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Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis
Endocrine disruptors (EDs) are chemical substances capable of affecting endocrine system functioning and interfering with organ morphogenesis and physiological functions. The development and regeneration of bone tissues have a complex hormonal regulation, and therefore, bone tissue cells can be cons...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9025575/ https://www.ncbi.nlm.nih.gov/pubmed/35454153 http://dx.doi.org/10.3390/biom12040564 |
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author | D’Amico, Ramona Gugliandolo, Enrico Cordaro, Marika Fusco, Roberta Genovese, Tiziana Peritore, Alessio Filippo Crupi, Rosalia Interdonato, Livia Di Paola, Davide Cuzzocrea, Salvatore Impellizzeri, Daniela Siracusa, Rosalba Di Paola, Rosanna |
author_facet | D’Amico, Ramona Gugliandolo, Enrico Cordaro, Marika Fusco, Roberta Genovese, Tiziana Peritore, Alessio Filippo Crupi, Rosalia Interdonato, Livia Di Paola, Davide Cuzzocrea, Salvatore Impellizzeri, Daniela Siracusa, Rosalba Di Paola, Rosanna |
author_sort | D’Amico, Ramona |
collection | PubMed |
description | Endocrine disruptors (EDs) are chemical substances capable of affecting endocrine system functioning and interfering with organ morphogenesis and physiological functions. The development and regeneration of bone tissues have a complex hormonal regulation, and therefore, bone tissue cells can be considered potential targets for endocrine disruptors. In that regard, the aim of this research was to investigate the impact of ED exposure on the inflammatory response and oxidative stress in an experimental model of collagen-induced arthritis (CIA). Arthritis was induced by an emulsion of type II collagen (CII) and complete Freund’s adjuvant, which was administered intradermally on days 0 and 21. Mice from day 21 to day 35 received the following EDs by oral gavage: cypermethrin (CP), diethyl phthalate (DEP), vinclozolin (VCZ), 17α-ethinylestradiol (EE), perfluorooctanesulfonic acid (PFOS) and atrazine (ATR). ED exposure caused worsening of clinical signs (erythema and edema in the hind paws), histological and radiographic changes, as well as behavioral deficits, induced by CII injections. Furthermore, ED exposure significantly increased the degree of inflammation and oxidative damage induced by arthritis; this upregulation was more evident after exposure to ATR than to other EDs. The results from our study suggest that exposure to EDs may play a deleterious role in the progression of RA; therefore, exposure to EDs should be limited. |
format | Online Article Text |
id | pubmed-9025575 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-90255752022-04-23 Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis D’Amico, Ramona Gugliandolo, Enrico Cordaro, Marika Fusco, Roberta Genovese, Tiziana Peritore, Alessio Filippo Crupi, Rosalia Interdonato, Livia Di Paola, Davide Cuzzocrea, Salvatore Impellizzeri, Daniela Siracusa, Rosalba Di Paola, Rosanna Biomolecules Article Endocrine disruptors (EDs) are chemical substances capable of affecting endocrine system functioning and interfering with organ morphogenesis and physiological functions. The development and regeneration of bone tissues have a complex hormonal regulation, and therefore, bone tissue cells can be considered potential targets for endocrine disruptors. In that regard, the aim of this research was to investigate the impact of ED exposure on the inflammatory response and oxidative stress in an experimental model of collagen-induced arthritis (CIA). Arthritis was induced by an emulsion of type II collagen (CII) and complete Freund’s adjuvant, which was administered intradermally on days 0 and 21. Mice from day 21 to day 35 received the following EDs by oral gavage: cypermethrin (CP), diethyl phthalate (DEP), vinclozolin (VCZ), 17α-ethinylestradiol (EE), perfluorooctanesulfonic acid (PFOS) and atrazine (ATR). ED exposure caused worsening of clinical signs (erythema and edema in the hind paws), histological and radiographic changes, as well as behavioral deficits, induced by CII injections. Furthermore, ED exposure significantly increased the degree of inflammation and oxidative damage induced by arthritis; this upregulation was more evident after exposure to ATR than to other EDs. The results from our study suggest that exposure to EDs may play a deleterious role in the progression of RA; therefore, exposure to EDs should be limited. MDPI 2022-04-10 /pmc/articles/PMC9025575/ /pubmed/35454153 http://dx.doi.org/10.3390/biom12040564 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article D’Amico, Ramona Gugliandolo, Enrico Cordaro, Marika Fusco, Roberta Genovese, Tiziana Peritore, Alessio Filippo Crupi, Rosalia Interdonato, Livia Di Paola, Davide Cuzzocrea, Salvatore Impellizzeri, Daniela Siracusa, Rosalba Di Paola, Rosanna Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title | Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title_full | Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title_fullStr | Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title_full_unstemmed | Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title_short | Toxic Effects of Endocrine Disruptor Exposure on Collagen-Induced Arthritis |
title_sort | toxic effects of endocrine disruptor exposure on collagen-induced arthritis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9025575/ https://www.ncbi.nlm.nih.gov/pubmed/35454153 http://dx.doi.org/10.3390/biom12040564 |
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