Selenium has a protective role in caspase-3-dependent apoptosis induced by H2O2 in primary cultured pig thyrocytes.

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MARC

Demelash, Abeba,1962Gothenburg University,Göteborgs universitet,Institutionen för anatomi och cellbiologi,Institute of Anatomy and Cell Biology (author)

Selenium has a protective role in caspase-3-dependent apoptosis induced by H2O2 in primary cultured pig thyrocytes.

Article/chapterEnglish2004

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2004

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LIBRIS-ID:oai:gup.ub.gu.se/60837
https://gup.ub.gu.se/publication/60837URI

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Language:English

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SwePubSwePub

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Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

Notes

OBJECTIVE: Hydrogen peroxide (H2O2), necessary for thyroid hormonogenesis, is produced at the apical surface of the thyroid follicular epithelium. Excess H2O2 is potentially cytotoxic and may contribute to the development of hypothyroidism, e.g. in severe selenium deficiency. Yet it is unclear how H2O2 contributes to thyroid cell death. DESIGN AND METHODS: H2O2-induced apoptosis and necrosis were studied in primary cultured pig thyroid cells. Glutathione peroxidase (GPx) activity was altered by culture in low serum with or without selenite substitution. Apoptosis was evaluated by spectrofluorometric measurement of caspase-3-specific substrate cleavage, and by analysis of DNA fragmentation by agarose gel electrophoresis. Necrosis was detected by 51Cr release from prelabeled cells. RESULTS: Exogenous H2O2 dose-dependently (100-400 micromol/l) activated caspase-3 within 3-12 h, and DNA degradation was observed after 24 h. The potency of H2O2 to induce apoptosis was low compared with that of staurosporine, a strong proapoptotic agent. H2O2-treated cells with reduced GPx activity showed increased caspase-3 activation. Incubation of serum-starved cells with selenite (10-100 nmol/l) normalized the GPx activity and reduced the activation of caspase-3 by H2O2. High H2O2 concentrations (400-800 micromol/l) were required to obtain necrosis. The H2O2-induced necrosis was exaggerated by both low GPx activity and catalase inhibition. CONCLUSIONS: Cytotoxic effects of H2O2 on thyroid cells include caspase-3-dependent apoptosis that occurs at H2O2 concentrations insufficient to induce necrosis. Selenium deficiency aggravates the apoptotic response, probably due to impaired capacity of GPx to degrade H2O2.

Subject headings and genre

Animals
Apoptosis
drug effects
Caspase 3
Caspases
metabolism
Cells
Cultured
Chromium Radioisotopes
metabolism
DNA Fragmentation
drug effects
Electrophoresis
Agar Gel
Enzyme Activation
drug effects
Glutathione Peroxidase
metabolism
Hydrogen Peroxide
pharmacology
Selenium
pharmacology
Spectrometry
Fluorescence
Staurosporine
pharmacology
Swine
Thyroid Gland
cytology

Added entries (persons, corporate bodies, meetings, titles ...)

Karlsson, Jan-Olof,1944Gothenburg University,Göteborgs universitet,Institutionen för anatomi och cellbiologi,Institute of Anatomy and Cell Biology(Swepub:gu)xkjanh (author)
Nilsson, Mikael,1958Gothenburg University,Göteborgs universitet,Institutionen för anatomi och cellbiologi,Institute of Anatomy and Cell Biology(Swepub:gu)xnimik (author)
Björkman, Ulla,1939Gothenburg University,Göteborgs universitet,Institutionen för anatomi och cellbiologi,Institute of Anatomy and Cell Biology (author)
Göteborgs universitetInstitutionen för anatomi och cellbiologi (creator_code:org_t)

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In:European journal of endocrinology / European Federation of Endocrine Societies150:6, s. 841-90804-4643

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