Thyroid hormones mediate metabolic rate and oxidative, anti-oxidative balance at different temperatures in Mongolian gerbils (Meriones unguiculatus) (original) (raw)
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Thyroid Hormones in Excess Induce Oxidativestress in Rats
Acta Endocrinologica (Bucharest), 2009
Thyroid hormones play a crucial role in the regulation of the mitochondrial oxidative metabolism. Hyperthyroidism caused by the acceleration of the energy metabolism leads to the occurrence of cellular oxidative stress. The aim is to evaluate the pro-oxidant / antioxidant balance and the effect of vitamin E supplementation in damage caused by the excessive administration of thyroid hormones. Materials and Methods. White, male Wistar rats were used in the study. Thirty male Wistar rats were divided into three groups (1:control group, 2:animals treated with L-Thyroxine 10 µg/animal/day for 30 days, 3:L-Thyroxin treated rats protected with vitamin E 10 mg/animal/day). Malondialdehyde (MDA), the marker of lipid peroxidation, carbonyl proteins, SH groups, glutathione (GSH) and superoxide dismutase (SOD) were determined from the serum, while MDA, carbonyl proteins, SH groups and GSH were determined from the thyroid tissue homogenates. The results showed increased levels of carbonyl proteins (1.31±0.33 nmol/mg protein, p=0.0001) in serum in thyrotoxic group versus control, while MDA levels did not differ significantly from the control. Significantly low values of the SH groups, GSH and SOD were found (p<0.001) in the plasma of Thyroxin treated rats. Vitamin E supplementation significantly increased plasma MDA levels in the Thyroxin treated group as compared with the control group (p=0.01) and with the animals treated only with Thyroxin (p=0.04). Carbonyl protein levels in plasma of the hyperthyroid supplemented rats were also increased as compared to controls (p=0.0002). Antioxidant capacity markers in plasma of group 3 were decreased compared with group 1. The marker of lipid peroxidation (MDA) significantly decreased in thyroid homogenates of the group 2 as compared with group 1 (p=0.004). Significantly high levels of the SH groups (p=0.0006) and low levels of GSH (p=0.0001) were found in thyroid homogenates of the L-Thyroxin treated group as compared with controls. These results suggest that experimental hyperthyroidism is accompanied with increased oxidative stress and with the consumption of antioxidant enzymes in induced oxidative aggressions. No protective effects of vitamin E on oxidative stress induced by excessive administration of thyroid hormones were detected.
The impact of thyroid activity variations on some oxidizing-stress parameters in rats
Comptes Rendus Biologies, 2007
The effect of the thyroid activity on the formation of lipid peroxidation and on liver and heart antioxidant enzyme activities was investigated in Wistar rats. Hypothyroidism and hyperthyroidism conditions were induced for five weeks by the administration of 0.05% benzythiouracile (BTU) and L-thyroxine sodium salt (0.0012%), in drinking water, respectively. No significant effect was observed on the rates of both lipid peroxidation and the vitamin E in hepatic and cardiac tissues of hypothyroidism rats compared to the controls, contrary to the hyperthyroidism rats, which expressed a pronounced increase. The increased glutathione peroxydase activity in rats suffering from hyperthyroidism was associated with a fall of the reduced glutathione in the homogenate and a marked increase in the glutathione reductase activity. An increase in superoxyde dismutase and catalase activities was also recorded in hyperthyroidism. Our results explain the thyroid activity variation in relation to the lipid peroxidation and the tissular contents of the enzymatic and the non-enzymatic antioxidants. To conclude, our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism. To cite this article: M.
Protein oxidation in thyroid hormone-induced liver oxidative stress: relation to lipid peroxidation
Toxicology Letters, 1999
The influence of thyroid hormone administration (daily doses of 0.1 mg of 3,3%,5-triiodothyranine (T 3)/kg for 1-3 consecutive days) on rat liver protein oxidation was investigated in relation to the calorigenic and lipid peroxidative actions of the hormone. T 3 treatment elicited a progressive enhancement in the serum levels of the hormone, the rectal temperature of the animals, and in the rate of O 2 uptake of the liver, changes that are significantly correlated and evidence the development of thyroid calorigenesis. Liver lipid peroxidation was augmented by T 3 administration as determined by the tissue content of thiobarbituric acid reactants, with a maximal effect (3.1-fold increase) being found at 2 days after treatment, whereas protein oxidation measured by the content of protein hydrazone derivatives exhibited a maximal 88% increase at 3 days. Maximal rates of lipid peroxidation occur at 1 day after the administration of T 3 , whereas those of protein oxidation are attained after treatment with three daily doses of T 3 , time at which the former levels off. It is concluded that T 3 administration induces a substantial enhancement in hepatic protein oxidation, in addition to lipid peroxidation, that seems to be due to the higher oxidative stress status conditioned in the liver by thyroid calorigenesis. Both processes exhibit a differential time course of changes, that may represent differences in the susceptibility of target molecules to free radical attack and/or in the efficiency of repair mechamisms.
Journal of Experimental Biology, 2009
SUMMARYWe compared the changes in tissue aerobic metabolism and oxidative damage elicited by hypothyroid rat treatment with T3 and its analog GC-1. Aerobic capacities, evaluated by cytochrome oxidase activities, were increased more by T3 than by GC-1. Furthermore, the response of the tissues to T3 was similar, whereas the response to GC-1 was high in liver,low in muscle and scarce in heart. Both treatments induced increases in ADP-stimulated O2 consumption, which were consistent with those in aerobic capacities. However, unlike T3, GC-1 differentially affected pyruvate/malate- and succinate-supported respiration, suggesting that respiratory chain components do not respond as a unit to GC-1 stimulation. According to the positive relationship between electron carrier levels and rates of mitochondrial generation of oxidative species, the most extensive damage to lipids and proteins was found in T3-treated rats. Examination of antioxidant enzyme activities and scavenger levels did not c...
Journal of Endocrinology, 1997
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 susceptib...
Journal of Medical Biochemistry, 2015
Background: Oxidative stress plays a role in the pathogenesis of many chronic diseases. It is recognized in overt hypothyroidism while its existence in subclinical hypothyroidism (SCH) is not well established. The aim of this study was to determine whether there was increased oxidation of lipids and proteins in SCH, and examine their association with lipids and thyroid hormones. Methods: Male adults (35-59 years) with SCH (n=467) and euthyroid controls (n=190) were studied. Anthropometric measurements, plasma lipids, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total antioxidant capacity (T-AOC), lipid peroxidation products, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and dityrosine concentrations were measured. Results: Plasma concentrations of MDA were significantly higher (p<0.05) in SCH (8.11±1.39 nmol/mL) compared with euthyroid controls (7.34±1.31 nmol/mL) while AOPP, dityrosine and T-AOC levels were not different. MDA was not associated with TSH (b=-0.019, P=0.759), FT4 (b=-0.062, P=0.323) and FT3 (b=-0.018, P=0.780) in SCH while levels increased with elevated total cholesterol (b=0.229, P=0.001), LDL (b=0.203, P=0.009) and triglycerides (b=0.159, P=0.036) after adjustment for age Kratak sadr`aj Uvod: Oksidativni stres u~estvuje u patogenezi mnogih hro-ni~nih oboljenja. Ima ulogu u manifestnoj hipotireozi, dok njegovo prisustvo u subklini~koj hipotireozi (SH) nije sasvim razja{njeno. Cilj ove studije bio je da se odredi da li postoji povi{ena oksidacija lipida i proteina u SH i da se istra`i njihova povezanost sa lipidima i tireoidnim hormonima. Metode: Ispitivani su odrasli mu{karci (35-59 godina) sa SH (n=467) i eutireoidne kontrolne osobe (n=190). Izmereni su antropometrijski parametri, koncentracije lipida u plazmi, tireostimuli{u}eg hormona (TSH), slobodnog tiroksina (FT4), slobodnog trijodtironina (FT3), ukupni antioksidantni kapacitet (T-AOC), proizvodi lipidne peroksidacije, malondialdehid (MDA), uznapredovali proizvodi proteinske oksidacije (AOPP) i ditirozin. Rezultati: Koncentracije MDA u plazmi bile su zna~ajno povi{ene (p<0,05) u SH (8,11±1,39 nmol/mL) u pore-|enju sa eutireoidnim kontrolnim osobama (7,34±1,31 nmol/mL) dok se nivoi AOPP, ditirozina i T-AOC nisu razlikovali. MDA nije bio povezan sa TSH (b=