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.
Mohamed A. Al-Griw, Abdul Hakim Elnfati, Naser M. Salama, Massaud S. Maamar, Soad A. Treesh, Taher Shaibi(10-2015)

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
Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, Emad M. Bennour(3-2016)

Background: The fat extracted from the nut of the African Shea tree (Vitellaria paradoxa) is called Shea butter. It has multiple uses at the local level as it is used in cosmetic products and as a cocoa butter substitute in chocolate industries. It has a high nutritious value and is also a valuable product on the local, national, and international markets, making it the ideal candidate to research and invest in. Aim: This study is a comparative experimental study of the possible burn healing effects between imported South African raw Shea butter and samples in a Libyan market. Method: The control samples were brought from South Africa (Benin traditional markets). A total of 18 different samples were collected from different sale centers in Tripoli, including pharmacies, beauty shops, and spices shops, in addition to one sample brought from Poland. Animal experiment on burn healing effect was carried out on nine male Sprague Dawley (350–400 g) rats aged 6–8 weeks old. After shaving the animal’s dorsum hair, a metal cube was used to create a deep second degree burn wound, and the cube was heated to 100°C for 20 seconds. Medication with Shea butter (control, T1, and T2) was initiated daily for one for these groups by the application of a thin film of the Shea butter samples on the burned areas. On days 1, 3, and 7, the rats were anesthetised and a sample from the burned scar tissue and skin adjacent were evaluated using pathological parameters. Results: The histological study indicates that the use of Shea butter T1 as topical treatment induces an immune response, which enhances the form of the presence of a large number of inflammatory cells in the epidermis and dermis layers. The treatment of burned skin with T2 lasted for 72 hours and it showed slightly significant healing in the normal structure of proliferative granulation tissue with accumulation of fibroblasts and inflammatory cells surrounding the sebaceous glands and hair follicles. Small areas of the epidermis which formed few layers were observed and some hair roots were grown. This was well seen in cases of T1 and T2. Shea butter bought as raw might have a bad effect on burned skin. Conclusion: Shea butter bought as raw might have bad effect on burned skin. On the other hand, the sample from Poland had a therapeutic effect, which was because of the additives such as avocado oil, grape seed oil, and others. arabic 18 English 101
Sakina Salem Mohammed Saadawi, Soad Ali Abdulsalam Treesh, ٍSuhera Mehemed Abdulsalam Aburawi, , , (11-2020)