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Chemosphere. 2016 Feb;144:459-66. doi: 10.1016/j.chemosphere.2015.09.023. Epub 2015 Sep 18.

Amelioration of particulate matter-induced oxidative damage by vitamin c and quercetin in human bronchial epithelial cells.

Author information

1
Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, China.
2
Institute of Environmental Science, Shanxi University, Taiyuan 030006, China.
3
Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.
4
Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, China; College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, China. Electronic address: lzy@sxu.edu.cn.

Abstract

Exposure to fine particulate matter (PM2.5) has a close association with respiratory damage. Vitamin c and quercetin have been documented to possess antioxidant and anti-inflammation properties. However, their potential protective effects against PM2.5-induced respiratory damage have not been evaluated yet. Hence, the study was aimed to investigate their protective effects and delineate the possible mechanisms. The results indicated that PM2.5 depleted the cell viability of 16HBE cells, elevated reactive oxygen species (ROS) generation, and inhibited mitochondrial genes expressions, including fusion proteins Mfn1 and OPA1, along with biogenesis markers SIRT1 and p53R2. Additionally, the damage of mitochondrial morphology was observed upon PM2.5 exposure using both JC-1 and MitoTracker Red staining. Expressions of mitochondrial respiratory chain genes including NDUFS2 and UQCRI1 were also attenuated by PM2.5 exposure. Furthermore, PM2.5 promoted the mRNA levels of NADPH oxidase and inflammation cytokines. However, the addition of vitamin c or quercetin strikingly antagonized the PM2.5-induced toxic effects. Collectively, these findings suggest that vitamin c and quercetin have repressive roles in respiratory oxidative damage incurred by PM2.5, which provide the theoretical basis about intervention and control of food nutrients on PM2.5-induced human adverse health.

KEYWORDS:

16HBE; Inflammation; Mitochondria; PM(2.5); Quercetin; Vitamin c

[Indexed for MEDLINE]

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