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Study on mechanism of thyroid cytotoxicity of ammonium perchlorate / 中华劳动卫生职业病杂志
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 418-421, 2013.
Artigo em Chinês | WPRIM | ID: wpr-343660
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of thyroid cytotoxicity mechanism of ammonium perchlorate (AP).</p><p><b>METHODS</b>Thyroid cells were cultured in vitro to a certain stage and then exposed to AP (0, 5, 10, 20, 40, and 60 mmol/L) in culture solution; the cultured cells and supernatant were collected. Cell viability was measured by MTT assay; cell apoptosis was determined by flow cytometry; the concentration of thyroglobulin was measured by enzyme-linked immunosorbent assay; the lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA) level, and so on were measured by colorimetry.</p><p><b>RESULTS</b>The cells exposed to 60 mmol/L AP for 12, 24, 48, and 72 h had cell viabilities of 74.93%, 42.26%, 2.66%, and 0.99%, respectively, and the cells exposed to 40 mmol/L AP for 24, 48, and 72 h had cell viabilities of 73.15%, 30.91%, and 3.03%, respectively, all significantly lower than that of the control group (100%)(P < 0.05 or P < 0.01). The overall apoptosis rate of all AP-exposed cells was significantly higher than that of the control group; the cells exposed to 20, 40, and 60 mmol/L AP had early apoptosis rates of 15.70%, 15.84%, and 16.96%, respectively, significantly higher than that of the control group (9.54%)(P < 0.05 or P < 0.01); the cells exposed to 60 mmol/L AP had a late apoptosis rate of 16.54%, significantly higher than that of the control group (6.11%)(P < 0.05 or P < 0.01). The cells exposed to 40 mmol/L AP had a significantly higher LDH activity than the control group (0.70 U/ml vs 0.55 U/ml, P < 0.01). The cells exposed to 5 mmol/L AP had a significantly higher MDA level than the control group (1.08 mmol/L vs 2.36 mmol/L, P < 0.05).</p><p><b>CONCLUSION</b>AP can markedly change the cell morphology and decrease the cell viability of thyroid cells, which may be because AP inhibits cell proliferation, induces cell apoptosis, and destroys cell membranes. However, AP does not result in significant oxidative damage to thyroid cells.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Tireoglobulina / Glândula Tireoide / Sobrevivência Celular / Células Cultivadas / Apoptose / Percloratos / Estresse Oxidativo / Proliferação de Células / Toxicidade Limite: Humanos Idioma: Chinês Revista: Chinese Journal of Industrial Hygiene and Occupational Diseases Ano de publicação: 2013 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Tireoglobulina / Glândula Tireoide / Sobrevivência Celular / Células Cultivadas / Apoptose / Percloratos / Estresse Oxidativo / Proliferação de Células / Toxicidade Limite: Humanos Idioma: Chinês Revista: Chinese Journal of Industrial Hygiene and Occupational Diseases Ano de publicação: 2013 Tipo de documento: Artigo