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<ArticleSet>
  <Article>
    <Journal>
      <PublisherName>Tabriz University of Medical Sciences</PublisherName>
      <JournalTitle>Advanced Pharmaceutical Bulletin</JournalTitle>
      <Issn>2228-5881</Issn>
      <Volume>10</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month>02</Month>
        <DAY>18</DAY>
      </PubDate>
    </Journal>
    <ArticleTitle>Cupric Oxide Nanoparticles Induce Cellular Toxicity in Liver and Intestine Cell Lines</ArticleTitle>
    <FirstPage>213</FirstPage>
    <LastPage>220</LastPage>
    <ELocationID EIdType="doi">10.34172/apb.2020.025</ELocationID>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName>Mahmoud</FirstName>
        <LastName>Abudayyak</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0003-2286-4777</Identifier>
      </Author>
      <Author>
        <FirstName>Elif</FirstName>
        <LastName>Guzel</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0001-9072-3322</Identifier>
      </Author>
      <Author>
        <FirstName>Gül</FirstName>
        <LastName>Özhan</LastName>
        <Identifier Source="ORCID">https://orcid.org/0000-0002-6926-5723</Identifier>
      </Author>
    </AuthorList>
    <PublicationType>Journal Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.34172/apb.2020.025</ArticleId>
    </ArticleIdList>
    <History>
      <PubDate PubStatus="received">
        <Year>2019</Year>
        <Month>07</Month>
        <Day>04</Day>
      </PubDate>
      <PubDate PubStatus="accepted">
        <Year>2019</Year>
        <Month>10</Month>
        <Day>09</Day>
      </PubDate>
    </History>
    <Abstract>Purpose: The wide application of cupric oxide nanoparticles (copper (II) oxide, CuO-NPs) in various fields has increased exposure to the kind of active nanomaterials, which can cause negative effects on human and environment health. Although CuO-NPs were reported to be harmful to human, there is still a lack information related to their toxic potentials. In the present study, the toxic potentials of CuO-NPs were evaluated in the liver (HepG2 hepatocarcinoma) and intestine (Caco-2 colorectal adenocarcinoma) cells. Methods: After the characterization of particles, cellular uptake and morphological changes were determined. The potential of cytotoxic, genotoxic, oxidative and apoptotic damage was investigated with several in vitro assays. Results: The average size of the nanoparticles was 34.9 nm, about 2%-5% of the exposure dose was detected in the cells and mainly accumulated in different organelles, causing oxidative stress, cell damages, and death. The IC50 values were 10.90 and 10.04 µg/mL by MTT assay, and 12.19 and 12.06 µg/mL by neutral red uptake (NRU) assay, in HepG2 and Caco-2 cells respectively. Apoptosis assumes to the main cell death pathway; the apoptosis percentages were 52.9% in HepG2 and 45.5% in Caco-2 cells. Comet assay result shows that the highest exposure concentration (20 µg/mL) causes tail intensities about 9.6 and 41.8%, in HepG2 and Caco-2 cells, respectively. Conclusion: CuO-NPs were found to cause significant cytotoxicity, genotoxicity, and oxidative and apoptotic effects in both cell lines. Indeed, CuO-NPs could be dangerous to human health even if their toxic mechanisms should be elucidated with further studies.</Abstract>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Copper oxide</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Nanoparticle</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">DNA damage</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Cytotoxicity</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Oxidative stress</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Apoptosis</Param>
      </Object>
    </ObjectList>
  </Article>
</ArticleSet>