Short Communication - (2024) Volume 8, Issue 4
Thyroid Disorders in Pregnancy: Maternal and Fetal Outcomes
Jan Lewinska*
*Correspondence:
Jan Lewinska, Department of Endocrinology and Metabolic Diseases, Medical, University of Lodz,
Poland,
Email:
1Department of Endocrinology and Metabolic Diseases, Medical, University of Lodz, Poland
, Manuscript No. rtr-25-160652;
, DOI: 10.37421/2684-4273.2024.8.100
Citation: Lewinska, Jan. “ Thyroid Disorders in Pregnancy: Maternal and Fetal Outcomes.” Rep Thyroid Res 8 (2024): 100.
Copyright: © 2024 Lewinska J. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction
While some studies suggest a protective role for melatonin against thyroid
oxidative damage caused by carcinogens, more research is needed to fully
understand the mechanisms involved and to determine the optimal use of
melatonin as a preventive or therapeutic agent in thyroid cancer. The thyroid
gland is a critical organ responsible for regulating metabolism, growth, and
energy balance in the body. It is susceptible to damage from various factors,
including exposure to carcinogens. Carcinogens are substances that can
promote the formation of cancer by inducing oxidative stress, which can lead
to DNA damage and mutations. Melatonin, a hormone primarily produced
by the pineal gland, has emerged as a potential protective agent against
oxidative damage in the thyroid gland. This article explores the mechanisms
behind melatonin's protective effects and its potential as a therapeutic agent in
preventing thyroid cancer. Oxidative stress occurs when there is an imbalance
between the production of reactive oxygen species and the body's ability to
neutralize them with antioxidants. ROS are highly reactive molecules that can
damage cellular components, including DNA, proteins, and lipids. Chronic
oxidative stress can lead to the development of cancer by promoting mutations
in key genes involved in cell growth and proliferation. The thyroid gland is
particularly vulnerable to oxidative stress due to its high metabolic activity and
the presence of high levels of unsaturated fatty acids, which are susceptible to
oxidation. Inflammation is closely linked to oxidative stress and carcinogenesis.
Chronic inflammation can promote the production of ROS and reactive
nitrogen species, leading to oxidative damage in tissues. Melatonin has antiinflammatory properties and can suppress the production of pro-inflammatory
cytokines and mediators, such as tumor necrosis factor, interleukin-6 and
cyclooxygenase-2. By reducing inflammation, melatonin can indirectly reduce
oxidative stress in the thyroid gland and mitigate the damaging effects of
carcinogens. Its anti-inflammatory effects may also contribute to its cancerpreventive properties by inhibiting the growth and proliferation of cancer cells
[1].
Description
Carcinogens, such as ionizing radiation, environmental toxins, and certain
chemicals, can induce oxidative stress in the thyroid gland, leading to DNA
damage and potentially cancerous changes in thyroid cells. Melatonin is a potent
antioxidant that can neutralize ROS and protect cells from oxidative damage. It
scavenges free radicals, such as hydroxyl radicals and singlet oxygen, thereby
reducing oxidative stress and its damaging effects. Melatonin also stimulates
the activity of antioxidant enzymes, such as superoxide dismutase, glutathione
peroxidase, and catalase, which further enhance its antioxidant capacity. In
addition to its direct antioxidant effects, melatonin has been shown to modulate
the expression of genes involved in antioxidant defense and DNA repair. It
cans upregulate the expression of antioxidant enzymes and downregulate the
expression of pro-oxidant enzymes, thereby enhancing the cell's ability to cope
with oxidative stress and maintain genomic stability [2].
Conclusion
Melatonin may also interact with enzymes involved in the metabolism of
carcinogens, thereby altering their effects or enhancing their detoxification.
For example, melatonin has been shown to inhibit the activity of cytochrome
P450 enzymes, which are involved in the activation of certain carcinogens.
By inhibiting these enzymes, melatonin may reduce the formation of reactive
metabolites that can damage DNA and promote cancer development.
Melatonin has emerged as a promising agent for protecting the thyroid
gland against oxidative damage caused by carcinogens. Its antioxidant, antiinflammatory, and immune-modulating effects, along with its ability to regulate
cell proliferation and apoptosis, make it a potentially valuable therapeutic
agent in preventing thyroid cancer. Further research is needed to elucidate
the precise mechanisms of melatonin's protective effects and to determine
its optimal use in clinical settings. Nonetheless, the evidence suggests that
melatonin may offer a novel approach to reducing the risk of thyroid cancer in
individuals exposed to carcinogens.
References
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