Effect of Thyroid Function on LDL Oxidation

Centro per lo Studio dell'Ipertensione Arteriosa, dell Dislipidemie e dell'Arteriosclerosi, University Gabriele D'Annunzio, School of Medicine, Chieti, Italy.
Arteriosclerosis Thrombosis and Vascular Biology (Impact Factor: 6). 06/1998; 18(5):732-7. DOI: 10.1161/01.ATV.18.5.732
Source: PubMed


In this study, the effect of different levels of thyroid hormone and metabolic activity on low density lipoprotein (LDL) oxidation was investigated. Thus, in 16 patients with hyperthyroidism, 16 with hypothyroidism, and 16 age- and sex-matched healthy normolipidemic control subjects, the native LDL content in lipid peroxides, vitamin E, beta-carotene, and lycopene, as well as the susceptibility of these particles to undergo lipid peroxidation, was assessed. Hyperthyroidism was associated with significantly higher lipid peroxidation, as characterized by a higher native LDL content in lipid peroxides, a lower lag phase, and a higher oxidation rate than in the other two groups. This elevated lipid peroxidation was associated with a lower LDL antioxidant concentration. Interestingly, hypothyroid patients showed an intermediate behavior. In fact, in hypothyroidism, LDL oxidation was significantly lower than in hyperthyroidism but higher than in the control group. Hypothyroidism was also characterized by the highest beta-carotene LDL content, whereas vitamin E was significantly lower than in control subjects. In hyperthyroidism but not in the other two groups, LDL oxidation was strongly influenced by free thyroxine blood content. In fact in this group, the native LDL lipid peroxide content and the lag phase were directly and indirectly, respectively, related to free thyroxine blood levels. On the contrary, in hypothyroidism LDL oxidation was strongly and significantly related to serum lipids. In conclusion, both hypothyroidism and hyperthyroidism are characterized by higher levels of LDL oxidation when compared with normolipidemic control subjects. In hyperthyroid patients, the increased lipid peroxidation was strictly related to free thyroxine levels, whereas in hypothyroidism it was strongly influenced by serum lipids.

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    • "Oxidative stress is well documented in hypothyroidism [22-24] and is even worsened through treatment with LT4[1,2]. The difference between the two conditions is that, in case of hypothyroidisms, oxidative stress is due to the reduction of AO [4], whereas, after the LT4 treatment it stems from overproduction of ROS from mitochondria [5,6]. "
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    ABSTRACT: Levothyroxine (LT4) treatment can lead to iatrogenic hyperthyroidism and oxidative stress that can cause patient discomfort. Oxidative stress is also recognized as one of the causes of chronic diseases and cancer. The prevalence of breast, colorectal, gastric and lung cancer in 18 Italian Regions during 2010 was correlated with the sales of LT4 in 2009. The cancer prevalence was analyzed in women aged 30--84. This age range corresponds to more than 80% of the consumers of the drug and to about 99% of all malignant cancers. The correlation between sales of LT4 and cancers was determined with the technique of Density Ellipses. The age and smoking contribution for lung cancer was determined with the Sequential test. No significant correlation was seen between LT4 sales and breast, colorectal and gastric cancers. A significant correlation was instead found for lung cancer (p < 0.05) corrected for smoking and age. LT4 consumption in Italy is about 0.7 boxes/women/year. There is a correlation between lung cancer and LT4 treatment and oxidative stress caused by LT4 supplementation can be one of the causes. Although we cannot exclude that dysthyroidism needing LT4 supplementation might be the ground for lung cancer itself and measuring oxidative stress could be helpful in avoiding excessive use of the drug.
    Reproductive Biology and Endocrinology 08/2013; 11(1):75. DOI:10.1186/1477-7827-11-75 · 2.23 Impact Factor
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    • "Besides the association with hypercholesterolemia, hypothyroidism can lead to intrinsic qualitative changes in circulating lipoproteins, thereby enhancing their atherogenicity [10]. The formation of oxidized LDL (oxLDL) in hypothyroidism can be attributed to increased LDLc levels [180] or, as recently suggested, to reduced serum paraoxonase 1 activity [181]. oxLDL contains lyso-phosphatidylcholine , a potent chemo-attractant for macrophages, leading to generation of foam cells; moreover, oxLDL up-regulates the expression of endothelial vascular cell adhesion molecules , increasing monocyte adhesion [182]. "
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    ABSTRACT: Endothelial dysfunction represents an important pathway thereby cardiovascular risk factors promote the development and progression of atherosclerosis. Hypothyroidism is associated with an increased cardiovascular risk, and the assessment of endothelium function is recognised an effective tool for the detection of evidence of preclinical cardiovascular alterations. Both vascular smooth muscle cells and endothelium play pivotal roles in modulating vascular tone and both are potential targets of thyroid hormone action. The pathogenesis of the association between endothelial dysfunction and hypothyroidism is complex and still not well established. The presence of traditional and emerging risk factors may contribute to the development of endothelium impairment, generating a chronic state of injury that triggers abnormal endothelial response. Levothyroxine replacement therapy is currently used for restoring euthyroidism and improving cardiovascular risk of hypothyroid patients. The decision to treat patients with subclinical hypothyroidism should depend on the presence of risk factors, rather than on a TSH threshold. However, the actual effectiveness of thyroid hormone substitution in reducing the risk of cardiovascular events, especially in subclinically hypothyroid patients, remains to be elucidated. Large multicenter, placebo-controlled prospective trials are necessary to address the issue. The article also discusses recent patents in this field.
    Recent Patents on Endocrine Metabolic & Immune Drug Discovery 05/2008; 2(2):79-96. DOI:10.2174/187221408784534222

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