Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells

Hexachlorobenzene (HCB) is a widespread environmental pollutant. Chronic exposure of humans to HCB produces a number of effects, such as triggering of porphyria, increased synthesis of liver microsomal enzymes, neurological symptoms, immunological disorders and thyroid dysfunctions. In rats, HCB ind...

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Autores principales:	Chiappini, F., Alvarez, L., Lux-Lantos, V., Randi, A.S., de Pisarev, D.L.K.
Formato:	JOUR
Materias:	Apoptosis Hexachlorobenzene Rat thyroid caspase 9 cytochrome c DNA nucleotidylexotransferase hexachlorobenzene messenger RNA procaspase 8 thyroid hormone thyroxine transforming growth factor beta1 animal cell animal experiment animal tissue apoptosis article cell count cell proliferation controlled study DNA fragmentation female gene expression growth regulation nick end labeling nonhuman protein secretion rat regulatory mechanism reverse transcription polymerase chain reaction thyroid follicle cell thyroid hormone blood level thyroid weight tissue structure upregulation Animals Blotting, Western Caspase 8 Caspase 9 Cell Proliferation DNA Fragmentation Endocrine Disruptors Environmental Pollutants Enzyme Induction Female In Situ Nick-End Labeling Mitochondria Organ Size Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Signal Transduction Subcellular Fractions Thyroid Gland Thyroid Hormones Transforming Growth Factor beta1 Animalia Rattus Rattus norvegicus
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_10966080_v108_n2_p301_Chiappini
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	todo:paper_10966080_v108_n2_p301_Chiappini2023-10-03T16:05:24Z Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells Chiappini, F. Alvarez, L. Lux-Lantos, V. Randi, A.S. de Pisarev, D.L.K. Apoptosis Hexachlorobenzene Rat thyroid caspase 9 cytochrome c DNA nucleotidylexotransferase hexachlorobenzene messenger RNA procaspase 8 thyroid hormone thyroxine transforming growth factor beta1 animal cell animal experiment animal tissue apoptosis article cell count cell proliferation controlled study DNA fragmentation female gene expression growth regulation nick end labeling nonhuman protein secretion rat regulatory mechanism reverse transcription polymerase chain reaction thyroid follicle cell thyroid hormone blood level thyroid weight tissue structure upregulation Animals Apoptosis Blotting, Western Caspase 8 Caspase 9 Cell Proliferation DNA Fragmentation Endocrine Disruptors Environmental Pollutants Enzyme Induction Female Hexachlorobenzene In Situ Nick-End Labeling Mitochondria Organ Size Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Signal Transduction Subcellular Fractions Thyroid Gland Thyroid Hormones Transforming Growth Factor beta1 Animalia Rattus Rattus norvegicus Hexachlorobenzene (HCB) is a widespread environmental pollutant. Chronic exposure of humans to HCB produces a number of effects, such as triggering of porphyria, increased synthesis of liver microsomal enzymes, neurological symptoms, immunological disorders and thyroid dysfunctions. In rats, HCB induced hepatic porphyria, neurotoxic effects, and toxic effects on the reproductive system, thyroid function, and immune system. HCB is also known to cause tumors of the liver, thyroid and mammary gland in laboratory animals. The aim of this study was to investigate parameters of thyroid growth regulation, mainly cell proliferation and apoptosis in thyroid tissue from HCB (0.1, 1, 10, 100, and 500 mg/kg body weight)-treated female Wistar rats. The current study demonstrates that only the exposure to the highest HCB dose for 30 days, has adverse effects on thyroid endpoints examined related to thyroid gland morphology, and 3,3′5,5′-tetraiodothyronine (T 4 , thyroxine) serum levels, without changes in thyroid-stimulating hormone concentrations or in thyroid gland weight. Morphological changes, included flattened epithelium and increased colloid size compared with control tissue. Transforming growth factor (TGF-β1) mRNA levels, evaluated by RT-PCR, revealed a significant upregulation after exposure to HCB (1, 10, 100 mg/kg body weight). Cell proliferation evaluated by 5′-Br deoxiuridine incorporation into DNA, was not altered at any dose. HCB (1, 10, 100 mg/kg body weight) induces apoptosis, evaluated by in situ end labeling of fragmented DNA, terminal deoxynucleotidyl transferase-mediated deoxy uridine triphosphate nick-end labeling, in rat thyroid glands. This process is associated with dose-dependent increases in cytochrome c release from the mitochondria and procaspase-9 processing to its active product. Caspase-8 was not activated. These studies indicate that doses of HCB that do not disrupt thyroid economy induce TGF-β1 expression and apoptosis in the thyroid gland, involving the mitochondrial pathway. © The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_10966080_v108_n2_p301_Chiappini
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Apoptosis Hexachlorobenzene Rat thyroid caspase 9 cytochrome c DNA nucleotidylexotransferase hexachlorobenzene messenger RNA procaspase 8 thyroid hormone thyroxine transforming growth factor beta1 animal cell animal experiment animal tissue apoptosis article cell count cell proliferation controlled study DNA fragmentation female gene expression growth regulation nick end labeling nonhuman protein secretion rat regulatory mechanism reverse transcription polymerase chain reaction thyroid follicle cell thyroid hormone blood level thyroid weight tissue structure upregulation Animals Apoptosis Blotting, Western Caspase 8 Caspase 9 Cell Proliferation DNA Fragmentation Endocrine Disruptors Environmental Pollutants Enzyme Induction Female Hexachlorobenzene In Situ Nick-End Labeling Mitochondria Organ Size Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Signal Transduction Subcellular Fractions Thyroid Gland Thyroid Hormones Transforming Growth Factor beta1 Animalia Rattus Rattus norvegicus
spellingShingle	Apoptosis Hexachlorobenzene Rat thyroid caspase 9 cytochrome c DNA nucleotidylexotransferase hexachlorobenzene messenger RNA procaspase 8 thyroid hormone thyroxine transforming growth factor beta1 animal cell animal experiment animal tissue apoptosis article cell count cell proliferation controlled study DNA fragmentation female gene expression growth regulation nick end labeling nonhuman protein secretion rat regulatory mechanism reverse transcription polymerase chain reaction thyroid follicle cell thyroid hormone blood level thyroid weight tissue structure upregulation Animals Apoptosis Blotting, Western Caspase 8 Caspase 9 Cell Proliferation DNA Fragmentation Endocrine Disruptors Environmental Pollutants Enzyme Induction Female Hexachlorobenzene In Situ Nick-End Labeling Mitochondria Organ Size Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Signal Transduction Subcellular Fractions Thyroid Gland Thyroid Hormones Transforming Growth Factor beta1 Animalia Rattus Rattus norvegicus Chiappini, F. Alvarez, L. Lux-Lantos, V. Randi, A.S. de Pisarev, D.L.K. Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
topic_facet	Apoptosis Hexachlorobenzene Rat thyroid caspase 9 cytochrome c DNA nucleotidylexotransferase hexachlorobenzene messenger RNA procaspase 8 thyroid hormone thyroxine transforming growth factor beta1 animal cell animal experiment animal tissue apoptosis article cell count cell proliferation controlled study DNA fragmentation female gene expression growth regulation nick end labeling nonhuman protein secretion rat regulatory mechanism reverse transcription polymerase chain reaction thyroid follicle cell thyroid hormone blood level thyroid weight tissue structure upregulation Animals Apoptosis Blotting, Western Caspase 8 Caspase 9 Cell Proliferation DNA Fragmentation Endocrine Disruptors Environmental Pollutants Enzyme Induction Female Hexachlorobenzene In Situ Nick-End Labeling Mitochondria Organ Size Rats Rats, Wistar Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Signal Transduction Subcellular Fractions Thyroid Gland Thyroid Hormones Transforming Growth Factor beta1 Animalia Rattus Rattus norvegicus
description	Hexachlorobenzene (HCB) is a widespread environmental pollutant. Chronic exposure of humans to HCB produces a number of effects, such as triggering of porphyria, increased synthesis of liver microsomal enzymes, neurological symptoms, immunological disorders and thyroid dysfunctions. In rats, HCB induced hepatic porphyria, neurotoxic effects, and toxic effects on the reproductive system, thyroid function, and immune system. HCB is also known to cause tumors of the liver, thyroid and mammary gland in laboratory animals. The aim of this study was to investigate parameters of thyroid growth regulation, mainly cell proliferation and apoptosis in thyroid tissue from HCB (0.1, 1, 10, 100, and 500 mg/kg body weight)-treated female Wistar rats. The current study demonstrates that only the exposure to the highest HCB dose for 30 days, has adverse effects on thyroid endpoints examined related to thyroid gland morphology, and 3,3′5,5′-tetraiodothyronine (T 4 , thyroxine) serum levels, without changes in thyroid-stimulating hormone concentrations or in thyroid gland weight. Morphological changes, included flattened epithelium and increased colloid size compared with control tissue. Transforming growth factor (TGF-β1) mRNA levels, evaluated by RT-PCR, revealed a significant upregulation after exposure to HCB (1, 10, 100 mg/kg body weight). Cell proliferation evaluated by 5′-Br deoxiuridine incorporation into DNA, was not altered at any dose. HCB (1, 10, 100 mg/kg body weight) induces apoptosis, evaluated by in situ end labeling of fragmented DNA, terminal deoxynucleotidyl transferase-mediated deoxy uridine triphosphate nick-end labeling, in rat thyroid glands. This process is associated with dose-dependent increases in cytochrome c release from the mitochondria and procaspase-9 processing to its active product. Caspase-8 was not activated. These studies indicate that doses of HCB that do not disrupt thyroid economy induce TGF-β1 expression and apoptosis in the thyroid gland, involving the mitochondrial pathway. © The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.
format	JOUR
author	Chiappini, F. Alvarez, L. Lux-Lantos, V. Randi, A.S. de Pisarev, D.L.K.
author_facet	Chiappini, F. Alvarez, L. Lux-Lantos, V. Randi, A.S. de Pisarev, D.L.K.
author_sort	Chiappini, F.
title	Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
title_short	Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
title_full	Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
title_fullStr	Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
title_full_unstemmed	Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
title_sort	hexachlorobenzene triggers apoptosis in rat thyroid follicular cells
url	http://hdl.handle.net/20.500.12110/paper_10966080_v108_n2_p301_Chiappini
work_keys_str_mv	AT chiappinif hexachlorobenzenetriggersapoptosisinratthyroidfollicularcells AT alvarezl hexachlorobenzenetriggersapoptosisinratthyroidfollicularcells AT luxlantosv hexachlorobenzenetriggersapoptosisinratthyroidfollicularcells AT randias hexachlorobenzenetriggersapoptosisinratthyroidfollicularcells AT depisarevdlk hexachlorobenzenetriggersapoptosisinratthyroidfollicularcells
_version_	1782026801986404352

Hexachlorobenzene triggers apoptosis in rat thyroid follicular cells

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