Perfluorononanoic acid-induced apoptosis in rat spleen involves oxidative stress and the activation of caspase-independent death pathway

Fang, X; Feng, Y; Wang, J; Dai, J

HERO ID

2919316

Reference Type

Journal Article

Year

2010

Language

English

PMID

19878704

HERO ID 2919316
In Press No
Year 2010
Title Perfluorononanoic acid-induced apoptosis in rat spleen involves oxidative stress and the activation of caspase-independent death pathway
Authors Fang, X; Feng, Y; Wang, J; Dai, J
Journal Toxicology
Volume 267
Issue 1-3
Page Numbers 54-59
Abstract Perfluoroalkyl acid (PFAA)-induced apoptosis has been reported in many cell types. However, minimal information on its mode of action is available. This study explored the possible involvement of apoptotic signaling pathways in a nine-carbon-chain length PFAA-perfluorononanoic acid (PFNA)-induced splenocyte apoptosis. After a 14-day exposure to PFNA, rat spleens showed dose-dependent levels of apoptosis. The production of pro-inflammatory and anti-inflammatory cytokines was significantly increased and decreased, respectively. However, protein levels of tumor necrosis factor receptor 1 (TNFR1), fas-associated protein with death domain (FADD), caspase 8 and caspase 3, which are involved in inflammation-related and caspase-dependent apoptosis, were discordant. Peroxisome proliferator-activated receptors alpha (PPARalpha) and PPARgamma genes expression was up-regulated in rats treated with 3 or 5 mg/kg/day of PFNA, and the level of hydrogen peroxide (H2O2) increased concurrently in rats treated with the highest dose. Moreover, superoxide dismutase (SOD) activity and Bcl-2 protein levels were dramatically decreased in spleens after treatment with 3 and 5 mg/kg/day of PFNA. However, protein levels of Bax were unchanged. Apoptosis-inducing factor (AIF), an initiator of caspase-independent apoptosis, was significantly increased in all PFNA-dosed rats. Thus, oxidative stress and the activation of a caspase-independent apoptotic signaling pathway contributed to PFNA-induced apoptosis in rat splenocytes.
Doi 10.1016/j.tox.2009.10.020
Pmid 19878704
Wosid WOS:000274588700008
Url https://search.proquest.com/docview/746076075?accountid=171501
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Environment Abstracts; Toxicology Abstracts; Tumor necrosis factor receptors; Oxidative stress; Hydrogen peroxide; Bax protein; Bcl-2 protein; Superoxide dismutase; Caspase-3; FADD protein; Fas-associated protein; Proteins; Signal transduction; Splenocytes; tumor necrosis factor receptor 1; Cytokines; Apoptosis-inducing factor; Mortality; Inflammation; Caspase-8; Peroxisome proliferator-activated receptors; Apoptosis; ENA 02:Toxicology & Environmental Safety; X 24490:Other