Genome-wide expression profiling of carbaryl and vinclozolin in human thyroid follicular carcinoma (FTC-238) cells

Authors
Song, MeeKim, Youn JungLee, Ji-NaRyu, Jae Chun
Issue Date
2010-06-20
Publisher
KOREAN BIOCHIP SOCIETY-KBCS
Citation
BIOCHIP JOURNAL, v.4, no.2, pp.89 - 98
Abstract
Environmental chemicals have attracted attention owing to their effects on thyroid functions, because thyroid hormones (THs) play key roles in the development of mammalian organs such as the brain and heart. Carbaryl, which is used as an insecticide, is a cholinesterase inhibitor and is toxic to humans. It is classified as a likely human carcinogen by the United States Environmental Protection Agency (EPA). It induces thyroid dysfunction by acting as a thyroid receptor (TR) antagonist and altering the circulating levels of THs; it increases triiodothryonine (13) levels. Vinclozolin is a fungicide and is known as an endocrine disruptor. Vinclozolin decreases circulating thyroxine (T-4) levels and increases thyroid stimulating hormone (TSH) levels. We examined the changes in gene expression profiles in human thyroid follicular carcinoma FTC-238 cells that were exposed to carbaryl and vinclozolin and various chemicals by using a human oligonucleotide chip. Several genes altered by carbaryl and vinclozolin belonged to the gene ontology (GO) categories of cell cycle, apoptosis, development, and metabolism. Further, we identified 106 classifiers represent in the contrast the reaction in thyroid systems by carbaryl and vinclozolin. These classifiers are potential biomarkers of the final symptoms (i.e., hyperthyroidism and hypothyroidism) that result from disruption of THs production. In conclusion, our study suggests potential biomarkers and biological functions related to thyroid dysfunction and biological functions to be investigated in response to the exposure of environmental chemicals such as carbaryl and vinclozolin.
Keywords
CARBOHYDRATE-METABOLISM; MEDIATED APOPTOSIS; HORMONE; HYPERTHYROIDISM; GENES; MICROARRAY; TOXICITY; PATHWAY; FAS; CARBOHYDRATE-METABOLISM; MEDIATED APOPTOSIS; HORMONE; HYPERTHYROIDISM; GENES; MICROARRAY; TOXICITY; PATHWAY; FAS; Carbaryl; Vinclozolin; Thyroid; Microarray; Gene ontology (GO)
ISSN
1976-0280
URI
https://pubs.kist.re.kr/handle/201004/131323
DOI
10.1007/s13206-010-4201-1
Appears in Collections:
KIST Article > 2010
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