Hdl Handle:
http://hdl.handle.net/10675.2/621302
Title:
Di-N-Octylphthalate Acts as a Proliferative Agent in Murine Cell Hepatocytes by Regulating the Levels of Pro-Apoptotic Proteins
Authors:
Pruitt, Allison; Miller, Laurence; Wiley, Faith
Abstract:
Hepatocellular carcinoma (HCC) is the fifth most common cancer in the US. Its development is thought to be associated with inactivation of tumor suppressors by methylation. Di-n-octylphthalate (DNOP), a common plasticizer, is believed to cause hepatic pre-neoplastic lesions. Because a number of tumor suppressors are shown to be not expressed in HCC, our goal was to identify tumor suppressor genes methylated upon treatment with 0.1 % DNOP at 24, 48, 72 h in mouse hepatocytes cell line AML-12 and isolated primary cultured mouse hepatocytes. None of tumor suppressors experienced a change in the methylation status in presence of DNOP. Because we found that DNOP causes an increase in cell proliferation, we studied whether the effect is paralleled to a suppression of apoptosis. We found that DNOP causes a decrease in pro-apoptotic proteins and no change in anti-apoptotic proteins. We studied the physiological effects of DNOP in mouse liver. Mice were treated with 0.1 % DNOP for a month. DNOP caused a decrease in bile secretion and an increase in the hepatic levels of bile acids and glutathione. Avoiding the use of DNOP as a plasticizer in products for human consumption can reduce the incidence of diseases related to its hepatotoxicity.
Affiliation:
Department of Biological Sciences
Issue Date:
Mar-2017
URI:
http://hdl.handle.net/10675.2/621302
Type:
Presentation
Language:
en
Description:
Presentation given at the 18th Annual Phi Kappa Phi Student Research and Fine Arts Conference
Appears in Collections:
Department of Biological Sciences: Student Research and Presentations; 18th Annual PKP Student Research and Fine Arts Conference: Oral Symposia I

Full metadata record

DC FieldValue Language
dc.contributor.authorPruitt, Allisonen
dc.contributor.authorMiller, Laurenceen
dc.contributor.authorWiley, Faithen
dc.date.accessioned2017-03-06T19:01:28Z-
dc.date.available2017-03-06T19:01:28Z-
dc.date.issued2017-03-
dc.identifier.urihttp://hdl.handle.net/10675.2/621302-
dc.descriptionPresentation given at the 18th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractHepatocellular carcinoma (HCC) is the fifth most common cancer in the US. Its development is thought to be associated with inactivation of tumor suppressors by methylation. Di-n-octylphthalate (DNOP), a common plasticizer, is believed to cause hepatic pre-neoplastic lesions. Because a number of tumor suppressors are shown to be not expressed in HCC, our goal was to identify tumor suppressor genes methylated upon treatment with 0.1 % DNOP at 24, 48, 72 h in mouse hepatocytes cell line AML-12 and isolated primary cultured mouse hepatocytes. None of tumor suppressors experienced a change in the methylation status in presence of DNOP. Because we found that DNOP causes an increase in cell proliferation, we studied whether the effect is paralleled to a suppression of apoptosis. We found that DNOP causes a decrease in pro-apoptotic proteins and no change in anti-apoptotic proteins. We studied the physiological effects of DNOP in mouse liver. Mice were treated with 0.1 % DNOP for a month. DNOP caused a decrease in bile secretion and an increase in the hepatic levels of bile acids and glutathione. Avoiding the use of DNOP as a plasticizer in products for human consumption can reduce the incidence of diseases related to its hepatotoxicity.en
dc.language.isoenen
dc.subjectCarcinoma, Hepatocellularen
dc.subjectMethylationen
dc.subjectMiceen
dc.subjectPlasticizersen
dc.titleDi-N-Octylphthalate Acts as a Proliferative Agent in Murine Cell Hepatocytes by Regulating the Levels of Pro-Apoptotic Proteinsen
dc.typePresentationen
dc.contributor.departmentDepartment of Biological Sciencesen
dc.description.advisorSabbatini, Mariaen
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