Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 Dec 27;5(1):25.
doi: 10.1186/1756-6614-5-25.

Oxidative damage to macromolecules in the thyroid - experimental evidence

Affiliations

Oxidative damage to macromolecules in the thyroid - experimental evidence

Małgorzata Karbownik-Lewińska et al. Thyroid Res. .

Abstract

Whereas oxidative reactions occur in all tissues and organs, the thyroid gland constitutes such an organ, in which oxidative processes are indispensable for thyroid hormone synthesis. It is estimated that huge amount of reactive oxygen species, especially of hydrogen peroxide (H2O2), are produced in the thyroid under physiological conditions, justifying the statement that the thyroid gland is an organ of "oxidative nature". Apart from H2O2, also other free radicals or reactive species, formed from iodine or tyrosine residues, participate in thyroid hormone synthesis. Under physiological conditions, there is a balance between generation and detoxification of free radicals. Effective protective mechanisms, comprising antioxidative molecules and the process of compartmentalization of potentially toxic molecules, must have been developed in the thyroid to maintain this balance. However, with additional oxidative abuse caused by exogenous or endogenous prooxidants (ionizing radiation being the most spectacular), increased damage to macromolecules occurs, potentially leading to different thyroid diseases, cancer included.

PubMed Disclaimer

References

    1. Halliwell B. Free radicals and antioxidants: updating a personal view. Nutr Rev. 2012;70:257–265. doi: 10.1111/j.1753-4887.2012.00476.x. - DOI - PubMed
    1. Ray PD, Huang BW, Tsuji Y. Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling. Cell Signal. 2012;24:981–990. doi: 10.1016/j.cellsig.2012.01.008. - DOI - PMC - PubMed
    1. Akhtar MJ, Kumar S, Murthy RC, Ashquin M, Khan MI, Patil G, Ahmad I. The primary role of iron-mediated lipid peroxidation in the differential cytotoxicity caused by two varieties of talc nanoparticles on A549 cells and lipid peroxidation inhibitory effect exerted by ascorbic acid. Toxicol In Vitro. 2010;24:1139–1147. doi: 10.1016/j.tiv.2010.03.002. - DOI - PubMed
    1. Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med. 2010;48:749–762. doi: 10.1016/j.freeradbiomed.2009.12.022. - DOI - PMC - PubMed
    1. Song Y, Driessens N, Costa M, De Deken X, Detours V, Corvilain B, Maenhaut C, Miot F, Van Sande J, Many MC, Dumont JE. Roles of hydrogen peroxide in thyroid physiology and disease. J Clin Endocrinol Metab. 2007;92:3764–3773. doi: 10.1210/jc.2007-0660. - DOI - PubMed

LinkOut - more resources