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Title: Effects of selenocystine on lead-exposed chinese hamster ovary (CHO) and PC-12 cells
Author (s): Aykin-Burns, N.
Ercal, Nuran
Department/Lab Affiliations: Chemistry
Environmental Research Center
Keywords: Lead toxicity
Reactive oxygen species
Selenocysteine
Thiol antioxidants
Issue Date: 2006
Publisher: Elsevier
Citation: Aykin-Burns, N., and Ercal, N. “Effects of Selenocystine on Lead-exposed Chinese Hamster Ovary (CHO) and PC-12 Cells” Toxicol Appl Pharmacol, 2006
Abstract: Lead is a pervasive environmental toxin that affects multiple organ systems, including the nervous, renal, reproductive, and hematological systems. Even though it is probably the most studied toxic metal, some of the symptoms of lead toxicity still cannot be explained by known molecular mechanisms. Therefore, lead-induced oxidative stress has recently started to gain attention. This in vitro study confirms the existence of oxidative stress due to lead exposure. Administration of lead acetate (PbA) to cultures of Chinese hamster ovary cells (CHO) had a concentration-dependent inhibitory effect on colony formation and cell proliferation. This inhibition was eliminated by 5 μM selenocystine (SeCys). In order to evaluate the nature of SeCys's effect, we measured glutathione (GSH), its oxidized form glutathione disulfide (GSSG), malondialdehyde (MDA), catalase, and GSH peroxidase (GPx) activities in lead-exposed CHO cells both in the presence and absence of SeCys. Increases in MDA, catalase, and GPx activities were observed in cultures that received only PbA, but supplementation with SeCys returned these measures to pretreatment levels. The ratio of GSH to GSSG increased in lead-exposed cells incubated in SeCys-enhanced media but declined in cultures treated with PbA only. In order to determine whether SeCys also reverses lead-induced neurotoxicity, a neuronal cell line, PC-12 cells, was used. Lead's inhibition on neurite formation was significantly eliminated by SeCys in PC-12 cells. Our results suggest that SeCys can confer protection against lead-induced toxicity in CHO cells and neurotoxicity in PC-12 cells.
Type: Article - Journal
text
In Title: Toxicology and Applied Pharmacology
Copyright Notice: This material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder.
FULL COPYRIGHT INFORMATION:
http://www.elsevier.com/wps/find/authorsview.authors/authorsrights
Publisher URL:
http://dx.doi.org/10.1016/j.taap.2005.12.002
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titleEffects of selenocystine on lead-exposed chinese hamster ovary (CHO) and PC-12 cells
contributor.authorAykin-Burns, N.
contributor.authorErcal, Nuran
contributor.deptlabChemistry
contributor.deptlabEnvironmental Research Center
contributor.sponsorNational Institute of Environmental Health
subjectLead toxicity
subjectReactive oxygen species
subjectSelenocysteine
subjectThiol antioxidants
date.issued2006
publisherElsevier
identifier.citationAykin-Burns, N., and Ercal, N. “Effects of Selenocystine on Lead-exposed Chinese Hamster Ovary (CHO) and PC-12 Cells” Toxicol Appl Pharmacol, 2006
identifier.pub.URI
http://dx.doi.org/10.1016/j.taap.2005.12.002
description.abstractLead is a pervasive environmental toxin that affects multiple organ systems, including the nervous, renal, reproductive, and hematological systems. Even though it is probably the most studied toxic metal, some of the symptoms of lead toxicity still cannot be explained by known molecular mechanisms. Therefore, lead-induced oxidative stress has recently started to gain attention. This in vitro study confirms the existence of oxidative stress due to lead exposure. Administration of lead acetate (PbA) to cultures of Chinese hamster ovary cells (CHO) had a concentration-dependent inhibitory effect on colony formation and cell proliferation. This inhibition was eliminated by 5 μM selenocystine (SeCys). In order to evaluate the nature of SeCys's effect, we measured glutathione (GSH), its oxidized form glutathione disulfide (GSSG), malondialdehyde (MDA), catalase, and GSH peroxidase (GPx) activities in lead-exposed CHO cells both in the presence and absence of SeCys. Increases in MDA, catalase, and GPx activities were observed in cultures that received only PbA, but supplementation with SeCys returned these measures to pretreatment levels. The ratio of GSH to GSSG increased in lead-exposed cells incubated in SeCys-enhanced media but declined in cultures treated with PbA only. In order to determine whether SeCys also reverses lead-induced neurotoxicity, a neuronal cell line, PC-12 cells, was used. Lead's inhibition on neurite formation was significantly eliminated by SeCys in PC-12 cells. Our results suggest that SeCys can confer protection against lead-induced toxicity in CHO cells and neurotoxicity in PC-12 cells.
typeArticle - Journal
type.DCMITypetext
type.statusFinal version
rightsThis material is presented to ensure timely dissemination of scholarly and technical work. Copyright and all rights therein are retained by authors or by other copyright holders. All persons copying this information are expected to adhere to the terms and constraints invoked by each author's copyright. In most cases, these works may not be reposted without the explicit permission of the copyright holder.
rights.URI
http://www.elsevier.com/wps/find/authorsview.authors/authorsrights
relation.isPartOfToxicology and Applied Pharmacology
date.accessioned2007-04-11T17:00:48Z
date.available2007-12-17T20:44:57Z
identifier.persist.URI
http://scholarsmine.mst.edu/post_prints/EffectsOfSelenocystine_09007dcc8042b2af.html