Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Ambrosio 2014 Free Radic Biol Med

From Bioblast
Revision as of 11:13, 28 March 2018 by Beno Marija (talk | contribs)
(diff) โ† Older revision | Latest revision (diff) | Newer revision โ†’ (diff)
The printable version is no longer supported and may have rendering errors. Please update your browser bookmarks and please use the default browser print function instead.
Publications in the MiPMap
Ambrosio F, Brown E, Stolz D, Ferrari R, Goodpaster BH, Deasy B, Distefano G, Roperti A, Cheikhi A, Garciafigueroa Y, Barchowsky A (2014) Arsenic induces sustained impairment of skeletal muscle and muscle progenitor cell ultrastructure and bioenergetics. Free Radic Biol Med 74C:64-73.

ยป PMID: 24960579

Ambrosio F, Brown E, Stolz D, Ferrari R, Goodpaster BH, Deasy B, Distefano G, Roperti A, Cheikhi A, Garciafigueroa Y, Barchowsky A (2014) Free Radic Biol Med

Abstract: Over 4 million individuals in the United States, and over 140 million individuals worldwide, are exposed daily to arsenic-contaminated drinking water. Human exposures can range from below the current limit of 10ฮผg/L to over 1mg/L, with 100ฮผg/L promoting disease in a large portion of those exposed. Although increased attention has recently been paid to myopathy following arsenic exposure, the pathogenic mechanisms underlying clinical symptoms remain poorly understood. This study tested the hypothesis that arsenic induces lasting muscle mitochondrial dysfunction and impairs metabolism. Compared to nonexposed controls, mice exposed to drinking water containing 100ฮผg/L arsenite for 5 weeks demonstrated impaired muscle function, mitochondrial myopathy, and altered oxygen consumption that were concomitant with increased mitochondrial fusion gene transcription. There were no differences in the levels of inorganic arsenic or its monomethyl and dimethyl metabolites between controls and exposed muscles, confirming that arsenic does not accumulate in muscle. Nevertheless, muscle progenitor cells isolated from exposed mice recapitulated the aberrant myofiber phenotype and were more resistant to oxidative stress, generated more reactive oxygen species, and displayed autophagic mitochondrial morphology, compared to cells isolated from nonexposed mice. These pathological changes from a possible maladaptive oxidative stress response provide insight into declines in muscle functioning caused by exposure to this common environmental contaminant. โ€ข Keywords: Metabolism, Mitochondria, Resistance to stress, Free radicals

โ€ข O2k-Network Lab: US FL Orlando Goodpaster BH


Labels: MiParea: Respiration, Pharmacology;toxicology 


Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, NS  HRR: Oxygraph-2k