American Journal of BioScience

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Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury

Received: 22 February 2016    Accepted: 01 March 2016    Published: 19 March 2016
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Abstract

The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.

DOI 10.11648/j.ajbio.20160401.11
Published in American Journal of BioScience (Volume 4, Issue 1, January 2016)
Page(s) 1-8
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Environmental Toxicant, Spleen, Toxicity, Oxidative Stress, DNA Damage, Apoptosis, Mice

References
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Author Information
  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Chemistry Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Department of Pathology and Clinical Pathology, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya

  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Department of Internal Medicine, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya

Cite This Article
  • APA Style

    Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. (2016). Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. American Journal of BioScience, 4(1), 1-8. https://doi.org/10.11648/j.ajbio.20160401.11

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    ACS Style

    Massaud S. Maamar; Mohamed A. Al-Griw; Rabia O. Al-Ghazeer; Seham A. Al-Azreg; Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am. J. BioScience 2016, 4(1), 1-8. doi: 10.11648/j.ajbio.20160401.11

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    AMA Style

    Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am J BioScience. 2016;4(1):1-8. doi: 10.11648/j.ajbio.20160401.11

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  • @article{10.11648/j.ajbio.20160401.11,
      author = {Massaud S. Maamar and Mohamed A. Al-Griw and Rabia O. Al-Ghazeer and Seham A. Al-Azreg and Naser M. Salama and Emad M. Bennour},
      title = {Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury},
      journal = {American Journal of BioScience},
      volume = {4},
      number = {1},
      pages = {1-8},
      doi = {10.11648/j.ajbio.20160401.11},
      url = {https://doi.org/10.11648/j.ajbio.20160401.11},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ajbio.20160401.11},
      abstract = {The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.},
     year = {2016}
    }
    

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  • TY  - JOUR
    T1  - Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury
    AU  - Massaud S. Maamar
    AU  - Mohamed A. Al-Griw
    AU  - Rabia O. Al-Ghazeer
    AU  - Seham A. Al-Azreg
    AU  - Naser M. Salama
    AU  - Emad M. Bennour
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    DO  - 10.11648/j.ajbio.20160401.11
    T2  - American Journal of BioScience
    JF  - American Journal of BioScience
    JO  - American Journal of BioScience
    SP  - 1
    EP  - 8
    PB  - Science Publishing Group
    SN  - 2330-0167
    UR  - https://doi.org/10.11648/j.ajbio.20160401.11
    AB  - The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.
    VL  - 4
    IS  - 1
    ER  - 

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