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)

Bisphenol A (BPA), an endocrine and metabolic disruptor, is widely used to manufacture polycarbonate plastics and epoxy resins. Accumulating evidence suggests that paternal BPA exposure adversely affects male germlines and results in atypical reproductive phenotypes that might persist for generations to come. Our study investigated this exposure on testicular architecture and sperm quality in mouse offspring, and characterised underlying molecular mechanism(s). A total of 18 immature male Swiss albino mice (3.5 weeks old) were randomly divided into three groups and treated as follows: Group I, no treatment (sham control); Group II, sterile corn oil only (vehicle control); Group III, BPA (400 μg/kg) in sterile corn oil. At 9.5 weeks old, F0 males were mated with unexposed females. F0 offspring (F1 generation) were monitored for postnatal development for 10 weeks. At 11.5 weeks old, the animals were sacrificed to examine testicular architecture, sperm parameters, including DNA integrity, and oxidative stress biomarkers (malondialdehyde (MDA), protein carbonylation (PC), and nitric oxide (NO)). Results showed that BPA significantly induced changes in the body and testis weights of the F0 and F1 generation BPA lineages compared to F0 and F1 generation control lineages. A decrease in sperm count and motility with further, increased sperm abnormalities, no or few sperm DNA alterations and elevated levels of MDA, PC, and NO were recorded. Similar effects were found in BPA exposed F0 males, but were more pronounced in the F0 offspring. In addition, BPA caused alterations in the testicular architecture. These pathological changes extended transgenerationally to F1 generation males’ mice, but the pathological changes were more pronounced in the F1 generation. Our findings demonstrate that the biological and health BPA impacts do not end in paternal adults, but are passed on to offspring generations. Hence, the linkage of seen testis and sperm pathologies in the F1 generation to BPA exposure of their parental line was evident in this work. The findings also illustrate that oxidative stress appears to be a molecular component of the testis and sperm pathologies. arabic 18 English 101
Mohamed A. Al-Griw(11-2020)

Background: During early development, environmental compounds can induce adult onset diseases and disrupt the circulating vitamin D (VitD) levels. Aim: This study aimed to examine the protective role of VitD against the adverse effects of BPA on male and female mice. Methods: A total of 60 male and female Swiss Albino mice (3 weeks old) were randomly divided into 5 groups; each consisted of 12 mice (6 males and 6 females) and was treated as follows: Group I received no treatment (sham control); Group II, sterile corn oil only (vehicle control); Group III, BPA (400 μg/kg); Group IV, VitD (2,195 IU/kg); and Group V, BPA + VitD. At 10.5 weeks, the animals were sacrificed to conduct histological examinations. Results: BPA-exposed mice were found to have neurobehavioral abnormalities, heart, kidney, and lung diseases with increased apoptotic indices in both sexes. On the other hand, the treatment of BPA mice with VitD altered this scenario with modulated motor activity, enhanced body and organ weights, and preserved the heart, kidney, and lung architecture, alongside a decreased percent apoptotic index. Conclusion: Our findings illustrate that VitD protects mice against BPA-induced heart, kidney, and lung abnormalities. arabic 20 English 103
Mohamed A. Al-Griw(8-2021)