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      8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) as a Cause of Autoimmune Thyroid Diseases (AITD) During Pregnancy?

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          Abstract

          The thyroid is not necessary to sustain life. However, thyroid hormones (TH) strongly affect the human body. Functioning of the thyroid gland affects the reproductive capabilities of women and men, as well as fertilization and maintaining a pregnancy. For the synthesis of TH, hydrogen peroxide (H 2O 2) is necessary. From the chemical point of view, TH is a reactive oxygen species (ROS) and serves as an oxidative stress (OS) promoter. H 2O 2 concentration in the thyroid gland is much higher than in other tissues. Therefore, the thyroid is highly exposed to OS. 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) are DNA lesions resulting from ROS action onto guanine moiety. Due to their abundance, they are recognized as biomarkers of OS. As thyroid function is correlated with the level of OS, 8-oxodG and 8-OHdG has been taken under consideration. Studies correlate the oxidative DNA damage with various thyroid diseases (TD) such as Hashimoto’s thyroiditis (HT), Graves’ disease (GD), and thyroid cancer. Human sexual function and fertility are also affected by OS and TD. Hypothyroidism and hyperthyroidism diagnosed in pregnant women have a negative effect on pregnancy as it may increase the risk of miscarriage or fetus mortality. In the case of TD in the mother, fetal health is also at risk – neurodevelopment and cognitive function of the child may be impaired in its future life. This review presents thyroid function in the context of TD during pregnancy. The authors introduce OS and describe oxidative DNA lesions as a crucial marker of thyroid pathologies.

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          Global epidemiology of hyperthyroidism and hypothyroidism

          Thyroid hormones are essential for growth, neuronal development, reproduction and regulation of energy metabolism. Hypothyroidism and hyperthyroidism are common conditions with potentially devastating health consequences that affect all populations worldwide. Iodine nutrition is a key determinant of thyroid disease risk; however, other factors, such as ageing, smoking status, genetic susceptibility, ethnicity, endocrine disruptors and the advent of novel therapeutics, including immune checkpoint inhibitors, also influence thyroid disease epidemiology. In the developed world, the prevalence of undiagnosed thyroid disease is likely falling owing to widespread thyroid function testing and relatively low thresholds for treatment initiation. However, continued vigilance against iodine deficiency remains essential in developed countries, particularly in Europe. In this report, we review the global incidence and prevalence of hyperthyroidism and hypothyroidism, highlighting geographical differences and the effect of environmental factors, such as iodine supplementation, on these data. We also highlight the pressing need for detailed epidemiological surveys of thyroid dysfunction and iodine status in developing countries.
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            Mitochondrial proton and electron leaks.

            Mitochondrial proton and electron leak have a major impact on mitochondrial coupling efficiency and production of reactive oxygen species. In the first part of this chapter, we address the molecular nature of the basal and inducible proton leak pathways, and their physiological importance. The basal leak is unregulated, and a major proportion can be attributed to mitochondrial anion carriers, whereas the proton leak through the lipid bilayer appears to be minor. The basal proton leak is cell-type specific and correlates with metabolic rate. The inducible leak through the ANT (adenine nucleotide translocase) and UCPs (uncoupling proteins) can be activated by fatty acids, superoxide or lipid peroxidation products. The physiological role of inducible leak through UCP1 in mammalian brown adipose tissue is heat production, whereas the roles of non-mammalian UCP1 and its paralogous proteins, in particular UCP2 and UCP3, are not yet resolved. The second part of the chapter focuses on the electron leak that occurs in the mitochondrial electron transport chain. Exit of electrons prior to the reduction of oxygen to water at cytochrome c oxidase causes superoxide production. As the mechanisms of electron leak are crucial to understanding their physiological relevance, we summarize the mechanisms and topology of electron leak from complexes I and III in studies using isolated mitochondria. We also highlight recent progress and challenges of assessing electron leak in the living cell. Finally, we emphasize the importance of proton and electron leak as therapeutic targets in body mass regulation and insulin secretion.
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              DNA base damage by reactive oxygen species, oxidizing agents, and UV radiation.

              Emphasis has been placed in this article dedicated to DNA damage on recent aspects of the formation and measurement of oxidatively generated damage in cellular DNA in order to provide a comprehensive and updated survey. This includes single pyrimidine and purine base lesions, intrastrand cross-links, purine 5',8-cyclonucleosides, DNA-protein adducts and interstrand cross-links formed by the reactions of either the nucleobases or the 2-deoxyribose moiety with the hydroxyl radical, one-electron oxidants, singlet oxygen, and hypochlorous acid. In addition, recent information concerning the mechanisms of formation, individual measurement, and repair-rate assessment of bipyrimidine photoproducts in isolated cells and human skin upon exposure to UVB radiation, UVA photons, or solar simulated light is critically reviewed.
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                Author and article information

                Journal
                Yale J Biol Med
                Yale J Biol Med
                yjbm
                YJBM
                The Yale Journal of Biology and Medicine
                YJBM
                0044-0086
                1551-4056
                30 September 2020
                September 2020
                : 93
                : 4
                : 501-515
                Affiliations
                DNA Damage Laboratory of Food Science Department, Faculty of Pharmacy, Medical University of Lodz, Lodz, Poland
                Author notes
                [* ]To whom all correspondence should be addressed: Bolesław T. Karwowski, Tel: +48 42 677 91 40; Email: boleslaw.karwowski@ 123456umed.lodz.pl ; ORCID iD: https://orcid.org/0000-0001-6922-7834.
                Article
                yjbm934501
                7513436
                33005115
                0cfea4c7-8ae6-4205-8c2a-8d3c0bfafafe
                Copyright ©2020, Yale Journal of Biology and Medicine

                This is an open access article distributed under the terms of the Creative Commons CC BY-NC license, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited. You may not use the material for commercial purposes.

                History
                Categories
                Review
                Focus: Sex & Reproduction

                Medicine
                thyroid diseases,oxidative stress,pregnancy,deoxyguanosine,dna damage,thyroid hormones
                Medicine
                thyroid diseases, oxidative stress, pregnancy, deoxyguanosine, dna damage, thyroid hormones

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