Selenoprotein P regulates 1-(4-Chlorophenyl)-benzo-2,5-quinone-induced oxidative stress and toxicity in human keratinocytes

Wusheng Xiao; Yueming Zhu; Ehab H Sarsour; Amanda L Kalen; Nukhet Aykin-Burns; Douglas R Spitz; Prabhat C Goswami

doi:10.1016/j.freeradbiomed.2013.06.010

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Selenoprotein P regulates 1-(4-Chlorophenyl)-benzo-2,5-quinone-induced oxidative stress and toxicity in human keratinocytes

Journal article

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Selenoprotein P regulates 1-(4-Chlorophenyl)-benzo-2,5-quinone-induced oxidative stress and toxicity in human keratinocytes

Wusheng Xiao, Yueming Zhu, Ehab H Sarsour, Amanda L Kalen, Nukhet Aykin-Burns, Douglas R Spitz and Prabhat C Goswami

Free radical biology & medicine, Vol.65, pp.70-77

12/2013

DOI: 10.1016/j.freeradbiomed.2013.06.010

PMCID: PMC3830697

PMID: 23770201

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Abstract

Polychlorinated biphenyls and their metabolites are environmental pollutants that are believed to have adverse health effects presumably by inducing oxidative stress. To determine if 1-(4-Chlorophenyl)-benzo-2,5-quinone (4-ClBQ; metabolite of 4-monochlorobiphenyl, PCB3)-induced oxidative stress is associated with changes in the expression of specific antioxidant genes, mRNA levels of 92 oxidative stress-response genes were analyzed using TaqMan Array Human Antioxidant Mechanisms (Life Technologies), and results were verified by performing quantitative RT-PCR assays. The expression of selenoprotein P (sepp1) was significantly downregulated (8- to 10-fold) in 4-ClBQ-treated HaCaT human skin keratinocytes, which correlated with a significant increase in MitoSOX oxidation. Overexpression of Mn-superoxide dismutase or catalase or treatment with N-acetyl-l-cysteine suppressed 4-ClBQ-induced toxicity. Sodium selenite supplementation also suppressed 4-ClBQ-induced decrease in sepp1 expression, which was associated with a significant inhibition in cell death. Furthermore, HaCaT cells overexpressing sepp1 were resistant to 4-ClBQ-induced oxidative stress and toxicity. These results demonstrate that SEPP1 represents a previously unrecognized regulator of PCB-induced biological effects. These results support the speculation that selenoproteins can be an attractive countermeasure for PCB-induced adverse biological effects.

Cell Line

Flow Cytometry

Keratinocytes - drug effects

Oligonucleotide Array Sequence Analysis

Keratinocytes - metabolism

Humans

Oxidative Stress - physiology

Selenoprotein P - metabolism

Benzoquinones - toxicity

Immunoblotting

Environmental Pollutants - toxicity

Real-Time Polymerase Chain Reaction

Details

Title: Subtitle: Selenoprotein P regulates 1-(4-Chlorophenyl)-benzo-2,5-quinone-induced oxidative stress and toxicity in human keratinocytes
Creators: Wusheng Xiao - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA
Yueming Zhu - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA; Department of Radiation Oncology, Feinberg Northwestern Medical School, Northwestern University, Chicago, IL 60611, USA
Ehab H Sarsour - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA
Amanda L Kalen - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA
Nukhet Aykin-Burns - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA; Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Douglas R Spitz - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA
Prabhat C Goswami - Free Radical and Radiation Biology Division, Department of Radiation Oncology, The University of Iowa, Iowa City, IA 52242, USA. Electronic address: prabhat-goswami@uiowa.edu
Resource Type: Journal article
Publication Details: Free radical biology & medicine, Vol.65, pp.70-77
DOI: 10.1016/j.freeradbiomed.2013.06.010
PMID: 23770201
PMCID: PMC3830697
NLM abbreviation: Free Radic Biol Med
ISSN: 0891-5849
eISSN: 1873-4596
Publisher: United States
Grant note: NIH 2R01CA111365 / NCI NIH HHS P30 ES005605 / NIEHS NIH HHS NIEHSP42ES013661 / NIEHS NIH HHS R01 CA111365 / NCI NIH HHS
Language: English
Date published: 12/2013
Academic Unit: Pathology; Radiation Oncology
Record Identifier: 9984047735402771

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