Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae

Carbonic anhydrase (CA) catalyzes reversible hydration of CO2 to HCO3− to mediate pH and ion homeostasis. Some chemical pollutants have been reported to have inhibitory effects on fish CA. In this study, we investigated effects of a CA inhibitor ethoxyzolamide (EZA) on neuromasts development during...

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Autores principales:	Hiroko Matsumoto, Hisako Miyagi, Nobuhiro Nakamura, Yasuhiro Shiga, Toshihiro Ohta, Shoko Fujiwara, Mikio Tsuzuki
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Zebrafish Carbonic anhydrase Ethoxyzolamide Hair cell Neuromast Apoptosis Toxicology. Poisons RA1190-1270
Acceso en línea:	https://doaj.org/article/332d19bc5d6d4be58741166b802e7a2d
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spelling	oai:doaj.org-article:332d19bc5d6d4be58741166b802e7a2d2021-12-04T04:34:22ZCarbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae2214-750010.1016/j.toxrep.2021.11.018https://doaj.org/article/332d19bc5d6d4be58741166b802e7a2d2021-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S221475002100202Xhttps://doaj.org/toc/2214-7500Carbonic anhydrase (CA) catalyzes reversible hydration of CO2 to HCO3− to mediate pH and ion homeostasis. Some chemical pollutants have been reported to have inhibitory effects on fish CA. In this study, we investigated effects of a CA inhibitor ethoxyzolamide (EZA) on neuromasts development during zebrafish embryogenesis, since embryogenesis in aquatic organisms can be particularly sensitive to water pollution. EZA caused alteration of pH and calcium concentration and production of reactive oxygen species (ROS) in larvae, and induced apoptosis in hair cells especially in the otic neuromast, in which CA2 was distributed on the body surface. mRNA levels of apoptotic genes and caspase activities were increased by EZA, whereas anti-oxidants and apoptotic inhibitors, Bax, NF-κB, and p53 inhibitors significantly relieved the induction of hair cell death. Also, mRNA levels of Bip and CHOP, which are induced in response to ER stress, were upregulated by EZA, suggesting that EZA induces otic hair cell apoptosis via the intrinsic mitochondrial pathway and ER stress. Our results demonstrated an essential role of CA in neuromast development via maintenance of ion transport and pH, and that the CA, which is directly exposed to the ambient water, shows marked sensitivity to EZA.Hiroko MatsumotoHisako MiyagiNobuhiro NakamuraYasuhiro ShigaToshihiro OhtaShoko FujiwaraMikio TsuzukiElsevierarticleZebrafishCarbonic anhydraseEthoxyzolamideHair cellNeuromastApoptosisToxicology. PoisonsRA1190-1270ENToxicology Reports, Vol 8, Iss , Pp 1937-1947 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Zebrafish Carbonic anhydrase Ethoxyzolamide Hair cell Neuromast Apoptosis Toxicology. Poisons RA1190-1270
spellingShingle	Zebrafish Carbonic anhydrase Ethoxyzolamide Hair cell Neuromast Apoptosis Toxicology. Poisons RA1190-1270 Hiroko Matsumoto Hisako Miyagi Nobuhiro Nakamura Yasuhiro Shiga Toshihiro Ohta Shoko Fujiwara Mikio Tsuzuki Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
description	Carbonic anhydrase (CA) catalyzes reversible hydration of CO2 to HCO3− to mediate pH and ion homeostasis. Some chemical pollutants have been reported to have inhibitory effects on fish CA. In this study, we investigated effects of a CA inhibitor ethoxyzolamide (EZA) on neuromasts development during zebrafish embryogenesis, since embryogenesis in aquatic organisms can be particularly sensitive to water pollution. EZA caused alteration of pH and calcium concentration and production of reactive oxygen species (ROS) in larvae, and induced apoptosis in hair cells especially in the otic neuromast, in which CA2 was distributed on the body surface. mRNA levels of apoptotic genes and caspase activities were increased by EZA, whereas anti-oxidants and apoptotic inhibitors, Bax, NF-κB, and p53 inhibitors significantly relieved the induction of hair cell death. Also, mRNA levels of Bip and CHOP, which are induced in response to ER stress, were upregulated by EZA, suggesting that EZA induces otic hair cell apoptosis via the intrinsic mitochondrial pathway and ER stress. Our results demonstrated an essential role of CA in neuromast development via maintenance of ion transport and pH, and that the CA, which is directly exposed to the ambient water, shows marked sensitivity to EZA.
format	article
author	Hiroko Matsumoto Hisako Miyagi Nobuhiro Nakamura Yasuhiro Shiga Toshihiro Ohta Shoko Fujiwara Mikio Tsuzuki
author_facet	Hiroko Matsumoto Hisako Miyagi Nobuhiro Nakamura Yasuhiro Shiga Toshihiro Ohta Shoko Fujiwara Mikio Tsuzuki
author_sort	Hiroko Matsumoto
title	Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
title_short	Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
title_full	Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
title_fullStr	Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
title_full_unstemmed	Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae
title_sort	carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and er stress in zebrafish larvae
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/332d19bc5d6d4be58741166b802e7a2d
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Carbonic anhydrase inhibitor induces otic hair cell apoptosis via an intrinsic pathway and ER stress in zebrafish larvae

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