Biochemical Changes During Goiter Induction by Methylmercaptoimidazol and Inhibition by δ-Iodolactone in Rat

Thomasz, Lisa; Oglio, Romina; Randi, Andrea; Fernández, M; Dagrosa, María Alejandra; Cabrini, R. L.; Juvenal, Guillermo; Pisarev, Mario A.

doi:10.1089/thy.2009.0257

Cited by 13 publications

(10 citation statements)

References 44 publications

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“…Some studies have shown increases in peroxide content, lipid peroxidation, and the activity of the antioxidant enzyme catalase and GPx during goitrogenesis in rats , Thomasz et al 2010. The source of ROS during goitrogenesis has not been demonstrated, but NOX4 is a good candidate, according to recent findings.…”

Section: Ros and Thyroid Pathophysiologymentioning

confidence: 99%

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fortunato¹,

Ferreira²,

Hecht³

et al. 2014

Journal of Endocrinology

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Thyroid diseases, such as autoimmune disease and benign and malignant nodules, are more prevalent in women than in men, but the mechanisms involved in this sex difference is still poorly defined. H 2 O 2 is produced at high levels in the thyroid gland and regulates parameters such as cell proliferation, migration, survival, and death; an imbalance in the cellular oxidant-antioxidant system in the thyroid may contribute to the greater incidence of thyroid disease among women. Recently, we demonstrated the existence of a sexual dimorphism in the thyrocyte redox balance, characterized by higher H 2 O 2 production, due to higher NOX4 and Poldip2 expression, and weakened enzymatic antioxidant defense in the thyroid of adult female rats compared with male rats. In addition, 17b-estradiol administration increased NOX4 mRNA expression and H 2 O 2 production in thyroid PCCL3 cells. In this review, we discuss the possible involvement of oxidative stress in estrogenrelated thyroid pathophysiology. Our current hypothesis suggests that a redox imbalance elicited by estrogen could be involved in the sex differences found in the prevalence of thyroid dysfunctions.

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Section: Ros and Thyroid Pathophysiologymentioning

confidence: 99%

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Fortunato¹,

Ferreira²,

Hecht³

et al. 2014

Journal of Endocrinology

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“…Moreover since excess iodine increases TGF-β1 mRNA expression in sheep thyroid cells [43] and its protein synthesis in porcine thyroid cells cultured in monolayer [41], as it was mentioned, it was expected that iodolactone could also induce TGF-β1 biosynthesis. However in porcine follicles [45] and in in vivo studies in rats IL-δ did not regulate TGF-β1 synthesis, while KI increased its expression [61].…”

Section: Iodolactonementioning

confidence: 83%

Thyroid: Iodine Beyond the Thyronines

Juvenal¹,

Thomasz²,

Oglio³

et al. 2011

curr chem biol

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Although thyroid gland function is mainly under the control of pituitary TSH, other factors may also play a role in this process. Iodine is not used only by the thyroid to synthesize thyroid hormones but also directly influences a number of parameters such as thyroid proliferation and function. Thyroid autoregulation has been related to intraglandular content of an unknown putative iodocompound. The thyroid is capable of producing different iodolipids such as 6-iododeltalactone (ILδ) and 2-iodohexadecanal (2-IHDA). Data from different laboratories have shown that these iodolipids can inhibit several thyroid parameters suggesting that these compounds may be the intermediates in the thyroid autoregulation process.

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“…17 Research shows that measurable concentrations of δ-iodolactone are found in the thyroid tissue, prevent excess iodide uptake and the generation of H 2 O 2 by NADPH oxidase, and regulate thyroid function. 18 Furthermore, specific iodolactones are able to inhibit signal transduction pathways to regulate cellular proliferation, modulate goiter formation, and normalize thyroid size. 14,[17][18][19][20] However, in iodine deficiency, iodolactones are obsolete, and the thyroid gland is susceptible to oxidative damage and loss of cellcycle control.…”

Section: Iodine Metabolism and Regulatory Mechanismsmentioning

confidence: 99%

“…As iodine concentrations decrease, the pituitary gland secretes thyroid-stimulating hormone (TSH) to induce NIS expression. 18…”

Section: Loss Of Autoregulation During Iodine Deficiencymentioning

confidence: 99%

“…36,38 As previously outlined, low concentrations of iodinated lipids increase oxidative damage, while sufficient levels regulate cell proliferation and apoptosis. [12][13][14]18 In vitro studies demonstrate that solutions of iodolactones effectively regulate cell proliferation and reduce malignancy in breast and thyroid tissue. 41 Thyroid carcinoma cells in the presence of δ-iodolactone show a dose-dependent decrease in cell proliferation and apoptosis.…”

Section: Thyroid Cancermentioning

confidence: 99%

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The Role of Iodine Deficiency and Subsequent Repletion in Autoimmune Thyroid Disease and Thyroid Cancer

Murphy¹,

Turek²,

Arseneau³

2016

j restorat med

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Iodine is an essential trace mineral that is necessary for thyroid hormone production. With the prevalence of iodine deficiency worldwide, universal salt iodization programs were successfully implemented to reduce the incidence of iodine deficiency disorders; however, unexpected increases in the prevalence of thyroid autoimmunity occurred, and iodine excess was implicated as the causative factor. Despite these observations, epidemiological studies are inconsistent, and the etiology of autoimmune thyroid disease remains undefined. A review of observational and in vitro studies revealed that iodine alone is not responsible for thyroid autoimmunity. Experimental models used to explain iodine excess as the culprit in thyroid autoimmunity fail to induce thyroid autoantibodies unless iodine is in the presence of excess inflammatory cytokines (interferon [IFN]-γ) and hydrogen peroxide (H 2 O 2 ). Within iodine-deficient populations, regulatory mechanisms to limit oxidative stress and excess iodine are lost. Thyroid-stimulating hormone persistently activates the sodium-iodide symporter, while iodine concentrations fail to achieve levels high enough to produce iodolactones, which are responsible for modulating NADPH oxidase and H 2 O 2 production. Subsequently, the thyroid becomes susceptible to oxidative stress as iodine is reintroduced. Oxidation of thyroid peroxidase and thyroglobulin initiate the release of inflammatory cytokines (IFN-γ) and lymphocytic infiltration, which induce autoantibody production and thyroid autoimmunity. Population studies revealed that iodine administration even below the recommended dietary allowance alters thyroid autoimmunity. Despite increases in thyroid antibodies, these changes are found to be transient. Interestingly, reports of iodine in combination with other nutrients and standardized botanical extracts have been used successfully to restore thyroid function. On the basis of our review of the literature, it is apparent that a loss of regulatory mechanisms due to preexisting iodine deficiency followed by iodine repletion, as opposed to iodine excess, is a causal factor in the development of thyroid autoimmunity.

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Biochemical Changes During Goiter Induction by Methylmercaptoimidazol and Inhibition by δ-Iodolactone in Rat

Cited by 13 publications

References 44 publications

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Sexual dimorphism and thyroid dysfunction: a matter of oxidative stress?

Thyroid: Iodine Beyond the Thyronines

The Role of Iodine Deficiency and Subsequent Repletion in Autoimmune Thyroid Disease and Thyroid Cancer

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