Antioxidants Protect Cell Damage from Free Radicals: A research study on Thyroid Hormones in Wistar Rats (original) (raw)
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www.ijsr.net Role of Antioxidants on Thyroid Hormones in Wister Rats
2015
Abstract: It is estimated that huge amount of ROS, especially of H2O2, are produced in the thyroid under physiological conditions, justifying the statement that the thyroid gland is an organ of “oxidative nature”. The present research work aimed to investigate the free radical scavenging activity, lipid peroxidation and antioxidant status in both hyperthyroid and hypothyroid patients.Adult male Wister rats, weighing around 150-200 gms used in this study. Rats were maintained in the animal care facilities. Under veterinary supervision, food and water were supplied ad labium to the animals. All rats were fed with normal diet (20 % protein). Animal studies were performed in compliance with generally accepted guidelines governing such work. Rats have been administered with known amount of Vitamin C, Vitamin E and turmeric. Results showed increased levels of thyroxin in rats after 15 days. ( Vit C-5.2 ± 1.2 NS,Vit E- 5.3 ± 0.5 NS and Turmeric-5.3 ± 0.87 NS)
Role of Antioxidants on Thyroid Hormones in Wister Rats
2014
It is estimated that huge amount of ROS, especially of H2O2, are produced in the thyroid under physiological conditions, justifying the statement that the thyroid gland is an organ of “oxidative nature”. The present research work aimed to investigate the free radical scavenging activity, lipid peroxidation and antioxidant status in both hyperthyroid and hypothyroid patients.Adult male Wister rats, weighing around 150-200 gms used in this study. Rats were maintained in the animal care facilities. Under veterinary supervision, food and water were supplied ad labium to the animals. All rats were fed with normal diet (20% protein). Animal studies were performed in compliance with generally accepted guidelines governing such work. Rats have been administered with known amount of Vitamin C, Vitamin E and turmeric. Results showed increased levels of thyroxin in rats after 15 days. ( Vit C-5.2 ± 1.2 NS,Vit E 5.3 ± 0.5 NS and Turmeric-5.3 ± 0.87 NS)
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.
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...
Toxicology Reports, 2020
Hypothyroidism is the most frequent consequence of the interaction of a large variety of drugs, environmental pollutants and industrial chemicals with the thyroid gland. It is associated with diminished endocrine function which may lead to hyperlipidemia, diabetes, Alzheimer's disease, weight gain, and other metabolic disorders. The present study evaluates the pro-thyroid activity of a bioactive fraction from a polyherbal teabag in rats with hypothyroidism induced by propylthiouracil. The teabag was formulated to stimulate synthesis and/or release of T4 and affectthe conversion of T4 to T3. Phytoconstituents of the polyherbal teabag are potent antioxidants that may be responsible for the pro-thyroid activity. The tea-extract (1000 mg) was found to contain 1076 μg of gallic acid and 1131 μg of rutin from HPTLC analysis. Rats received propylthiouracil (8 mg/kg) for the first 15days followed by the polyherbal tea-extract (500, 1000 and 1500 mg/kg), the standard drug levothyroxine (0.1 mg/ kg), aerobic exercise, and a combination of tea-extract (1000 mg/kg) and aerobic exercise daily along with propylthiouracil for the next 30 days. Finally, rats received their respective treatments alone without propylthiouracil for 15 more days. Lipid profile and levels of glucose, insulin, T3, T4, TSH, cortisol, homocysteine, creatinine, uric acid, malondialdehyde, glucose-6 phosphatase, and endogenous antioxidants were determined. All treatments attenuated significantly the propylthiouracil-elevated TSH, homocysteine, creatinine, uric acid, glucose-6-phosphatase, insulin, and malondialdehyde levels, and restored favorably the propylthiouracil-altered lipid profile, T3, T4, and endogenous antioxidant levels. The polyherbal tea-extract (1000 and 1500 mg/kg) treatment and thecombination treatment of tea-extract (1000 mg/kg) with aerobic exercise displayed significant restoration of the suboptimalthyroid function. This may be due to a favorablemodulation ofthe hypothalamicpituitary-thyroid and the hypothalamic-pituitary-adrenal axes.
Dr. K.M.Priyadharshini., Asst Professor, PSG CAS Coimbatore and Dr.G.Vanithakumari.
Ciprofloxacin is a widely prescribed antimicrobial drug belonging to a class of drugs called quinolones. The first 1 – cyclopropyl theroquinolone ciprofloxacin was synthesized in 1983 (Wentland, 1990) and this drug was remarkable among the quinolones for its high activity. Currently, the most important benefit claimed for vitamins A, C and E is their role as antioxidants, which are scavengers of particles known as oxygen free radicals (or oxidants). According to Goldberg (2005) without sufficient vitamin A, thyroid gland cannot produce thyroxine. Vitamin A is a key nutrient to produce thyroxine (Gary Null, 2005), Vitamin C is necessary for tyrosine metabolism and it is quite a delicate balance (http://www.what reallyworks.co.uk /start / fact sheets.asp? article ID = 410). Vitamin E works with iodine for proper thyroid function (Earl Mindell, 2005). Development of the thyroid gland is controlled by the thyroid stimulating hormone (TSH) secreted by the hypothalamus; TSH is also called thyrotropin (The Medicine Journal, 2000). The main function of the thyroid gland is to synthesis the iodothyronine, hormone 3, 5, 3/ , 5/ tetraiodothyronine (T4, thyroxine) and 3, 5, 3/ triiodothyronine (T3). These are peptides containing iodine. The two most important hormones are T3 and T4, and these hormones are essential for life and have many effects on body metabolizing growth and development (Thyroid foundation of Canada, 1999).NSAIDs produce abnormal thyroid functions and there by alter the synthesis, transport and metabolism of thyroid hormones (Davis and Franklyn, 1991). They alter TSH response to TRH and thereby influence TSH release (Lim et al., 1995), and also compete for T3 binding sites in serum and at the cell surface, which act as T3 antagonists. Disturbances of the gastro intestinal tract are the most frequent side effects observed with fluoroquinolones and occur in about 5% of treated patients. Microsomal metabolism of ciprofloxacin generates free radicals. Free radicals formation might play a role in the mechanism of producing adverse effects. Microsomal metabolism of ciprofloxacin generates free radicals. Free radicals formation might play a role in the mechanism of producing adverse effects. Ciprofloxacin is a potent inhibitor of the thyroid hormone regulated P 450 enzyme system in the liver since ciprofloxacin and enoxacin have shown the greatest inhibitory capacity (Clinical Toxicology Review, 1997).
Effect of chronic excess iodine intake on thyroid function and oxidative stress in hypothyroid rats
Our objective was to investigate the effects of chronic excess iodine intake on thyroid functions and thyroid oxi-dative stress state in hypothyroid rats. Sixty rats were divided into euthyroid and hypothyroid (thiocyanate-induced) groups with or without administration of excess iodine (3000 or 6000 mg/L) for 8 weeks. Serum thyroxine (T 4), triiodothyronine (T 3), thyroid-stimulating hormone (TSH), thyroid antioxidants (catalase, superoxide dismutase enzymes, and total antioxi-dants), and lipid peroxide (malondialdehyde; MDA) were measured. Reverse transcription – PCR gene expression for thyroi-dal Na + /I – symporter (NIS), D1 deiodinase, and thyroid peroxidase (TPO) were performed. Thiocyanate significantly decreased thyroid hormones (T3, T4), increased lipid peroxides and antioxidants, and increased gene expression of NIS, D1 deiodinase, and TPO. Excess iodine intake in hypothyroid rats increased T3 and T4. Also, high iodine intake by hypothy-roid rats significantly decreased NIS, D1 deiodinase, and TPO genes expression. Excess iodine significantly increased MDA and antioxidants in euthyroid and hypothyroid rats. In conclusion, thiocyanate-hypothyroidism increases gene expression of NIS, TPO, and TPO and induces oxidative stress. High iodine intake decreases NIS and D1 deiodinase gene expression in hypothyroid rats. Moreover, excess iodine increase thyroid hormones, lipid peroxides, and antioxidants in hypothyroid rats. Résumé : Notre objectif était d'examiner les effets d'une prise chronique d'iode en excès sur les fonctions thyroïdiennes et sur l'état de stress oxydant de la thyroïde chez le rat hypothyroïdien. Soixante rats ont été divisés en groupes euthyroïdiens et hypothyroïdiens (induction par le thiocyanate), avec ou sans administration d'iode en excès (3000 ou 6000 mg/L) pendant 8 semaines. La thyroxine (T4), la triiodothyronine (T3) et l'hormone stimulant la thyroïde (TSH) sériques, les antioxydants de la thyroïde (catalase, superoxyde dismutase et antioxydants totaux) et le malondialdéhyde (MDA) ont été mesurés. Une analyse de l'expression génique du symporteur Na + /I – (NIS), de la déiodinase D1 et de la thyroperoxydase (TPO) a été réa-lisée par RT–PCR. Le thiocyanate a diminué significativement les niveaux d'hormones thyroïdiennes (T3, T4), augmenté les niveaux de peroxydes lipidiques et d'antioxydants, et augmenté l'expression génique du NIS, de la déiodinase D1 et de la TPO. Une prise d'iode en excès par les rats hypothyroïdiens augmentait les niveaux de T 3 et de T 4. Aussi, une forte prise d'iode diminuait significativement l'expression génique du NIS, de la déiodinase D1 et de la TPO chez les rats hypothyroï-diens. L'iode en excès augmentait de manière significative les niveaux de MDA et d'antioxydants chez les rats euthyroïdiens et hypothyroïdiens. En conclusion, l'hypothyroïdie induite par le thiocyanate augmente l'expression génique du NIS, de la diodinase D1 et de la TPO et induit un stress oxydant. Une prise d'iode à haute dose diminue l'expression génique du NIS et de la diodinase D1 chez les rats hypothyroïdiens. De plus, l'iode en excès augmente les niveaux d'hormones thyroïdien-nes, de peroxydes lipidiques et d'antioxydants chez les rats hypothyroïdiens.