The Minimal Arsenic Concentration Required to Inhibit the Activity of Thyroid Peroxidase Activity In Vitro

Palazzolo, Dominic L.; Jansen, Kevin P.

doi:10.1007/s12011-008-8183-y

Cited by 27 publications

(12 citation statements)

References 21 publications

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“…TSH was positively associated with arsenic in the present study, which is consistent with experimental data demonstrating that arsenic trioxide inhibits thyroid peroxidase activity (TPO) in vitro (Palazzolo and Jansen 2008). TPO is the major enzyme involved in thyroid hormone synthesis, and TPO inhibition likely results in declined thyroid hormone levels, which, through feedback mechanisms, would result in increased TSH.…”

Section: Discussionsupporting

confidence: 92%

Multiple metals predict prolactin and thyrotropin (TSH) levels in men

Meeker

Rossano

Protas

et al. 2009

Environmental Research

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Exposure to a number of metals can affect neuroendocrine and thyroid signaling, which can result in adverse effects on development, behavior, metabolism, reproduction, and other functions. The present study assessed the relationship between metal concentrations in blood and serum prolactin (PRL) and thyrotropin (TSH) levels, markers of dopaminergic and thyroid function, respectively, among men participating in a study of environmental influences on male reproductive health. Blood samples from 219 men were analyzed for concentrations of 11 metals and serum levels of PRL and TSH. In multiple linear regression models adjusted for age, BMI and smoking, PRL was inversely associated with arsenic, cadmium, copper, lead, manganese, molybdenum, and zinc, but positively associated with chromium. Several of these associations (Cd, Pb, Mo) are consistent with limited studies in humans or animals, and a number of the relationships (Cr, Cu, Pb, Mo) remained when additionally considering multiple metals in the model. Lead and copper were associated with non-monotonic decreases in TSH, while arsenic was associated with a dose-dependent increase in TSH. For arsenic these findings were consistent with recent experimental studies where arsenic inhibited enzymes involved in thyroid hormone synthesis and signaling. More research is needed for a better understanding of the role of metals in neuroendocrine and thyroid function and related health implications.

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Section: Discussionsupporting

confidence: 92%

Multiple metals predict prolactin and thyrotropin (TSH) levels in men

Meeker

Rossano

Protas

et al. 2009

Environmental Research

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“…Heavy metals such as arsenic (As), cadmium (Cd), lead (Pb) and mercury (Hg) are environmental toxins that interfere with the normal functioning of the thyroid gland. Arsenic has been shown to inhibit TPO activity [ 446 ]. Cadmium affects TPO activity [ 329 , 447 ] and alters thyroid hormone metabolism [ 329 , 448 ].…”

Section: Environmental Factors That Influence Tsh and Thyroid Hormone Levelsmentioning

confidence: 99%

Environmental Factors Affecting Thyroid-Stimulating Hormone and Thyroid Hormone Levels

Leko

Gunjača

Pleić

et al. 2021

IJMS

131

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Thyroid hormones are necessary for the normal functioning of physiological systems. Therefore, knowledge of any factor (whether genetic, environmental or intrinsic) that alters the levels of thyroid-stimulating hormone (TSH) and thyroid hormones is crucial. Genetic factors contribute up to 65% of interindividual variations in TSH and thyroid hormone levels, but many environmental factors can also affect thyroid function. This review discusses studies that have analyzed the impact of environmental factors on TSH and thyroid hormone levels in healthy adults. We included lifestyle factors (smoking, alcohol consumption, diet and exercise) and pollutants (chemicals and heavy metals). Many inconsistencies in the results have been observed between studies, making it difficult to draw a general conclusion about how a particular environmental factor influences TSH and thyroid hormone levels. However, lifestyle factors that showed the clearest association with TSH and thyroid hormones were smoking, body mass index (BMI) and iodine (micronutrient taken from the diet). Smoking mainly led to a decrease in TSH levels and an increase in triiodothyronine (T3) and thyroxine (T4) levels, while BMI levels were positively correlated with TSH and free T3 levels. Excess iodine led to an increase in TSH levels and a decrease in thyroid hormone levels. Among the pollutants analyzed, most studies observed a decrease in thyroid hormone levels after exposure to perchlorate. Future studies should continue to analyze the impact of environmental factors on thyroid function as they could contribute to understanding the complex background of gene–environment interactions underlying the pathology of thyroid diseases.

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“…Also, some histological alterations such as a flattened cell lining epithelium, hyperplasia, edema, atrophy, colloid vacuoles, and destructive degeneration were observed in the fetal thyroid gland at ED 20. Previously, ATO accumulates in the thyroid follicles 70 and binds the protein sulfhydryl group of thyroid peroxidase (THs synthesis) 20,71 decreasing THs levels, 13,72 altering THs-metabolism, 73 perturbing thyroid receptors (TRs), 72,74 and thus initiating goiter. 75 Another possible mechanism is that exposure to arsenic can decrease the levels of selenium (necessary for conversion of T4 to T3) in blood and tissue causing a negative action on thyroid functions.…”

Section: Discussionmentioning

confidence: 99%

Gestational Arsenic Trioxide Exposure Acts as a Developing Neuroendocrine-Disruptor by Downregulating Nrf2/PPARγ and Upregulating Caspase-3/NF-ĸB/Cox2/BAX/iNOS/ROS

Ahmed

El-Gareib

2019

Dose-Response

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The goal of this investigation was to evaluate the effects of gestational administrations of arsenic trioxide (ATO; As 2 O 3) on fetal neuroendocrine development (the thyroid-cerebrum axis). Pregnant Wistar rats were orally administered ATO (5 or 10 mg/kg) from gestation day (GD) 1 to 20. Both doses of ATO diminished free thyroxine and free triiodothyronine levels and augmented thyrotropin level in both dams and fetuses at GD 20. Also, the maternofetal hypothyroidism in both groups caused a dose-dependent reduction in the fetal serum growth hormone, insulin growth factor-I (IGF-I), and IGF-II levels at embryonic day (ED) 20. These disorders perturbed the maternofetal body weight, fetal brain weight, and survival of pregnant and their fetuses. In addition, destructive degeneration, vacuolation, hyperplasia, and edema were observed in the fetal thyroid and cerebrum of both ATO groups at ED 20. These disruptions appear to depend on intensification in the values of lipid peroxidation, nitric oxide, and H 2 O 2 , suppression of messenger RNA (mRNA) expression of nuclear factor erythroid 2-related factor 2 and peroxisome proliferator-activated receptor gamma, and activation of mRNA expression of caspase-3, nuclear factor kappa-light-chain-enhancer of activated B cells, cyclooxygenase-2, Bcl-2-associated X protein, and inducible nitric oxide synthase in the fetal cerebrum. These data suggest that gestational ATO may disturb thyroid-cerebrum axis generating fetal neurodevelopmental toxicity.

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The Minimal Arsenic Concentration Required to Inhibit the Activity of Thyroid Peroxidase Activity In Vitro

Cited by 27 publications

References 21 publications

Multiple metals predict prolactin and thyrotropin (TSH) levels in men

Multiple metals predict prolactin and thyrotropin (TSH) levels in men

Environmental Factors Affecting Thyroid-Stimulating Hormone and Thyroid Hormone Levels

Gestational Arsenic Trioxide Exposure Acts as a Developing Neuroendocrine-Disruptor by Downregulating Nrf2/PPARγ and Upregulating Caspase-3/NF-ĸB/Cox2/BAX/iNOS/ROS

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