Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice

Epidemiological studies suggest that ambient particulate matter exposure may be a new risk factor of glaucoma, but it lacks solid experimental evidence to establish a causal relationship. In this study, young mice (4 weeks old) were exposed concentrated ambient PM2.5 (CAP) for 9 months, which is thr...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Liping Li, Ji Zhou, Wenpei Fan, Liangliang Niu, Maomao Song, Bo Qin, Xinghuai Sun, Yuan Lei
Formato: article
Lenguaje:EN
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://doaj.org/article/d162ae196ee44d81b5df3086d7f85d76
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:d162ae196ee44d81b5df3086d7f85d76
record_format dspace
spelling oai:doaj.org-article:d162ae196ee44d81b5df3086d7f85d762021-11-14T04:28:20ZLifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice0147-651310.1016/j.ecoenv.2021.112963https://doaj.org/article/d162ae196ee44d81b5df3086d7f85d762021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321010757https://doaj.org/toc/0147-6513Epidemiological studies suggest that ambient particulate matter exposure may be a new risk factor of glaucoma, but it lacks solid experimental evidence to establish a causal relationship. In this study, young mice (4 weeks old) were exposed concentrated ambient PM2.5 (CAP) for 9 months, which is throughout most of the life span of a mouse under heavy pollution. CAP was introduced using a versatile aerosol concentration enrichment system which mimics natural PM2.5 exposure. CAP exposure caused a gradual elevation of intraocular pressure (IOP) and an increase in aqueous humor outflow resistance. In the conventional outflow tissues that regulates IOP, inducible nitric oxide synthase (iNOS) was up-regulated and 3-nitrotyrosine (3-NT) formation increased. At the cellular level, PM2.5 exposure increased the transendothelial electrical resistance of cells that control IOP (AAP cells). This is accompanied by increased reactive oxygen species (ROS), iNOS and 3-NT levels. Peroxynitrite scavenger MnTMPyP successfully treated the IOP elevation and restored it to normal levels by reducing 3-NT formation in outflow tissues. This study provides the novel evidence that in young mice, lifetime whole-body PM2.5 exposure has a direct toxic effect on intraocular tissues, which imposes a significant risk of IOP elevation and may initiate the development of ocular hypertension and glaucoma. This occurs as a result of protein nitration of conventional aqueous humor outflow tissues.Liping LiJi ZhouWenpei FanLiangliang NiuMaomao SongBo QinXinghuai SunYuan LeiElsevierarticlePM2.5GlaucomaIntraocular pressure3-nitrotyrosineNitrative stressEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 112963- (2021)
institution DOAJ
collection DOAJ
language EN
topic PM2.5
Glaucoma
Intraocular pressure
3-nitrotyrosine
Nitrative stress
Environmental pollution
TD172-193.5
Environmental sciences
GE1-350
spellingShingle PM2.5
Glaucoma
Intraocular pressure
3-nitrotyrosine
Nitrative stress
Environmental pollution
TD172-193.5
Environmental sciences
GE1-350
Liping Li
Ji Zhou
Wenpei Fan
Liangliang Niu
Maomao Song
Bo Qin
Xinghuai Sun
Yuan Lei
Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
description Epidemiological studies suggest that ambient particulate matter exposure may be a new risk factor of glaucoma, but it lacks solid experimental evidence to establish a causal relationship. In this study, young mice (4 weeks old) were exposed concentrated ambient PM2.5 (CAP) for 9 months, which is throughout most of the life span of a mouse under heavy pollution. CAP was introduced using a versatile aerosol concentration enrichment system which mimics natural PM2.5 exposure. CAP exposure caused a gradual elevation of intraocular pressure (IOP) and an increase in aqueous humor outflow resistance. In the conventional outflow tissues that regulates IOP, inducible nitric oxide synthase (iNOS) was up-regulated and 3-nitrotyrosine (3-NT) formation increased. At the cellular level, PM2.5 exposure increased the transendothelial electrical resistance of cells that control IOP (AAP cells). This is accompanied by increased reactive oxygen species (ROS), iNOS and 3-NT levels. Peroxynitrite scavenger MnTMPyP successfully treated the IOP elevation and restored it to normal levels by reducing 3-NT formation in outflow tissues. This study provides the novel evidence that in young mice, lifetime whole-body PM2.5 exposure has a direct toxic effect on intraocular tissues, which imposes a significant risk of IOP elevation and may initiate the development of ocular hypertension and glaucoma. This occurs as a result of protein nitration of conventional aqueous humor outflow tissues.
format article
author Liping Li
Ji Zhou
Wenpei Fan
Liangliang Niu
Maomao Song
Bo Qin
Xinghuai Sun
Yuan Lei
author_facet Liping Li
Ji Zhou
Wenpei Fan
Liangliang Niu
Maomao Song
Bo Qin
Xinghuai Sun
Yuan Lei
author_sort Liping Li
title Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
title_short Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
title_full Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
title_fullStr Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
title_full_unstemmed Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice
title_sort lifetime exposure of ambient pm2.5 elevates intraocular pressure in young mice
publisher Elsevier
publishDate 2021
url https://doaj.org/article/d162ae196ee44d81b5df3086d7f85d76
work_keys_str_mv AT lipingli lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT jizhou lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT wenpeifan lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT liangliangniu lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT maomaosong lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT boqin lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT xinghuaisun lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
AT yuanlei lifetimeexposureofambientpm25elevatesintraocularpressureinyoungmice
_version_ 1718430044115697664