Various oxidative stress and histopathological biomarkers in gill tissues of Nile tilapia Oreochromis niloticus were investigated. Fish were collected from four sites that differ in their extent of pollution load, including heavy metals: the southeast basin (SEB), main basin (MB), and northwest basin (NWB) of Lake Mariut; and Boughaz El-Maadiya, a channel in Lake Edku. The oxidative stress biomarkers that were analyzed included lipid peroxidation (LPO), superoxide dismutase (SOD), catalase (CAT), and glutathione redox cycle enzymes (glutathione peroxidase [GPx] and glutathione reductase [GR]). Levels of reduced glutathione (GSH) were also evaluated. Gill morphology was analyzed by light microscopy and scanning electron microscopy (SEM). Gill LPO was significantly higher in gill tissues of fish collected from the more heavily contaminated MB (40.0%) and NWB (51.4%) sites than in gill samples from the less-contaminated (reference) site, the SEB. Gill LPO in fish from Lake Edku was intermediate but was not significantly higher (17.1%) than the reference. The activities of antioxidant enzymes and the redox-sensitive thiol compound GSH were significantly lower in gill samples from the disturbed sites than in samples from the reference site. Specifically, SOD in MB, NWB, and Lake Edku samples; CAT and GPx in NWB samples; and GR activity and GSH content in MB and NWB samples were lower than those in SEB samples. In most cases, gill tissues from Lake Edku fish had intermediate levels of antioxidants. The main histopathological alterations observed in gills were epithelial lifting, hyperplasia and hypertrophy of the respiratory epithelium, lamellar fusion, and aneurysms. In addition, SEM results demonstrated transformation of the surface structure of epithelial pavement cells. Pathological reactions in the gills of Nile tilapia were most severe at the MB and NWB sites. Our findings suggest that Nile tilapia responded differently according to the environmental stress index in each sampling area. This study is the first to report gill oxidative stress and histopathologies in Nile tilapia from Egyptian aquatic environments.

This study focuses on finding if the hazards produced by gasoline 90 (vehicle fuel in Egypt) are less than those produced by gasoline 80 in healthy Swiss albino mice. Sixty mice were equally divided into 3 groups: group one (control), group two (topically treated with 0.5ml gasoline 90 /kg B.W.) and group three (topically treated with 0.5ml gasoline 80 /kg B.W.). The specimens were taken after 4 and 8 weeks. Determination of bioaccumulation of some heavy metals, biochemical examination and a light microscopical study were performed. It was found that the accumulation of lead, cadmium and nickel in the liver had the following order lead > cadmium > nickel. After topically treated with gasoline 90 and 80 for 8 weeks, there was an increase in the activities of the serum liver function enzymes (alkaline phosphatase, alanine aminotransferase and aspartate amino transferase) and adenosine deaminase and a decrease in the total protein content of the liver homogenate. There were pathological changes which were more pronounced by treatment with gasoline 80 than with gasoline 90 depending upon treatment duration from 4 to 8 weeks. After 4 weeks of topically treating mice with gasoline 90, cellular infiltration, dilatation of blood sinusoid and cytoplasmic vaculation were demonstrated. After 8 weeks the liver architecture of the mice was disrupted with liquid infiltration and the presence of foamy areas. After 4 weeks of topically treating mice with gasoline 80, we observed a shrinking of the blood sinusoid, hypatocyte vaculation with pyknotic nuclei and different stages of karyolysis. After 8 weeks, there was a noticeable hypatocyte degeneration and complete disappearance of blood sinusoids in the liver sections of the mice.

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The present work aims to evaluatethe cytotoxic effects on lung cells exerted by gasoline. 60 male albino mice were used in the present experiment, divided equally into 3 groups: first group (control) was left access to fresh air, second group (experimental) was subjected to gasoline 80vapor/1h./day and third group (experimental) was subjected to gasoline 90-vapor/1h./day along eight consecutive weeks. The study comprises determination of body weight, bioaccumulation of some heavy metals ,histological and ultra-changes . Histological changes increased according to duration of exposure as, infiltration of inflammatory cells, detachment and necrosis of the epithelial cells .The electron micrographs revealed dilatation of the smooth endoplasmic reticulum, loss of the secretory granules in the Clara cells and loss of cilia in the ciliated cells that exhibited bleb formation. Necrotic type II pneumocytes, exhibited vacuolation, fragmentation of the rough endoplasmic reticulum,mitochondrial degeneration , nuclear alterations, degeneration of lamellar bodies and microvillar atrophy. In conclusion, gasoline vapour inhalation induced lung tissue injury and cellular damage concomitant with impairment of the lung antioxidant defense system. These effects were more pronounced with the unleaded than with the leaded gasoline.