Oxidative DNA Base Damage, Antioxidant Enzyme Activities and Selenium Status in Highly Iodine-deficient Goitrous Children

Abstract

The objective of this study was to investigate oxidative DNA damage, and the levels of antioxidant enzymes (AOE) and selenium (Se) in relation to iodine deficiency and/or goiter in children. The study was performed in a group of goitrous high school children (15 -18 years of age) ðn ¼ 14Þ with severe or moderate iodine deficiency. Thyroid hormones (TSH, FT 4 , TT 4 , FT 3 , TT 3 ), urinary iodine (UI) and plasma Se levels, and erythrocyte glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were determined and compared with those of a control group consisting of nongoitrous high school children ðn ¼ 14Þ with normal UI levels or mild iodine deficiency. In the goitrous group, concentrations of FT 4 , TT 4 , plasma Se and UI, and activities of GSHPx and SOD were found to be significantly lower. Six typical hydroxyl radical-induced base lesions in genomic DNA of peripheral blood were identified and quantified by gas chromatography/isotope-dilution mass spectrometry (GC/IDMS), and higher levels of DNA base lesions were observed in the goitrous group. The results suggest that highly iodine-deficient goitrous children may be under oxidative stress, which may lead to greater level of oxidative damage to DNA. This study supports the evidence for the reported relationship between iodine deficiency and the increased incidence of thyroid malignancies.

Thyroid volume, goiter prevalence, and selenium levels in an iodine-sufficient area: a cross-sectional study

“…The abnormality of iodine and selenium nutrition in populations can result in thyroid dysfunction and abnormal thyroid structure. Studies have shown that concurrent severe selenium and iodine deficiency can lead to an increase in thyroid volume and/or TSH levels [4-6], possibly because thyroid iodine deficiency stimulates the synthesis of thyroid hormones, under TSH control, leading to an increased production of hydrogen peroxide , which is the electron acceptor for the thyroid peroxidase reaction in the synthesis of thyroid hormones. However, when produced excessively, hydrogen peroxide is toxic for thyroid cells [18].…”

“…Researchers have investigated the relationship between thyroid volume, goiter, and serum selenium, but some have not taken into account the influence of iodine nutrition status on thyroid volume. Some trials have investigated populations with concurrent iodine deficiency [4-6], while others have failed to describe the iodine status of a population [7]. However, iodine nutritional status in a population seems to be a key factor in maintaining normal thyroid volume and function [8,9].…”

Diagnostic and Therapeutic Significance of the Oxidative Stress Parameters in Children

“…Diabetes mellitus (19-23), glutathione synthetase deficiency (24), hyperthyroidism (25), iodinedeficient goiter (26), mitochondrial disorder (27,28), multimetabolic syndrome (29), phenylketonuria (30) and X-linked adrenoleukodystrophy (31) are endocrinologic/metabolic diseases in children where the link with oxidative stress has also been shown.…”

Trace elements in growth: Iodine and selenium status of Turkish children

“…Prevalence of goiter was 39.6%, and goitrous group consisting ''severely and moderately iodine-deficient'' children had significantly lower Se levels and antioxidant enzyme (AOE: erythrocyte GSHPx, SOD and CAT) activities than their non-goitrous ''normal in iodine status or mildly iodine-deficient'' controls (NMID-C). Modified DNA base levels (8-OH-Gua, 5-OH-Cyt, 8-OH-Ade) were also found to be significantly higher in the goitrous group [28]. These results, thus, indicated the presence of an oxidative activity and enhancement of free radical reactions in severely plus moderately iodine-deficient goitrous children.…”