4.7 Article

NMR Spectroscopy Identifies Chemicals in Cigarette Smoke Condensate That Impair Skeletal Muscle Mitochondrial Function

期刊

TOXICS
卷 10, 期 3, 页码 -

出版社

MDPI
DOI: 10.3390/toxics10030140

关键词

cigarette smoke extract; tobacco; mitochondria; chronic obstructive pulmonary disease; skeletal muscle; bioenergetics; smoking

资金

  1. James and Esther King Biomedical Research Program (Florida Department of Health) [20K05]
  2. American Heart Association [POST836216]
  3. Ruth L. Kirschstein National Research Service Award Fellowship from the NIH/NIDDK [F31-DK128920]

向作者/读者索取更多资源

Tobacco smoke-related diseases such as chronic obstructive pulmonary disease (COPD) are associated with high healthcare burden and mortality rates. Many COPD patients were reported to have muscle atrophy and weakness, with several studies suggesting intrinsic muscle mitochondrial impairment as a possible driver of this phenotype. However, little is known about how active tobacco smoking might impact skeletal muscle physiology or mitochondrial health. In this study, acute exposure of muscle mitochondria to cigarette smoke condensate (CSC) was found to cause a dose-dependent decrease in skeletal muscle mitochondrial respiratory capacity.
Tobacco smoke-related diseases such as chronic obstructive pulmonary disease (COPD) are associated with high healthcare burden and mortality rates. Many COPD patients were reported to have muscle atrophy and weakness, with several studies suggesting intrinsic muscle mitochondrial impairment as a possible driver of this phenotype. Whereas much information has been learned about muscle pathology once a patient has COPD, little is known about how active tobacco smoking might impact skeletal muscle physiology or mitochondrial health. In this study, we examined the acute effects of cigarette smoke condensate (CSC) on muscle mitochondrial function and hypothesized that toxic chemicals present in CSC would impair mitochondrial respiratory function. Consistent with this hypothesis, we found that acute exposure of muscle mitochondria to CSC caused a dose-dependent decrease in skeletal muscle mitochondrial respiratory capacity. Next, we applied an analytical nuclear magnetic resonance (NMR)-based approach to identify 49 water-soluble and 12 lipid-soluble chemicals with high abundance in CSC. By using a chemical screening approach in the Seahorse XF96 analyzer, several CSC-chemicals, including nicotine, o-Cresol, phenylacetate, and decanoic acid, were found to impair ADP-stimulated respiration in murine muscle mitochondrial isolates significantly. Further to this, several chemicals, including nicotine, o-Cresol, quinoline, propylene glycol, myo-inositol, nitrosodimethylamine, niacinamide, decanoic acid, acrylonitrile, 2-naphthylamine, and arsenic acid, were found to significantly decrease the acceptor control ratio, an index of mitochondrial coupling efficiency.

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