Experimental simulation for accidental exposure to uranium pollutants in drinking water a histological study on the possible impact to the cerebral cortex of adult albino rats

The international racing between countries for using uranium element and its isotopes led to renewal of the efforts evaluating its health impacts. The present study aimed at assessing the possible histological alterations in the cerebral cortex of albino rats ingesting a soluble uranium compound as an experimental simulation to the long term exposure to uranium pollutants in drinking water. Ten control adult male albino rats have received daily 1 ml of ordinary tap water by orogastric intubation for 90 days. Another group of 15 experimental rats have received 60 micro g / kg body weight dissolved uranium in 14.21 micro ml uranyl acetate added to 1 ml tap water by the same route and for the same duration. Specimens from the left fronto-temporal area of the cerebral cortices of both groups of animals were processed for light microscopic examination by routine hematoxylin and eosin stain and immunohistochemical labeling for glial fibrillary acidic protein as well as for transmission electron microscopy. The applied dose and duration of exposure to uranyl acetate in drinking water proved to induce focal degenerative changes in some neurons of the cerebral cortex, which was associated with moderate increase in the neuroglial reaction. Regular, short-termed monitoring of uranium levels in all sources of drinking water is mandatory at the local as well as the national ranges. The population at risk for high rates of exposure should be subjected to periodic assessment of uranium level in urine. The efforts of the national and international health organizations together with the governments should be directed to limit the expanding utilization of uranium compounds in civilian and military applications

inner ear neuroepithelium is a vulnerable target for impact during cisplatin chemotherapy a histological study in albino rabbits

Cisplatin is a widely used chemotherapeutic agent with potential toxicity to normal tissues including the inner ear. Cochlear damage has been always recognized as its primary ototoxic side effect with negligence to the vestibular involvement. The present study aimed to provide a histological assessment for the vulnerability of the inner car cochlear and vestibular tissues in albino rabbits to the impact by cisplatin administration. Ten adult male albino rabbits were divided among a control group and another experimented group. The latter received 8 therapeutic - equivalent doses of cisplatin [2mg/kg body weight/ dose; intraperitoneal injection every other day]. Two days after the last injection, animals were subjected to intravital perfusion by 5% gluteraldehyd under light ether anaesthesia then sacrificed by decapitation. The petrous temporal bones were dissected out, fixed, properly decalcified, and further processed for examination by the light microscope using routine hematoxylin and eosin stain and by the scanning electron microscope. Light microsopic findings showed histological degenerative changes involving the outer and inner hair cells of the organ of Corti, the supporting cells, the spiral ganglion cells and the epithelium of the stria vascularis. It also revealed degeneration of the epithelium of the crista ampullaris. The scanning electron microscopic examination explored the architectural damages affecting the cochlear hair cells and the vestibular otoconia. Cisplatin can affect both the cochlear as well as the vestibular epithelium of the inner ear in albino rabbits. Emesis in patients receiving cisplatin therapy should not mask the possibility for a vestibular impact. Accordingly, an ongoing counseling of an otolaryngeologist is mandatory for the follow up assessment of the auditory-vestibular functions during the cisplatin chemotherapy. On the other hand, multidisciplinary research studies should be expanded, particularly on the molecular level, to came out with new generations of platinum drugs that could be selectively targeted to cancer cells and escape the damage to the normal tissues