Thyroid hormone (T3) and its acetic derivative (TA3) protect low-density lipoproteins from oxidation by different mechanisms

Fauré, Philippe; Oziol, Lucie; Artur, Yves; Chomard, P

doi:10.1016/j.biochi.2004.04.009

Cited by 29 publications

(20 citation statements)

References 33 publications

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“…Гипотиреоз уже на ранней (субклинической) стадии ассоциируется с повышением риска развития ИБС, инфаркта миокарда, ХСН и смертности от сердечно-сосудистых заболеваний независимо от пола, возрас-та и предшествующих сердечно-сосудистых заболе-ваний [6].…”

Section: Rhythm and Conductivity In A Pa-tient With Hypothyroidism (Cunclassified

Complex Disorders of Heart Rhythm and Conductivity in a Patient With Hypothyroidism (Clinical Observation)

Козлова¹,

Кучма²,

Турмухамбетова³

et al. 2017

Arhivʺ vnutr. med.

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Section: Rhythm and Conductivity In A Pa-tient With Hypothyroidism (Cunclassified

Complex Disorders of Heart Rhythm and Conductivity in a Patient With Hypothyroidism (Clinical Observation)

Козлова¹,

Кучма²,

Турмухамбетова³

et al. 2017

Arhivʺ vnutr. med.

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“…Thyroid compounds may also chelate cell transition metals. Indeed, T 3 and TA 3 have been shown to disturb LDL Cu 2+ binding suggesting that they have chelating properties for this metal (Faure et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of in vitro macrophage-induced low density lipoprotein oxidation by thyroid compounds

Oziol¹,

Fauré²,

Bertrand³

et al. 2003

Journal of Endocrinology

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Oxidized low density lipoproteins (LDL) are highly suspected of initiating the atherosclerosis process. Thyroid hormones and structural analogues have been reported to protect LDL from lipid peroxidation induced by Cu 2+ or the free radical generator 2,2 -azobis-[2-amidinopropane] dihydrochloride in vitro. We have examined the effects of thyroid compounds on macrophage-induced LDL oxidation. Human monocyte-derived macrophages (differentiated U937 cells) were incubated for 24 h with LDL and different concentrations (0-20 µM) of 3,5,3 -triiodo--thyronine (T 3 ), 3,5,3 ,5 -tetraiodo-L-thyronine (T 4 ), 3,3 ,5 -tri-iodo--thyronine (rT 3 ), the T 3 acetic derivative (3,5,3 -tri-iodothyroacetic acid; TA 3 ) or L-thyronine (T 0 ) (experiment 1). Cells were also preincubated for 24 h with 1 or 10 µM of the compounds, washed twice, then incubated again for 24 h with LDL (experiment 2). Oxidation was evaluated by measurement of thiobarbituric acid-reactive substances (TBARS) and cell viability by lactate deshydrogenase release. In experiment 1, T 0 had no effect, whereas the other compounds decreased LDL TBARS production, but T 3 and TA 3 were less active than T 4 and rT 3 (IC 50 : 11·0 2·6 and 8·1 0·8 vs 1·4 0·5 and 0·9 0·3 µM respectively). In experiment 2, the compounds at 1 µM had no effect; at 10 µM, T 3 and rT 3 slightly reduced LDL TBARS production, whereas TA 3 and T 4 inhibited it by about 50% and 70% respectively. TBARS released by the cells were also highly decreased by T 3 , T 4 , rT 3 and TA 3 in experiment 1, but only by T 3 (30%) and T 4 (70%) in experiment 2. Cell viability was not affected by the compounds except slightly by TA 3 at 10 µM. The data suggested that the physicochemical antioxidant capacity of thyroid compounds was modulated by their action on the intracellular redox systems of macrophage. Overall cellular effects of T 3 led to a reduction of its antioxidant capacity whereas those of T 4 increased it. Thus T 4 might protect LDL against cellular oxidation in vivo more than T 3 .

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“…16 Faure et al also reported that T3 protects LDL from oxidation. 17 Thyroid hormones has been documented to affect HDL metabolism by enhancing cholesteryl ester transfer protein (CETP) activity which is involved in the conversion of cholesteryl esters from HDL2 to the very low density lipoproteins (VLDL) and TGs to the opposite direction. 18 Thyroid hormones have also been shown to induce lipoprotein lipase which catabolizes the TG-rich lipoproteins, and the hepatic lipase (HL).…”

Section: Introductionmentioning

confidence: 99%

“…[22][23][24] Lipid peroxidation is also affected by thyroid function with studies however showing controversial outcomes. [17][18][19][20][21][22][23][24][25] This study thus determines the effect of dysthyroidism on lipid profile, cardiac TNF-α and lipid peroxidation, and whether the effect is estradiol-dependent.…”

Section: Introductionmentioning

confidence: 99%

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

Ajayi¹,

Akhigbe²,

Ajayi³

2017

JCDR

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Background: It is a known fact that altered thyroid state is associated with cardiometabolic disturbances. Raised TNF-α and lipid peroxidation have also been reported to be involved in the pathogenesis of cardiometabolic disorders. Aim: The present study evaluates the effect of dysthyroidism on cardiac TNF-α and lipid peroxidation, and whether the effect is estradiol-dependent. Methods: Male white New Zealand rabbits were randomized into three groups; control, carbimazole-induced hypothyroidism, and levothyroxine-induced hyperthyroidism. Results: Dysthyroidism led to altered glucose metabolism and dyslipidaemia with elevated LDL, TNF-α, and MDA. There was also decreased HDL, GSH, catalase, and 17β-estradiol. Serum electrolytes and hemorheological variables were not significantly affected. Conclusion: These findings demonstrate that dysthyroidism-induced cardiometabolic disturbance is associated with elevated cardiac TNF-α and oxidative stress via an estradiol-dependent mechanism.

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Thyroid hormone (T3) and its acetic derivative (TA3) protect low-density lipoproteins from oxidation by different mechanisms

Cited by 29 publications

References 33 publications

Complex Disorders of Heart Rhythm and Conductivity in a Patient With Hypothyroidism (Clinical Observation)

Complex Disorders of Heart Rhythm and Conductivity in a Patient With Hypothyroidism (Clinical Observation)

Inhibition of in vitro macrophage-induced low density lipoprotein oxidation by thyroid compounds

Activation of Cardiac TNF-α in Altered Thyroid State-Induced Cardiometabolic Disorder

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