2017
DOI: 10.1177/0748233717707361
|View full text |Cite
|
Sign up to set email alerts
|

Ascorbic acid prevents zinc oxide nanoparticle–induced intracellular oxidative stress and inflammatory responses

Abstract: Exposure to zinc oxide nanoparticles (ZnO NPs) promotes acute pulmonary toxicity through oxidative stress and inflammation. Furthermore, dissolved zinc from ZnO NPs induces the formation of intracellular reactive oxygen species (ROS). We previously reported that supplemental ascorbic acid (AA) inhibits ZnO NP-induced acute pulmonary toxicity in a rat model; however, the mechanism of this action remains unclear. Therefore, we investigated the effects of AA on ZnO NP-induced cytotoxicity in human lung carcinoma … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
12
0

Year Published

2018
2018
2023
2023

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 16 publications
(13 citation statements)
references
References 35 publications
1
12
0
Order By: Relevance
“…As‐2P displayed slightly better effect than L‐AA, which was consistent with its stability in solution. As‐2P may exert its effect within the cells or by modifying the extracellular environment (Fukui et al, ). As‐2P can be taken up by cells through sodium‐dependent Vc transporters (SVCTs) after modification by cell membrane esterases (Du et al, ).…”
Section: Resultsmentioning
confidence: 99%
“…As‐2P displayed slightly better effect than L‐AA, which was consistent with its stability in solution. As‐2P may exert its effect within the cells or by modifying the extracellular environment (Fukui et al, ). As‐2P can be taken up by cells through sodium‐dependent Vc transporters (SVCTs) after modification by cell membrane esterases (Du et al, ).…”
Section: Resultsmentioning
confidence: 99%
“…The current study was designed to determine the possible toxic effect of chronic oral administration of environmental-equivalent doses of pulmonary toxicity induced by ZnO-NPs. It was proved recently that, the mechanisms underlying the toxicity of ZnO-NPs depend on the induction of apoptosis [23,24]. Significant increase in the levels of pro-inflammatory mediator (COX-2) in lung tissue indicated pulmonary damage.…”
Section: Discussionmentioning
confidence: 99%
“…Qiao et al provided evidence that the pulmonary inflammation induced by exposure to ZnO-NPs is through modulation of miRNA expression [27]. Fukui et al reported that the inflammatory response and also the oxidative stress induced by ZnO-NPs were prevented by co-treatment with ascorbic acid in human lung carcinoma A549 cells [24]. However, further studies are recommended to investigate this protective effect on chronic lung inflammation induced by long term exposure to oral ingestion of ZnO-NPs.…”
Section: Discussionmentioning
confidence: 99%
“…In in vitro assays, in human lung carcinoma, A549 cells showed significant toxicity of ZnO-NPs. Exposure to vitamin C leads to a decrease in intracellular ROS production which lowered the inflammation level [91]. The proposed mechanism of vitamin C action was based on its antioxidant activity and chelating reaction with Zn leading to the formation of a stable complex.…”
Section: Antioxidantsmentioning
confidence: 99%