Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury
American Journal of BioScience
Volume 4, Issue 1, January 2016, Pages: 1-8
Received: Feb. 22, 2016; Accepted: Mar. 1, 2016; Published: Mar. 19, 2016
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Authors
Massaud S. Maamar, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Mohamed A. Al-Griw, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Rabia O. Al-Ghazeer, Chemistry Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Seham A. Al-Azreg, Department of Pathology and Clinical Pathology, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya
Naser M. Salama, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Emad M. Bennour, Department of Internal Medicine, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya
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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.
Keywords
Environmental Toxicant, Spleen, Toxicity, Oxidative Stress, DNA Damage, Apoptosis, Mice
To cite this article
Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, Emad M. Bennour, Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury, American Journal of BioScience. Vol. 4, No. 1, 2016, pp. 1-8. doi: 10.11648/j.ajbio.20160401.11
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Copyright © 2016 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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