Published October 15, 2013 | Version v1
Journal article

Cadmium sulfate and CdTe-quantum dots alter DNA repair in zebrafish (Danio rerio) liver cells

  • 1. The Institute of Environmental and Human Health, Texas Tech University, Lubbock, TX 79416 (United States)
  • 2. Department of Biomedical Engineering, McGill University, Montréal, QC H3A 2B4 (Canada)

Description

Increasing use of quantum dots (QDs) makes it necessary to evaluate their toxicological impacts on aquatic organisms, since their contamination of surface water is inevitable. This study compares the genotoxic effects of ionic Cd versus CdTe nanocrystals in zebrafish hepatocytes. After 24 h of CdSO4 or CdTe QD exposure, zebrafish liver (ZFL) cells showed a decreased number of viable cells, an accumulation of Cd, an increased formation of reactive oxygen species (ROS), and an induction of DNA strand breaks. Measured levels of stress defense and DNA repair genes were elevated in both cases. However, removal of bulky DNA adducts by nucleotide excision repair (NER) was inhibited with CdSO4 but not with CdTe QDs. The adverse effects caused by acute exposure of CdTe QDs might be mediated through differing mechanisms than those resulting from ionic cadmium toxicity, and studying the effects of metallic components may be not enough to explain QD toxicities in aquatic organisms. - Highlights: • Both CdSO4 and CdTe QDs lead to cell death and Cd accumulation. • Both CdSO4 and CdTe QDs induce cellular ROS generation and DNA strand breaks. • Both CdSO4 and CdTe QDs induce the expressions of stress defense and DNA repair genes. • NER repair capacity was inhibited with CdSO4 but not with CdTe QDs

Availability note (English)

Available from http://dx.doi.org/10.1016/j.taap.2013.06.004

Additional details

Identifiers

DOI
10.1016/j.taap.2013.06.004;
PII
S0041-008X(13)00271-8;

Publishing Information

Journal Title
Toxicology and Applied Pharmacology
Journal Volume
272
Journal Issue
2
Journal Page Range
p. 443-452
ISSN
0041-008X
CODEN
TXAPA9

Optional Information

Copyright
Copyright (c) 2013 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.