Environmental toxicants such as chemicals, heavy metals, and pesticides have been shown to promote transgenerational inheritance of abnormal phenotypes and/or diseases to multiple subsequent generations following parental and/ or ancestral exposures. This study was designed to examine the potential transgenerational action of the environmental toxicant trichloroethane (TCE) on transmission of liver abnormality, and to elucidate the molecular etiology of hepatocyte cell damage. A total of thirty two healthy immature female albino mice were randomly divided into three equal groups as follows: a sham group, which did not receive any treatment; a vehicle group, which received corn oil alone, and TCE treated group (3 weeks, 100 μg/kg i.p., every 4th day). The F0 and F1 generation control and TCE populations were sacrificed at the age of four months, and various abnormalities histpathologically investigated. Cell death and oxidative stress indices were also measured. The present study provides experimental evidence for the inheritance of environmentally induced liver abnormalities in mice. The results of this study show that exposure to the TCE promoted adult onset liver abnormalities in F0 female mice as well as unexposed F1 generation offspring. It is the first study to report a transgenerational liver abnormalities in the F1 generation mice through maternal line prior to gestation. This finding was based on careful evaluation of liver histopathological abnormalities, apoptosis of hepatocytes, and measurements of oxidative stress biomarkers (lipid peroxidation, protein carbonylation, and nitric oxide) in control and TCE populations. There was an increase in liver histopathological abnormalities, cell death, and oxidative lipid damage in F0 and F1 hepatic tissues of TCE treated group. In conclusion, this study showed that the biological and health impacts of environmental toxicant TCE do not end in maternal adults, but are passed on to offspring generations. Hence, linking observed liver abnormality in the offspring to environmental exposure of their parental line. This study also illustrated that oxidative stress and apoptosis appear to be a molecular component of the hepatocyte cell injury.
Mohamed A. Al-Griw , Soad A. Treesh, Rabia O. Alghazeer, Sassia O. Regeai (7-2017)

The ever-increasing demand for natural products and biotechnology, derived from bees and ultramodernization of various analytical devices, has facilitated the rational and planned development of biotechnology products with a focus on human health to treat chronic and neglected diseases. This study aimed to prepare, characterize and examine the stability and evaluation of the antioxidant and the antibacterial activity of Libyan propolis. Propolis Nanoparticles PNP were prepared using particle size reduction, then Transmission Electron Microscope (TEM) at a magnification of X 25000, was used for accurate evaluation of the size distribution of NPs. Three different concentration (10, 5, 2.5 mg/ml) of propolis and nano-propolis powder were tested for their 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity. The quantitative antioxidant activity test results using UV Spectrophotometer absorbance at 517 nm. The antibacterial activities of propolis and prepared nano propolis at different concentrations (10, 5 and 2.5mg/ml) were tested on bacterial strain, Klebsiella, human mouth, skin, and surface bacteria using cup cut diffusion method. The findings exhibited that the prepared propolis Nanoparticles (PNPs) were generally non-spherical with a size 100-200 nm. The PNP was a nano-sized particle around 316 nm in diameter. Zeta potential of PNP showed a negative surface charge value (− 48 mV) which was sufficiently high to avoid NPs aggregation. This value represents a stable and dispersed suspension of NPs and disables the tendency of aggregations in a short in period of time. Poly dispersity index (PdI) of synthetized PNP was used as a measurement of the size distribution. PdI values for PrNP were generally uniform with PdI 0.3 indicating monodispersity of the prepared systems. The propolis and PNPs displayed good antioxidant activity with inhibition percentage (77%, 46% and 18%) for propolis and (82%, 66% and 37%) for PNPs. Propolis nanoparticles showed to have more antibacterial effect compared to propolis. Libyan propolis nanoparticles has shown to be potential candidates as antioxidant and antibacterial agent.
sakina Salem Saadawi, Rabia O Alghazeer, Hanin N. Mughrbi, Bushra M. Dakhil, Rokaya O. Amara, Khairi A. Alennabi, Riham M. El-Moslemany, Khadija O. Turkman, Masarra A. Daraweel(3-2022)

Accumulating evidence indicates the role of endocrine disruptor bisphenol A (BPA) in many pathological conditions. Histone deacetylase (HDAC) inhibition has potential for the treatment of many diseases/abnormalities. Using a mouse BPA exposure model, this study investigated the hepatoprotective effects of the Food and Drug Administration–approved HDAC2 inhibitor valproic acid (VPA) against BPA-induced liver pathology. We randomly divided 30 adult male Swiss albino mice (8 weeks old; N = 6) into five groups: group 1, no treatment (sham control (SC)); group 2, only oral sterile corn oil (vehicle control (VC)); group 3, 4 mg/kg/day of oral BPA (single dose (BPA group)); group 4, 0.4% oral VPA (VPA group); and group 5, oral BPA + VPA (BPA + VPA group). At the age of 10 weeks, the mice were euthanized for biochemical and histological examinations. BPA promoted a significant decrease in the body weight (BW), an increase in the liver weight, and a significant increase in the levels of liver damage markers aspartate aminotransferase and alanine aminotransferase in the BPA group compared to SC, as well as pathological changes in liver tissue. We also found an increase in the rate of apoptosis among hepatocytes. In addition, BPA significantly increased the levels of oxidative stress indices, malondialdehyde, and protein carbonylation but decreased the levels of reduced glutathione (GSH) in the BPA group compared to SC. In contrast, treatment with the HDAC2 inhibitor VPA significantly attenuated liver pathology, oxidative stress, and apoptosis and also enhanced GSH levels in VPA group and BPA + VPA group. The HDAC2 inhibitor VPA protects mice against BPA-induced liver pathology, likely by inhibiting oxidative stress and enhancing the levels of antioxidant-reduced GSH.
Mohamed A. Al-Griw, Zaynab Osama Alshibani, Rabia Omar abdullah Alghazeer, Mohamed Elhensheri, Refaat. M. Tabagh, Areej A. Eskandrani, Wafa S. Alansari, Mahmoud M. Habibulla, Ghalia Shamlan(6-2022)