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Mode of Cell Death in Mouse Brain Following Early Exposure to Low-Dose Trichloroethane: Apoptosis or Necrosis
Current Issue
Volume 3, 2015
Issue 6 (December)
Pages: 232-240   |   Vol. 3, No. 6, December 2015   |   Follow on         
Paper in PDF Downloads: 38   Since Oct. 24, 2015 Views: 1241   Since Oct. 24, 2015
Authors
[1]
Mohamed A. Al-Griw, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya.
[2]
Abdul Hakim Elnfati, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya.
[3]
Naser M. Salama, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya.
[4]
Massaud S. Maamar, Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya.
[5]
Soad A. Treesh, Department of Histology and Medical Genetics, Faculty of Medicine, University of Tripoli, Tripoli, Libya.
[6]
Taher Shaibi, Division of Ecological Sciences, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya; National Centre for Disease Control, Ministry of Health, Tripoli, Libya.
Abstract
The goal of this study was to investigate, in-vivo, the predominant mechanism of cell death, apoptosis versus necrosis, in the mature mouse brain exposed early to a ubiquitous environmental toxicant trichloroethane (TCE). A subset of male albino mice was injected intraperitoneally twice weekly for three weeks with TCE (100 and 400µg/kg). All animals were followed up for signs of toxicity and mortality. Changes in neural tissues were histpathologically evaluated. Biomarkers of brain cell number were also studied. The results showed that TCE insult triggered significant alterations in the microstructure of the brain tissues compared to controls. Mitotic figures and apoptotic changes such as chromatin condensation and nuclear fragments were also identified. Cell death analysis demonstrates that cell apoptosis with necrosis was evident in the TCE-treated groups. The percent of necrosis was quantified as 20.09 ± 2.57% at 100µg/kg TCE, 30.57 ± 5.18% at 400µg/kg TCE, and 12.67 ± 1.25% in controls. However, the percent of apoptosis was quantified as 29.18 ± 1.51% at 100µg/kg TCE, 20.14 ± 2.12% at 400µg/kg TCE, and 8 ± 1.25% in controls. There was also a significant reduction in the brain DNA content in the TCE-treated groups. Agarose gel electrophoresis is also provided further biochemical evidence of apoptosis by showing internucleosomal DNA fragmentation. These results correlated with neurobehavioral impairment. These findings indicate that TCE induces degeneration and apoptotic cell death in mouse brain, suggesting a crucial role played by apoptosis in TCE neurotoxicity.
Keywords
Trichloroethane, Neurotoxicity, Neurobehavior Abnormalities, Apoptosis, DNA Fragmentation, Mouse
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