ABSTRACT
Although there are many applications of silver nanoparticles (Ag-NPs) in human activities, there is still little known about their potential environmental toxicity, particularly to fish. In the present study, the effects of Ag-NPs on African catfish (Clarias gariepinus) were studied using melanomacrophage centers as immunohistological biomarkers. Fish were exposed to 25 mg/L, 50 mg/L and 75 mg/L 100-nm Ag-NPs. We studied the effects on the size and number of melanomacrophage centers in all target tissues. Many histopathological alterations in those tissues were observed. The histological changes were represented as dislocation of the epithelium, dilatation of central veins associated with inflammatory leukocytic infiltration, necrosis, and pyknotic nuclei of hepatocytes. There was shrinkage of Malpighian corpuscles, dislocation of nuclei of convoluted tubules, cellular degeneration, and dispersed infiltration of leukocytes in kidney tissue. Examination of spleen sections after exposure to Ag-NPs showed rupture within the red pulp and hemorrhage, dislocation of nuclei, accumulation of inflammatory leukocytes, and congestion in blood vessels. In conclusion, exposure to Ag-NPs induced alterations in tissues, suggesting a possible increase in oxidative stress in those tissues.
ABSTRACT
Oxygen deficiency during critical illness may cause profound changes in cellular metabolism and subsequent tissue and organ dysfunction. Thus, the present study was designed to determine the effects of hypoxia and reoxygenation on the levels of lipid peroxidation and the morphological changes in the liver of male mice as well as the protective role of melatonin as an antioxidant. Two experiments were carried out in this study. Experiment I includes three groups of mice (control, hypoxic, and hypoxic+melatonin) while the experiment II includes two groups (reoxygenated and reoxygenated+melatonin). The levels of oxidized lipids were measured and the morphological changes were investigated using light and electron microscopy. In experiment I, hypoxia strongly stimulated lipid peroxidation levels (88%) while melatonin administration inhibited this increase (69%). Severe morphological changes (necrosis, dilated congested blood vessels, collection of inflammatory cells, condensed heterochromatic with irregular outlines nuclei, and mitochondrial degeneration) were detected in the liver of hypoxic mice. In experiment II, reoxygenation inhibited the levels of oxidized lipids (42%) versus hypoxic mice and some morphological changes were detected. When melatonin was given before reoxygenation, it inhibited the levels of lipid peroxidation by 66% versus hypoxic mice. Also, melatonin enhanced the recovery profile by 41% when compared with mice that reoxygenated with room air only. All morphological alterations that detected in both hypoxic and reoxygenated mice were repaired when melatonin administered. These results indicate that hypoxia and reoxygenation induce severe alterations in the liver and that melatonin exerts beneficial role in restoring tissue alterations after subjection to hypoxia.
