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Proteomic changes driven by urban pollution suggest particulate matter as a deregulator of energy metabolism, mitochondrial activity, and oxidative pathways in the rat brain

Author:
Araújo, J.E., Jorge, Susana, Santos, H.M., Chiechi, A., Galstyan, A., Lodeiro, Carlos, Diniz, M., Kleinman, M.T., Ljubimova, Julia Y., Capelo, J.L.
Source:
The Science of the total environment 2019 v.687 pp. 839-848
ISSN:
0048-9697
Subject:
adverse effects, air pollution, astrocytes, brain, carcinogenesis, computer software, electron transport chain, lungs, mass spectrometry, mitochondria, neurodegenerative diseases, neurons, particulates, protein synthesis, proteins, proteomics, rats, two-dimensional gel electrophoresis
Abstract:
The adverse effects of air pollution have been long studied in the lung and respiratory systems, but the molecular changes that this causes at the central nervous system level have yet to be fully investigated and understood. To explore the evolution with time of protein expression levels in the brain of rats exposed to particulate matter of different sizes, we carried out two-dimensional gel electrophoresis followed by determination of dysregulated proteins through Coomassie blue staining-based densities (SameSpots software) and subsequent protein identification using MALDI-based mass spectrometry. Expression differences in dysregulated proteins were found to be statistically significant with p-value <0.05. A systems biology-based approach was utilized to determine critical biochemical pathways involved in the rats' brain response. Our results suggest that rats' brains have a particulate matter size dependent-response, being the mitochondrial activity and the astrocyte function severely affected. Our proteomic study confirms the dysregulation of different biochemical pathways involving energy metabolism, mitochondrial activity, and oxidative pathways as some of the main effects of PM exposure on the rat brain.Rat brains exposed to particulate matter with origin in car engines are affected in two main areas: mitochondrial activity, by the dysregulation of many pathways linked to the respiratory chain, and neuronal and astrocytic function, which stimulates brain changes triggering tumorigenesis and neurodegeneration.
Agid:
6465961