Dichloroacetate Decreases Cell Health and Activates Oxidative Stress Defense Pathways in Rat Alveolar Type II Pneumocytes.

Content Provider	Europe PMC
Author	Valauri-Orton, Alexis Bschorer, Frizzi Bernd, Karen K.
Copyright Year	2015
Abstract	Dichloroacetate (DCA) is a water purification byproduct that is known to be hepatotoxic and hepatocarcinogenic and to induce peripheral neuropathy and damage macrophages. This study characterizes the effects of the haloacetate on lung cells by exposing rat alveolar type II (L2) cells to 0–24 mM DCA for 6–24 hours. Increasing DCA concentration and the combination of increasing DCA concentration plus longer exposures decrease measures of cellular health. Length of exposure has no effect on oxidative stress biomarkers, glutathione, SOD, or CAT. Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway. These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.
ISSN	23146133
Journal	Biomed Research International
Volume Number	2015
PubMed Central reference number	PMC4537706
PubMed reference number	26301238
e-ISSN	23146141
DOI	10.1155/2015/129031
Language	English
Publisher	Hindawi
Publisher Date	2015-08-02
Access Restriction	Open
Rights License	This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2015 Alexis Valauri-Orton et al.
Content Type	Text
Resource Type	Article
Subject	Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology