Thyroid status modulates glycoxidative and lipoxidative modification of tissue proteins

Pamplona, Reinald; Portero-Otı́n, Manel; Ruiz, César; Bellmunt, Marı́a Josep; Requena, Jesús R.; Thorpe, Suzanne R.; Baynes, John W.; Romero, María Cristina; López-Torres, Mónica; Barja, Gustavo

doi:10.1016/s0891-5849(99)00135-5

Cited by 50 publications

(31 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hepatocytes from ZDF rats exhibit increased lipogenesis, glycogen synthesis, and glycolysis and decreased gluconeogenesis, glycogenolysis, and fatty acid oxidation [11]. Hypothyroidism increases the lipid gain and decreases the fatty acid oxidation activity [13,22]. In addition, overt hypothyroidism is widely recognized as a risk factor for atherosclerosis by its association with different factors, including lipid disturbances [8,10].…”

Section: Discussionmentioning

confidence: 99%

Effects of Methimazole on the Onset of Type 2 Diabetes in Leptin Receptor-Deficient Rats

Hwang

Kim

et al. 2009

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

We investigated the effects of methimazole, an anti-thyroid drug, on the onset of type 2 diabetes in Zucker diabetic fatty (ZDF) rats. For this, 0.03% methimazole was administered to 7-week-old, pre-diabetic ZDF rats in drinking water for 5 weeks and the animals were sacrificed at 12 weeks of age. Methimazole treatment to ZDF rats significantly reduced blood glucose levels, food intake, body weight, and serum T3 levels. Hepatocytes in ZDF-methi rats were more densely stained with eosin than those in ZDF rats because of low fat accumulation in ZDF-methi hepatocytes. The pancreatic islet in ZDF-methi rats was normal compared to that in ZDF rats. Glucagon, not insulin, immunoreactivity in ZDF-methi rats was significantly higher than that in ZDF-methi rats. These suggest that methimazole treatment may delay the onset of type 2 diabetes in leptin receptor-deficient rats and also suggests that thyroid hormones may be necessary for the onset of diabetes.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Methimazole on the Onset of Type 2 Diabetes in Leptin Receptor-Deficient Rats

Hwang

Kim

et al. 2009

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

show abstract

“…≠, Ø, and´indicate hyperthyroid tissue levels increased, decreased and unchanged, respectively, in comparison with euthyroid controls. dehyde (MDA) and lysine residue in proteins, was found in T 3 -treated rats [19]. Although this might be viewed as an indication of decreased oxidative stress, the finding that protein degradation was the most relevant variable in determining the decrease in MDAL levels suggested increased oxidative stress in hyperthyroid liver [19].…”

Section: Lipid Peroxidationmentioning

confidence: 99%

“…Vol. 63,2006 ≠ (11)(12)(13)(14)(15)(16) ≠ (12,14) ≠ (11,17) Ø (19) ≠ (15) ≠(45) (18)´ (19) Ø (35) Heart ≠ (14,18,(22)(23)(24) ≠ (14)´(44) ´ (24,34) Ø (32) EDL ´ (18,28) Soleus ≠ (18,25,28) Gastrocnemious ≠ (14,31) ≠ (14) White portion Ø (25) Hindlimb ≠ (33) Ø (33) Brain ≠ (20,21) ≠ (20) MLN ≠ (25) Thymus ≠ (25) Spleen ´ (25) Kidney ´ (32) Testis´ (27) Ø (27) ≠ (27) BAT ≠ (36) ´ (36) Blood ≠ (37)(38)…”

Section: Lipid Peroxidationunclassified

Thyroid hormone-induced oxidative stress

Venditti

Meo

2006

Cell. Mol. Life Sci.

337

230

View full text Add to dashboard Cite

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.

show abstract

“…The latter indicates that the mitochondrial antioxidant defence system is considerably influenced by hypothyroidism. Pamplona et al (1999) suggest that thyroid hormones acting as physiologic modulators of tissue oxidative stress and protein degradation are more effective in cytosol, whereas DNA is more protected from oxidative damage. In humans, the low density lipoprotein (LDH) oxidation was shown to be significantly lower in hypothyroid than in hyperthyroid subjects (Constantini et al, 1998).…”

Section: Acta Veterinaria Hungarica 51 2003mentioning

confidence: 99%

Influence of hypothyroidism on lipid peroxidation, erythrocyte resistance and antioxidant plasma properties in rabbits

Brzezińska-Ślebodzińska

2003

Acta Veterinaria Hungarica

View full text Add to dashboard Cite

The effect of hypothyroidism on some oxidative stress parameters is reported. Moderate hypothyroid state was induced in two groups of female rabbits (3 and 12 months old) by giving 50 mg/kg body weight (BW) of propylthiouracil (PTU) per os for 6 days and 20 mg/kg BW of methimazole (MMI) for further 14 days. Serum T 4 and T 3 concentrations decreased by about 38-40 and 32-36%, respectively. The induced hypothyroidism resulted in a significant decrease in the serum concentration of the lipid peroxidation end-product malondialdehyde, as measured by the thiobarbituric-acid assay. Erythrocytes of hypothyroid animals exhibited higher resistance to oxidative stress, while submitted to free radicals generator 2,2'-azo-bis(2-amidinopropane) hydrochloride (AAPH) in vitro. Using two detector systems (phospholipid liposomes and deoxyribose), sensitive to either organic or inorganic oxygen radical damage, the ability of euthyroid and hypothyroid rabbit plasma to protect against oxygen radicals was evaluated. The plasma of hypothyroid animals showed about 20% higher ability to protect against iron-binding organic radicals, but about 50% lower chain-breaking antioxidant activity. The antioxidant capacity of plasma against inorganic radicals was not affected by hypothyroidism. In conclusion, the results show that thyroid hormones modulate the free-radical-induced oxidative damage of lipids and that hypothyroidism offers some protection against lipid peroxidation.Key words: Hypothyroidism, oxidative stress, lipid peroxidation, free radicals While the biochemical knowledge on free radical metabolism is well documented, there is little information on the endocrine control of oxidative stress. The involvement of thyroid hormones in lipid peroxidation and antioxidant enzyme activities has been studied mainly in liver tissue (Venditti et al

show abstract

Thyroid status modulates glycoxidative and lipoxidative modification of tissue proteins

Cited by 50 publications

References 43 publications

Effects of Methimazole on the Onset of Type 2 Diabetes in Leptin Receptor-Deficient Rats

Effects of Methimazole on the Onset of Type 2 Diabetes in Leptin Receptor-Deficient Rats

Thyroid hormone-induced oxidative stress

Influence of hypothyroidism on lipid peroxidation, erythrocyte resistance and antioxidant plasma properties in rabbits

Contact Info

Product

Resources

About