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Related Concept Videos

Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Biological Effects of Radiation02:59

Biological Effects of Radiation

All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they produce ions...

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The Lambda Select cII Mutation Detection System
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The Lambda Select cII Mutation Detection System

Published on: April 26, 2018

UVC radiation-induced effect on human primary thyroid cell proliferation and HLA-DR expression.

I Kostic1, B Toffoletto, M Toller

  • 1Institute of Pathophysiology, School of Medicine, University of Kragujevac, Kragujevac, Serbia.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|October 2, 2010
PubMed
Summary

UVC irradiation inhibits thyroid cell proliferation and induces apoptosis, potentially via oxidative stress. This UVC-induced increase in HLA-DR expression may contribute to autoimmune thyroid disease development.

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Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells

Published on: July 22, 2021

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Ultraviolet C (UVC) irradiation is known to affect cellular processes.
  • The role of UVC in thyroid cell function and its potential link to autoimmune thyroid diseases (AITD) requires further investigation.

Purpose of the Study:

  • To investigate the effects of UVC irradiation on normal human thyroid cell proliferation and HLA-DR expression.
  • To explore the involvement of oxidative stress and apoptosis in UVC-induced thyroid cell damage.

Main Methods:

  • Primary human thyroid cells were exposed to UVC (254 nm).
  • Buthionine sulfoximine (BSO), a glutathione synthesis inhibitor, was used to induce oxidative stress.
  • Apoptosis was assessed using Annexin V, immunoblot analysis of apoptotic proteins (p53, Bax, Bcl-2, caspase 3, and 9), and cell cycle analysis.
  • HLA-DR expression was measured by Flow Cytometry (FACS).

Main Results:

  • UVC induced cell cycle arrest in G0/G1 phase and subsequent accumulation in S phase, leading to increased apoptosis.
  • BSO pretreatment enhanced and accelerated apoptosis, suggesting a role for oxidative stress.
  • UVC irradiation altered the expression of apoptosis-related proteins (increased p53, caspase 3, 9; decreased Bax, Bcl-2).
  • A transient increase in HLA-DR expression was observed following UVC exposure.

Conclusions:

  • UVC irradiation inhibits normal human thyroid cell proliferation and induces apoptosis through the intrinsic mitochondrial pathway.
  • Oxidative stress appears to play a significant role in UVC-induced thyroid cell apoptosis.
  • The transient increase in HLA-DR expression post-UVC irradiation may be implicated in the pathogenesis of autoimmune thyroid diseases.