weight). In tissues of hypothyroid rats the lipid peroxidation was not modified, whereas in hyperthyroid rats lipid peroxidation increased in liver and heart but not in skeletal muscle. The glutathione peroxidase activity increased significantly in heart and muscle of hypothyroid rats and in muscle of hyperthyroid rats. The glutathione reductase activity was not modified in tissues of hypothyroid and hyperthyroid rats. In both rat groups the whole antioxidant capacity of tissues decreased, but significantly only in liver and heart. The results obtained studying the response to oxidative stress in vitro indicated that the susceptibility to oxidative challenge was increased in all tissues of hyperthyroid rats and in heart and muscle of hypothyroid animals. These results are explainable in terms of tissue variations in haemoprotein content and/or of antioxidant capacity. Since it has been reported that hypothyroidism offers in vivo protection against free radical damage, we suggest that such an effect could be due to greater effectiveness of cellular defence systems different from antioxidant ones.

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

“…In addition, Kupffer cells isolated from acutely T 3 -treated rats exhibited upregulation of UCP2 mRNA, which may limit mitochondrial ROS production by these cells (30). Consequently, T 3 -induced ROS production is associated with diminution in antioxidant defenses (28,(31)(32)(33), thus increasing the oxidative stress status in the liver with enhancement of hepatic lipid peroxidation (22,28,(34)(35)(36), protein carbonylation (37), and DNA oxidation (38). This pro-oxidant state induced in the liver of experimental animals by thyroid hormone administration is considered as a mild redox alteration, considering the lack of occurrence of morphological changes in liver parenchyma, except for significant hyperplasia and hypertrophy of Kupffer cells ( Fig.…”

Comparison of therapeutic effects of L-Thyroxin, apelin and a combination of both on antioxidant enzymes in the heart of PTU-induced hypothyroid rats

“…Findings about stress oxidative and activity of antioxidants in hypothyroidism are limited and controversial. There are some data that show in patients with hypothyroidism, oxidative stress, is increased (Lampka et al 2006;Sarandol et al 2005), decreased (Venditti et al 1997) or remain unchanged (Coria et al 2009). In agreement with the results of the current study, Reddy, et al demonstrated that the serum level of MDA and GPx activity increase in hypothyroid and subclinical hypothyroid patients (Reddy et al 2013).…”

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

“…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.…”

“…Thyroid hormones are the major regulators of oxidative energy metabolism (1) at the level of the mitochondrion (2) inducing increase in oxygen consumption (3) and heat production in mammalian tissues (4,5) and are responsible for increased metabolic rate (6) in hyperthyroidism. Therefore, excess secretion of thyroid hormone or hyperthyroidism leads to hypermetabolic state, causing accelerated mitochondrial electron transport that could enhance generation of reactive oxygen species (ROS), thereby leading to oxidative stress.…”