Proteomic identification of carbonylated proteins in the kidney of trichloroethene-exposed MRL+/+ mice

Xiuzhen Fan, Gangduo Wang, Robert D. English, M Khan

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Trichloroethene (TCE), a common environmental and occupational pollutant, is associated with multiorgan toxicity. Kidney is one of major target organs affected as a result of TCE exposure. Our previous studies have shown that exposure to TCE causes increased protein oxidation (protein carbonylation) in the kidneys of autoimmune-prone MRL+/+ mice, and suggested a potential role of protein oxidation in TCE-mediated nephrotoxicity. To assess the impact of chronic TCE exposure on protein oxidation, particularly to identify the carbonylated proteins in kidneys, female MRL+/+ mice were treated with TCE at the dose of 2mg/ml via drinking water for 36 weeks and kidney protein extracts were analyzed for protein carbonyls and carbonylated proteins identified using proteomic approaches (2D gel, Western blot, MALDI TOF/TOF MS/MS, etc.). TCE treatment led to significantly increased protein carbonyls in the kidney protein extracts (20000g pellet fraction). Interestingly, among 18 identified carbonylated proteins, 10 were found only in the kidneys of TCE-treated mice, whereas other 8 were present in the kidneys of both control and TCE-treated mice. The identified carbonylated proteins represent skeletal proteins, chaperones, stress proteins, enzymes, plasma protein and proteins involved in signaling pathways. The findings provide a map for further exploring the role of carbonylated proteins in TCE-mediated nephrotoxicity.

Original languageEnglish (US)
Pages (from-to)21-30
Number of pages10
JournalToxicology Mechanisms and Methods
Volume24
Issue number1
DOIs
StatePublished - Jan 2014

Fingerprint

Trichloroethylene
Proteomics
Kidney
Proteins
Oxidation
Protein Carbonylation
Environmental Pollutants
Carbonylation
Matrix-Assisted Laser Desorption-Ionization Mass Spectrometry
Heat-Shock Proteins
Drinking Water

Keywords

  • Autoimmune nephritis
  • Oxidative stress
  • Protein carbonylation
  • Proteomics
  • Trichloroethene

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Proteomic identification of carbonylated proteins in the kidney of trichloroethene-exposed MRL+/+ mice. / Fan, Xiuzhen; Wang, Gangduo; English, Robert D.; Khan, M.

In: Toxicology Mechanisms and Methods, Vol. 24, No. 1, 01.2014, p. 21-30.

Research output: Contribution to journalArticle

@article{4eef748d4c0547a8b5b5f449a9cb1af4,
title = "Proteomic identification of carbonylated proteins in the kidney of trichloroethene-exposed MRL+/+ mice",
abstract = "Trichloroethene (TCE), a common environmental and occupational pollutant, is associated with multiorgan toxicity. Kidney is one of major target organs affected as a result of TCE exposure. Our previous studies have shown that exposure to TCE causes increased protein oxidation (protein carbonylation) in the kidneys of autoimmune-prone MRL+/+ mice, and suggested a potential role of protein oxidation in TCE-mediated nephrotoxicity. To assess the impact of chronic TCE exposure on protein oxidation, particularly to identify the carbonylated proteins in kidneys, female MRL+/+ mice were treated with TCE at the dose of 2mg/ml via drinking water for 36 weeks and kidney protein extracts were analyzed for protein carbonyls and carbonylated proteins identified using proteomic approaches (2D gel, Western blot, MALDI TOF/TOF MS/MS, etc.). TCE treatment led to significantly increased protein carbonyls in the kidney protein extracts (20000g pellet fraction). Interestingly, among 18 identified carbonylated proteins, 10 were found only in the kidneys of TCE-treated mice, whereas other 8 were present in the kidneys of both control and TCE-treated mice. The identified carbonylated proteins represent skeletal proteins, chaperones, stress proteins, enzymes, plasma protein and proteins involved in signaling pathways. The findings provide a map for further exploring the role of carbonylated proteins in TCE-mediated nephrotoxicity.",
keywords = "Autoimmune nephritis, Oxidative stress, Protein carbonylation, Proteomics, Trichloroethene",
author = "Xiuzhen Fan and Gangduo Wang and English, {Robert D.} and M Khan",
year = "2014",
month = "1",
doi = "10.3109/15376516.2013.843112",
language = "English (US)",
volume = "24",
pages = "21--30",
journal = "Toxicology Mechanisms and Methods",
issn = "1537-6516",
publisher = "Informa Healthcare",
number = "1",

}

TY - JOUR

T1 - Proteomic identification of carbonylated proteins in the kidney of trichloroethene-exposed MRL+/+ mice

AU - Fan, Xiuzhen

AU - Wang, Gangduo

AU - English, Robert D.

AU - Khan, M

PY - 2014/1

Y1 - 2014/1

N2 - Trichloroethene (TCE), a common environmental and occupational pollutant, is associated with multiorgan toxicity. Kidney is one of major target organs affected as a result of TCE exposure. Our previous studies have shown that exposure to TCE causes increased protein oxidation (protein carbonylation) in the kidneys of autoimmune-prone MRL+/+ mice, and suggested a potential role of protein oxidation in TCE-mediated nephrotoxicity. To assess the impact of chronic TCE exposure on protein oxidation, particularly to identify the carbonylated proteins in kidneys, female MRL+/+ mice were treated with TCE at the dose of 2mg/ml via drinking water for 36 weeks and kidney protein extracts were analyzed for protein carbonyls and carbonylated proteins identified using proteomic approaches (2D gel, Western blot, MALDI TOF/TOF MS/MS, etc.). TCE treatment led to significantly increased protein carbonyls in the kidney protein extracts (20000g pellet fraction). Interestingly, among 18 identified carbonylated proteins, 10 were found only in the kidneys of TCE-treated mice, whereas other 8 were present in the kidneys of both control and TCE-treated mice. The identified carbonylated proteins represent skeletal proteins, chaperones, stress proteins, enzymes, plasma protein and proteins involved in signaling pathways. The findings provide a map for further exploring the role of carbonylated proteins in TCE-mediated nephrotoxicity.

AB - Trichloroethene (TCE), a common environmental and occupational pollutant, is associated with multiorgan toxicity. Kidney is one of major target organs affected as a result of TCE exposure. Our previous studies have shown that exposure to TCE causes increased protein oxidation (protein carbonylation) in the kidneys of autoimmune-prone MRL+/+ mice, and suggested a potential role of protein oxidation in TCE-mediated nephrotoxicity. To assess the impact of chronic TCE exposure on protein oxidation, particularly to identify the carbonylated proteins in kidneys, female MRL+/+ mice were treated with TCE at the dose of 2mg/ml via drinking water for 36 weeks and kidney protein extracts were analyzed for protein carbonyls and carbonylated proteins identified using proteomic approaches (2D gel, Western blot, MALDI TOF/TOF MS/MS, etc.). TCE treatment led to significantly increased protein carbonyls in the kidney protein extracts (20000g pellet fraction). Interestingly, among 18 identified carbonylated proteins, 10 were found only in the kidneys of TCE-treated mice, whereas other 8 were present in the kidneys of both control and TCE-treated mice. The identified carbonylated proteins represent skeletal proteins, chaperones, stress proteins, enzymes, plasma protein and proteins involved in signaling pathways. The findings provide a map for further exploring the role of carbonylated proteins in TCE-mediated nephrotoxicity.

KW - Autoimmune nephritis

KW - Oxidative stress

KW - Protein carbonylation

KW - Proteomics

KW - Trichloroethene

UR - http://www.scopus.com/inward/record.url?scp=84890404137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84890404137&partnerID=8YFLogxK

U2 - 10.3109/15376516.2013.843112

DO - 10.3109/15376516.2013.843112

M3 - Article

C2 - 24024666

AN - SCOPUS:84890404137

VL - 24

SP - 21

EP - 30

JO - Toxicology Mechanisms and Methods

JF - Toxicology Mechanisms and Methods

SN - 1537-6516

IS - 1

ER -