Abstract

Particulate air pollution is recognized as a potential risk factor for neurological disorders; however, the underlying mechanisms of neurodegenerative diseases that occur due to particulate air pollution remain unclear. The objective of the present study was to evaluate the neurotoxic effects caused by diesel exhaust particles (DEPs). We determined the ability of DEPs and carbon black (CB) to induce neurotoxicity, oxidative stress and inflammation, and to disrupt the expression of tau and autophagy proteins in human neuroblastoma IMR-32 cells. Spherical CB (dominated by C, N, and S) and DEPs (dominated by C, N, and O) in aggregates were observed using a field emission-scanning electron microscope (FE-SEM) equipped with energy-dispersive x-ray (EDX) microanalysis. Cell viability was significantly decreased by CB and DEPs in IMR-32 cells, but neither particle altered malondialdehyde (MDA) production. We observed that exposure to DEPs significantly increased 8-isoprostane and tumor necrosis factor (TNF)-α levels. Significantly increased expression of tau was induced in IMR-32 cells by DEPs but not by CB. Expression of beclin 1 was increased by DEPs, whereas the light chain 3II (LC3II)/LC3I ratio was increased by CB. Results of the present study suggested that DEPs induced neuroinflammation, oxidative stress, and neurodegenerative-related tau overexpression and regulation by autophagy in IMR-32 cells. We demonstrated that DEPs are able to induce neurotoxicity, which could be associated with the development of neurodegenerative diseases.

Original languageEnglish
Pages (from-to)54-59
Number of pages6
JournalEnvironmental Toxicology and Pharmacology
Volume62
DOIs
Publication statusPublished - Sep 1 2018

Fingerprint

Vehicle Emissions
tau Proteins
Autophagy
Neuroblastoma
Soot
Proteins
Neurodegenerative diseases
8-epi-prostaglandin F2alpha
Oxidative stress
Air Pollution
Air pollution
Neurodegenerative Diseases
Oxidative Stress
Nervous System Diseases
Malondialdehyde
Field emission
Cell Survival
Electron microscopes
Tumor Necrosis Factor-alpha
Cells

Keywords

  • Beclin 1
  • Central nervous system
  • Inflammation
  • Neurotoxicity
  • Oxidative stress

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Health, Toxicology and Mutagenesis

Cite this

@article{617dcb8848924618b1b4ea405ddc761e,
title = "Effects of diesel exhaust particles on the expression of tau and autophagy proteins in human neuroblastoma cells",
abstract = "Particulate air pollution is recognized as a potential risk factor for neurological disorders; however, the underlying mechanisms of neurodegenerative diseases that occur due to particulate air pollution remain unclear. The objective of the present study was to evaluate the neurotoxic effects caused by diesel exhaust particles (DEPs). We determined the ability of DEPs and carbon black (CB) to induce neurotoxicity, oxidative stress and inflammation, and to disrupt the expression of tau and autophagy proteins in human neuroblastoma IMR-32 cells. Spherical CB (dominated by C, N, and S) and DEPs (dominated by C, N, and O) in aggregates were observed using a field emission-scanning electron microscope (FE-SEM) equipped with energy-dispersive x-ray (EDX) microanalysis. Cell viability was significantly decreased by CB and DEPs in IMR-32 cells, but neither particle altered malondialdehyde (MDA) production. We observed that exposure to DEPs significantly increased 8-isoprostane and tumor necrosis factor (TNF)-α levels. Significantly increased expression of tau was induced in IMR-32 cells by DEPs but not by CB. Expression of beclin 1 was increased by DEPs, whereas the light chain 3II (LC3II)/LC3I ratio was increased by CB. Results of the present study suggested that DEPs induced neuroinflammation, oxidative stress, and neurodegenerative-related tau overexpression and regulation by autophagy in IMR-32 cells. We demonstrated that DEPs are able to induce neurotoxicity, which could be associated with the development of neurodegenerative diseases.",
keywords = "Beclin 1, Central nervous system, Inflammation, Neurotoxicity, Oxidative stress",
author = "Bai, {Kuan Jen} and Chuang, {Kai Jen} and Wu, {Sheng Ming} and Chang, {Li Te} and Chang, {Ta Yuan} and Ho, {Kin Fai} and Chuang, {Hsiao Chi}",
year = "2018",
month = "9",
day = "1",
doi = "10.1016/j.etap.2018.06.007",
language = "English",
volume = "62",
pages = "54--59",
journal = "Environmental Toxicology and Pharmacology",
issn = "1382-6689",
publisher = "Elsevier",

}

TY - JOUR

T1 - Effects of diesel exhaust particles on the expression of tau and autophagy proteins in human neuroblastoma cells

AU - Bai, Kuan Jen

AU - Chuang, Kai Jen

AU - Wu, Sheng Ming

AU - Chang, Li Te

AU - Chang, Ta Yuan

AU - Ho, Kin Fai

AU - Chuang, Hsiao Chi

PY - 2018/9/1

Y1 - 2018/9/1

N2 - Particulate air pollution is recognized as a potential risk factor for neurological disorders; however, the underlying mechanisms of neurodegenerative diseases that occur due to particulate air pollution remain unclear. The objective of the present study was to evaluate the neurotoxic effects caused by diesel exhaust particles (DEPs). We determined the ability of DEPs and carbon black (CB) to induce neurotoxicity, oxidative stress and inflammation, and to disrupt the expression of tau and autophagy proteins in human neuroblastoma IMR-32 cells. Spherical CB (dominated by C, N, and S) and DEPs (dominated by C, N, and O) in aggregates were observed using a field emission-scanning electron microscope (FE-SEM) equipped with energy-dispersive x-ray (EDX) microanalysis. Cell viability was significantly decreased by CB and DEPs in IMR-32 cells, but neither particle altered malondialdehyde (MDA) production. We observed that exposure to DEPs significantly increased 8-isoprostane and tumor necrosis factor (TNF)-α levels. Significantly increased expression of tau was induced in IMR-32 cells by DEPs but not by CB. Expression of beclin 1 was increased by DEPs, whereas the light chain 3II (LC3II)/LC3I ratio was increased by CB. Results of the present study suggested that DEPs induced neuroinflammation, oxidative stress, and neurodegenerative-related tau overexpression and regulation by autophagy in IMR-32 cells. We demonstrated that DEPs are able to induce neurotoxicity, which could be associated with the development of neurodegenerative diseases.

AB - Particulate air pollution is recognized as a potential risk factor for neurological disorders; however, the underlying mechanisms of neurodegenerative diseases that occur due to particulate air pollution remain unclear. The objective of the present study was to evaluate the neurotoxic effects caused by diesel exhaust particles (DEPs). We determined the ability of DEPs and carbon black (CB) to induce neurotoxicity, oxidative stress and inflammation, and to disrupt the expression of tau and autophagy proteins in human neuroblastoma IMR-32 cells. Spherical CB (dominated by C, N, and S) and DEPs (dominated by C, N, and O) in aggregates were observed using a field emission-scanning electron microscope (FE-SEM) equipped with energy-dispersive x-ray (EDX) microanalysis. Cell viability was significantly decreased by CB and DEPs in IMR-32 cells, but neither particle altered malondialdehyde (MDA) production. We observed that exposure to DEPs significantly increased 8-isoprostane and tumor necrosis factor (TNF)-α levels. Significantly increased expression of tau was induced in IMR-32 cells by DEPs but not by CB. Expression of beclin 1 was increased by DEPs, whereas the light chain 3II (LC3II)/LC3I ratio was increased by CB. Results of the present study suggested that DEPs induced neuroinflammation, oxidative stress, and neurodegenerative-related tau overexpression and regulation by autophagy in IMR-32 cells. We demonstrated that DEPs are able to induce neurotoxicity, which could be associated with the development of neurodegenerative diseases.

KW - Beclin 1

KW - Central nervous system

KW - Inflammation

KW - Neurotoxicity

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=85049304417&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85049304417&partnerID=8YFLogxK

U2 - 10.1016/j.etap.2018.06.007

DO - 10.1016/j.etap.2018.06.007

M3 - Article

VL - 62

SP - 54

EP - 59

JO - Environmental Toxicology and Pharmacology

JF - Environmental Toxicology and Pharmacology

SN - 1382-6689

ER -