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Toxicol Sci. 2016 Sep;153(1):55-69. doi: 10.1093/toxsci/kfw102. Epub 2016 Jun 2.

From the Cover: Thirdhand Cigarette Smoke Causes Stress-Induced Mitochondrial Hyperfusion and Alters the Transcriptional Profile of Stem Cells.

Author information

1
*Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, California 92521 Environmental Toxicology Graduate Program University of California Riverside.
2
*Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, California 92521.
3
*Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, California 92521 Bioengineering Interdepartmental Graduate Program, University of California Riverside.
4
Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, California 94243.
5
*Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, California 92521 talbot@ucr.edu.

Abstract

Thirdhand cigarette smoke (THS) was recently recognized as an environmental health hazard; however, little is known about it effects on cells. Mitochondria are sensitive monitors of cell health and report on environmentally induced stress. We tested the effects of low levels of THS extracted from terry cloth on mitochondrial morphology and function using stem cells with well-defined mitochondria. Concentrations of THS that did not kill cells caused stress-induced mitochondrial hyperfusion (SIMH), which was characterized by changes in mitochondrial morphology indicative of fusion, increased mitochondrial membrane potential (MMP), increased ATP levels, increased superoxide production, and increased oxidation of mitochondrial proteins. SIMH was accompanied by a decrease in Fis1 expression, a gene responsible for mitochondrial fission, and a decrease in apoptosis-related genes, including Aifm2, Bbc3, and Bid There was also down regulation of Ucp2, Ucp4, and Ucp5, genes that decrease MMP thereby reducing oxidative phosphorylation, while promoting glycolysis. These effects, which collectively accompany SIMH, are a prosurvival mechanism to rescue damaged mitochondria and protect cells from apoptosis. Prolonged exposure to THS caused a reduction in MMP and decreased cell proliferation, which likely leads to apoptosis.

KEYWORDS:

cigarette; fusion; mitochondria; oxidation; reactive oxygen species.; smoke; stress; thirdhand smoke; tobacco

PMID:
27255386
DOI:
10.1093/toxsci/kfw102
[Indexed for MEDLINE]
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