Effects of Iodotyrosines, Thyronines, Iodothyroacetic Acids and Thyromimetic Analogues on In Vitro Copper-Induced Oxidation of Low-Density Lipoproteins

Chomard, P; Séguin, Carole; Loireau, Annie; Autissier, N; Artur, Yves

doi:10.1016/s0006-2952(97)00675-8

Cited by 7 publications

(11 citation statements)

References 30 publications

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“…It has been reported that thyroid hormones and structural analogues limited in vitro LDL oxidation induced by Cu 2+ (Hanna et al 1993, Chomard et al 1998 or human endothelial cells (Hanna et al 1995). Here, we show that it was also true using the free radical generator, AAPH, and that thyroid compounds revealed free radical scavenging properties.…”

Section: Discussionsupporting

confidence: 68%

“…However, it may be suspected that thyroid compounds also disturb Cu 2+ binding on apolipoprotein B100. Indeed, during Cu 2+ -induced LDL oxidation (Chomard et al 1998), i) TA 3 had a much greater antioxidant effect than T 3 , whereas it was similar in the present study, ii) TA 4 strongly decreased V max by about 80%, more than T 3 (45%), whereas it only decreased it by 9% here, and iii) rT 3 had an antioxidant effect similar to that of T 3 , whereas it had practically no effect here.…”

Section: +supporting

confidence: 72%

“…They found that thyroxine (T 4 ), 3,5,3 -tri-iodothyronine (T 3 ) and 3,3 ,5 -tri-iodothyronine (rT 3 ) similarly decreased Cu 2+ -induced LDL oxidation. Using the same pro-oxidant system, we previously showed that not only thyroid hormones, but also their acetic derivatives and thyronines lacking iodine, had LDL-antioxidant properties (Chomard et al 1998). More precisely, our data suggested that the antioxidant efficiency was related to the 4 -hydroxydiphenylether structure and depended upon the nature and the position of substituents in this structure.…”

Section: Introductionsupporting

confidence: 52%

“…The plasma was supplemented with 1 g/l EDTA-Na 2 . LDLs (density 1·019-1·063 g/m) were immediately isolated by density-gradient ultracentrifugation at 4 C, as previously described (Chomard et al 1998). Fresh LDLs were kept under argon and in darkness at 4 C for up to 15 days.…”

Section: Aaph-induced Ldl Oxidation Experimentsmentioning

confidence: 99%

See 3 more Smart Citations

In vitro free radical scavenging capacity of thyroid hormones and structural analogues

Oziol¹,

Fauré²,

Vergely³

et al. 2001

Journal of Endocrinology

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It was reported that thyroid hormones decreased Cu 2+ -induced low-density lipoprotein (LDL) oxidation in vitro. Here, we investigated free radical scavenging capacities of thyroid hormones (3,5,3 -tri-iodo-L-thyronine (T 3 ), thryoxine (T 4 ) and 3,3 ,5 -tri-iodo-L-thyronine (rT 3 )) and structural analogues (L-thryonine (T 0 ), 3,5,3 -tri-iodothyroacetic acid (TA 3 ) and 3,5,3 ,5 -tetraiodothyroacetic acid (TA 4 )), using three different models of free radical generation. T 0 , T 3 and TA 3 slowed down production of conjugated diene and thiobarbituric acidreactive substances during LDL oxidation by 2,2 -azobis-[2-amidinopropane] (water-soluble), whereas rT 3 , T 4 and TA 4 had practically no effect. In this system, T 0 was the more active compound. Using a 1,1-diphenyl-2-picrylhydrazyl (lipid-soluble) test, all compounds also revealed free radical scavenging capacities, but rT 3 , T 4 and TA 4 were more active than T 0 , T 3 and TA 3 . T 3 was able to scavenge superoxide anion and hydroxyl radicals generated in an aqueous phase by a xanthine-xanthine oxidase system, as measured by electron paramagnetic resonance spectroscopy. It may be concluded that: (1) thyroid hormones and analogues with a 4 -hydroxy diphenylether structure have free radical scavenging capacities, (2) this property is influenced by the number of iodines on the phenolic ring, and (3) thyroid hormone scavenging capacity should not be the only mechanism explaining their protective effect on Cu 2+ -induced LDL oxidation. The physiological significance of the findings is discussed.

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Section: Discussionsupporting

confidence: 68%

Section: +supporting

confidence: 72%

Section: Introductionsupporting

confidence: 52%

Section: Aaph-induced Ldl Oxidation Experimentsmentioning

confidence: 99%

See 2 more Smart Citations

In vitro free radical scavenging capacity of thyroid hormones and structural analogues

Oziol¹,

Fauré²,

Vergely³

et al. 2001

Journal of Endocrinology

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show abstract

“…Thyroid hormones and structural analogues have been shown to decrease the in vitro LDL oxidation induced by cuprous ions (Cu 2+ ) (Hanna et al 1993, Chomard et al 1998, the free radical generator 2,2 -azobis-[2-amidinopropane] dihydrochloride (AAPH) (Oziol et al 2001) or human endothelial cells (Hanna et al 1995). However, their effect on macrophage-induced LDL oxidation is unknown.…”

Section: Introductionmentioning

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

Fauré¹,

Oziol²,

Artur³

et al. 2004

Biochimie

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Effects of Iodotyrosines, Thyronines, Iodothyroacetic Acids and Thyromimetic Analogues on In Vitro Copper-Induced Oxidation of Low-Density Lipoproteins

Cited by 7 publications

References 30 publications

In vitro free radical scavenging capacity of thyroid hormones and structural analogues

In vitro free radical scavenging capacity of thyroid hormones and structural analogues

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

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

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