An acetyl-L-carnitine switch on mitochondrial dysfunction and rescue in the metabolomics study on aluminum oxide nanoparticles

Particle and Fibre Toxicology
Xiaobo LiRui Chen

Abstract

Due to the wide application of engineered aluminum oxide nanoparticles and increased aluminum containing particulate matter suspending in air, exposure of human to nano-scale aluminum oxide nanoparticles (Al2O3 NPs) is becoming inevitable. In the present study, RNA microarray coupled with metabolomics analysis were used to uncover mechanisms underlying cellular responses to Al2O3 NPs and imply the potential rescue. We found that Al2O3 NPs significantly triggered down-regulation of mitochondria-related genes located in complex I, IV and V, which were involved in oxidative phosphorylation and neural degeneration pathways, in human bronchial epithelial (HBE) cells. Subsequent cell- and animal- based assays confirmed that Al2O3 NPs caused mitochondria-dependent apoptosis and oxidative stress either in vitro or in vivo, which were consistent with the trends of gene regulation. To rescue the Al2O3 NPs induced mitochondria dysfunction, disruption of small molecular metabolites of HBE were profiled using metabolomics analysis, which facilitates identification of potential antagonizer or supplement against nanoparticle-involved damages. Supplementation of an antioxidant, acetyl-L-carnitine, completely or partially restored the Al2O3 NPs...Continue Reading

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Citations

Nov 22, 2017·Journal of Nanobiotechnology·Eleonore Fröhlich
Nov 21, 2018·Nanomedicine·Liang ChenWan-Xi Yang
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Jan 29, 2021·Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)·Liuyan WuZhaoxin Tang

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Methods Mentioned

BETA
MDA
PCA
chip
Feature Extraction
flow cytometry
ELISA
PCR

Software Mentioned

SPSS12
DAVID
limma
MetaboAnalyst
Agilent Feature Extraction
GeneSpring Gx

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