Nickel Oxide (NiO) Nanoparticles Induce Loss of Cell Viability in Yeast Mediated by Oxidative Stress

• Type: Article in International Scientific Journal
• Date: 2018

Authors

Cátia A. Sousa (Author) Other; Helena M. V. M. Soares (Author) FEUP; Eduardo V. Soares (Author) Other

Journal

Title: Chemical Research in Toxicology

Vol. 31 No. 8

Pages: 658-665

ISSN: 0893-228X

Publisher: American Chemical Society

Indexing

ISI Web of Knowledge - 3 Citations

Scopus - 14 Citations

Other information

Authenticus ID: P-00P-HFB

DOI: 10.1021/acs.chemrestox.8b00022

Abstract (EN): The present work aimed to elucidate whether the toxic effects of nickel oxide (NiO) nanoparticles (NPs) on the yeast Saccharomyces cerevisiae were associated with oxidative stress (OS) and what mechanisms may have contributed to this OS. Cells exposed to NiO NPs accumulated superoxide anions and hydrogen peroxide, which were intracellularly generated. Yeast cells coexposed to NiO NPs and antioxidants (L-ascorbic acid and N-tert-butyl-alpha-phenylnitrone) showed quenching of reactive oxygen species (ROS) and increased resistance to NiO NPs, indicating that the loss of cell viability was associated with ROS accumulation. Mutants lacking mitochondrial DNA (rho(0)) displayed reduced levels of ROS and increased resistance to NiO NPs, which suggested the involvement of the mitochondrial respiratory chain in ROS production. Yeast cells exposed to NiO NPs presented decreased levels of reduced glutathione (GSH). Mutants deficient in GSH1 (gsh1 Delta) or GSH2 (gsh2 Delta) genes displayed increased levels of ROS and increased sensitivity to NiO NPs, which underline the central role of GSH against NiO NPs-induced OS. This work suggests that the increased levels of intracellular ROS (probably due to the perturbation of the electron transfer chain in mitochondria) combined with the depletion of GSH pool constitute important mechanisms of NiO NPs-induced loss of cell viability in the yeast S. cerevisiae.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 8