Neuropathology changed by 3- and 6-months low-level PM2.5 inhalation exposure in spontaneously hypertensive rats
Journal
Particle and fibre toxicology
Journal Volume
17
Journal Issue
1
Date Issued
2020
Author(s)
Chuang, Hsiao-Chi
Chai, Pei-Jui
Liao, Ho-Tang
Chen, Chia-Ling
Jhan, Ming-Kai
Hsieh, Hui-I
Abstract
Epidemiological evidence has linked fine particulate matter (PM2.5) to neurodegenerative diseases; however, the toxicological evidence remains unclear. The objective of this study was to investigate the effects of PM2.5 on neuropathophysiology in a hypertensive animal model. We examined behavioral alterations (Morris water maze), lipid peroxidation (malondialdehyde (MDA)), tau and autophagy expressions, neuron death, and caspase-3 levels after 3 and 6 months of whole-body exposure to urban PM2.5 in spontaneously hypertensive (SH) rats.
Subjects
Air pollution; Autophagy; Central nervous system toxicity; Particulate matter; Tau
Other Subjects
beclin 1; caspase 3; malonaldehyde; tau protein; air pollution; animal experiment; animal model; Article; autophagy (cellular); behavior disorder; brain cortex; cerebellum; controlled study; degenerative disease; exposure; hippocampus; hypertension; lipid peroxidation; male; nerve cell necrosis; neuropathology; neurotoxicity; nonhuman; particulate matter 2.5; priority journal; rat; spontaneously hypertensive rat; air pollutant; animal; brain; drug effect; female; particle size; particulate matter; toxicity; Air Pollutants; Animals; Brain; Female; Hippocampus; Inhalation Exposure; Male; Neuropathology; Particle Size; Particulate Matter; Rats; Rats, Inbred SHR
Type
journal article