Mechanism of cytotoxic action of perfluorinated acids II. Disruption of mitochondrial bioenergetics

Kleszczynski, K; Stepnowski, P; Skladanowski, AC

HERO ID

488418

Reference Type

Journal Article

Year

2009

Language

English

PMID

19135466

HERO ID 488418
In Press No
Year 2009
Title Mechanism of cytotoxic action of perfluorinated acids II. Disruption of mitochondrial bioenergetics
Authors Kleszczynski, K; Stepnowski, P; Skladanowski, AC
Journal Toxicology and Applied Pharmacology
Volume 235
Issue 2
Page Numbers 182-190
Abstract PFAs and derivatives due to perfect technological properties are broadly applied in industry and consumer goods, and in consequence widely disseminated, environmentally bioaccumulative and found at ppb level in human serum. Earlier we revealed that in vitro cytotoxicity increases with chain length (CF6-CF14). The compounds dissipate plasma membrane potential and acidify of cytosol. Here we determine whether there is an association between the protonophoric uncoupling of respiration and disruption of bioenergetics caused by CF6-CF12 on HCT116 cell apoptosis. Again the effects were stronger for longer molecules. Incubation of cells with CF10 stimulated time-dependent generation of reactive oxygen species, opening of mitochondrial permeability transition (MPT) pore, release of cytochrome c, activation of caspases and depletion of intracellular level of ATP occurring in intrinsic pathway of apoptosis. Incubation with decanoic acid (DA) did not lead to mitochondrial dysfunctions neither to cell cycle disturbances. Synchronized removal of the phosphorylated state of Akt, ERK1/2 and PKC6/0 kinases by CF10 suggests presence of concerted action to uninhibit Bad protein activation and a cascade of intrinsic pathway of apoptosis. Blocking MPT pore by cyclosporin A (CsA) led to a reduction of mitochondrial potential dissipation (mt Delta Psi). Such cells neither showed cytochrome c release nor the downstream activation of caspase-9 and caspase-3. Our results confirm that mitochondria play a crucial role in perfluorochemicals induced apoptosis by releasing apoptotic signals through MPT pore. (C) 2008 Elsevier Inc. All rights reserved.
Doi 10.1016/j.taap.2008.11.021
Pmid 19135466
Wosid WOS:000263994900006
Url http://www.sciencedirect.com/science/article/pii/S0041008X08005012
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Perfluorinated acid; Mitochondrial transmembrane potential; Reactive; oxygen species; Cytochrome c; Cyclosporin A; Apoptosis; Cell signaling; HCT116 cells; rodent peroxisome proliferator; cytochrome-c release; hepatoma hepg2; cells; fatty-acids; permeability transition; perfluorooctanoic acid; in-vitro; induced apoptosis; arachidonic-acid; rat-liver
Is Qa No
Relationship(s)