Journal
REDOX BIOLOGY
Volume 3, Issue -, Pages 47-55Publisher
ELSEVIER
DOI: 10.1016/j.redox.2014.10.005
Keywords
Zinc; H2O2; Live cell imaging; Mitochondria; Catalase; Genetically encoded redox probes
Categories
Funding
- NIEHS Toxicology Training Grant [T32 ES007126]
- UNC-EPA Training Agreement [CR-83515201-0]
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Human exposure to particulate matter (PM) is a global environmental health concern. Zinc (Zn2+) is a ubiquitous respiratory toxicant that has been associated with PM health effects. However, the molecular mechanism of Zn2+ toxicity is not fully understood. H2O2 and Zn2+ have been shown to mediate signaling leading to adverse cellular responses in the lung and we have previously demonstrated Zn2+ to cause cellular H2O2 production. To determine the role of Zn2+-induced H2O2 production in the human airway epithelial cell response to Zn2+ exposure. BEAS-2B cells expressing the redox-sensitive fluorogenic sensors HyPer (H2O2) or roGFP2 (E-GSH) in the cytosol or mitochondria were exposed to 50 mu M Zn2+ for 5 min in the presence of 1 mu M of the zinc ionophore pyrithione. Intracellular H2O2 levels were modulated using catalase expression either targeted to the cytosol or ectopically to the mitochondria. HO-1 mRNA expression was measured as a downstream marker of response to oxidative stress induced by Zn2+ exposure. Both cytosolic catalase overexpression and ectopic catalase expression in mitochondria were effective in ablating Zn2+-induced elevations in H2O2. Compartment-directed catalase expression blunted Zn2+-induced elevations in cytosolic E-GSH and the increased expression of HO-1 mRNA levels. Zn2+ leads to multiple oxidative effects that are exerted through H2O2-dependent and independent mechanisms. Published by Elsevier B.V.
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