Maternal exposure to environmental chemicals can adversely affect fetal health. This study aims to identify, in-vivo, the risk of maternal exposure to trichloroethane (TCE) on the birth weight and the neurobehavioral performance of newborns. Groups of female albino mice (F0 generation) were injected intraperitoneally twice weekly for three weeks with TCE (100 and 400 µg/kg BW). Animals were followed up for signs of toxicity and mortality. Neonate's motor behavior including large movement (crawling, pivoting, righting) and small movement (tremor) were assessed. No toxicity adverse signs or mortality were observed in the animals (F0 generation) treated with TCE. The results showed that TCE exposure led to a significant increase in the F1 mouse body weight compared to controls. The results also showed that tremor of neonates of dams exposed to TCE (100µg/kg and 400µg/kg BW) were significantly increased when assessed on postnatal day-1 (PND-1). These findings provide support to a role of the environmental toxicant, TCE, in abnormalities in birth weight and neonatal neurobehavior.
Mohamed A. Al-Griw, Massaud S. Maamar, Naser M. Salama, Lubna N. Algadi, Abdul Hakim S. Elnfati, Emad M. Bennour(9-2015)

Factor V Leiden G1691A (FVL) and Factor II prothrombin G20210A (PGM) mutations are the leading causes of thrombophilia. In this study, we have investigated the prevalence of the FVL G1691A and PGM G20210A single nucleotide polymorphisms (SNPs) among Libyan deep vein thrombosis (DVT) and myocardial infarction (MI) patients. SNP genotyping was performed using high-resolution melt analysis (HRM) and DNA sequencing. Biochemical parameters conducted on 112 males and 93 females showed no significant difference in means between the control group and the deep vein thrombosis and myocardial infarction groups. For Factor V Leiden, 40 samples were genotyped. Of the 40 samples, 6 (15.0%) of them were heterozygous and no one was homozygous. As for Factor II SNP, 59 samples were genotyped and only 2 (3.3%) were heterozygous. All the heterozygous samples showed 100% concordance between the HRM-PCR and DNA sequence analysis. Our study showed, for the first time, that both the FVL and PGM mutations are present among Libyan DVT and MI patients and that the FVL mutation is significantly associated with DVT but not with MI. However, our results do not support the association of PGM G20210A mutation with DVT or MI. arabic 18 English 117
Abdulghani Msalati, Abdulla Bashein, Murad Ghrew, Khaled Sedaa, Abushawashi Ali, Ahmed Zaid, (1-2021)

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)