الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
 |  | from | 16 |  |  |
| | | from | 16 | | |
Abstract
SUMMARY
Lead is an important element present naturally in some areas of the world and used on alarqe scale in industry, in
•addilion the enviromental lead pollution is agreal problem in human and animal health,several sources of lead pois oning to animals were reported and the animals were pooned through different ways. Lead is one of the paronchymatous poisions that cause regressive disturbances of cell melabolism principally in the liver and kidney in spite of the Prevalence of lead pois .oning b-oth in humans and animals its pathogenesis is still rathor obscure. but the author added that it is like other heavy metals is usually as protoplasmic poision and it exet its deleterious effect on the nervous tissue with light degree of specificity.
In the piesent study, male albino mice, ranging from 30 to 50 gm in weight were obtained from the experimental
animal house. Assiut University and acclimatized to
laboratory conditions fifteen days before testing. Two
experiments were conducted in the first, 72 male mice were exposed to asingle dose (1 ml) of lead acetate. Three different coflcentration (1, 1.5, 2%) as well as two routes of adminstration (per os or introperitoneal injection) were used. In the second experiment, 72 mice, the same design using lead nitrate was used. Half of the control animals were intr,peritoneally injected with 1 ml sterile distelled water and the others were left without treatment.
Three mice from each subqroup were randomly chosen and sacrificied after 1, 3,5 and 7 days o”f treatment.
Animals were necropsied and tissue specimens from the liver, kidneys, spleen, stomach, intestines testicles, lungs, heart and brain were taken for histopathological examination.
In the present work, the clinical manifestations were inconstant and insignificant and included inactivity, in appetance, drowsiness and palness of the conjunctival mucosa. Difficult breathing, collapse and coma were observed before death of the animals.
Post mortem examination of sacrificied and dead mice revealed gross changes in the liver, kidney, lung, heart and brain. However no gross detectable alteration could be observed in stomach, intestine, spleen and testicles.
The subgroups which injected intraperitoneally with 2% either lead acetate or nitrate showed more pronounced changes.
Regarding the lead hepatopathic alterations noticed, could related to the time post adminstrations. Twenty four hours after treatment features of toxic hepatitis including parenchymatous degeneration, hyperaemia of the vascular ramifications, activation and proliferation of the retiw. culoendothelial cells and occassional slight perivascular round cell infiltrations. Three days post lead adminstration hyDROPic degeneration of the cytoplasm and intranuclear glycogenic infiltration were prominent features five days
rafter treatment fatty metamorphosisfocal necrosis and appearance of nuclear and nucleolar acid fast-positive
bodies could be seen.
Seven days post adminstration the degenerative process was more pronounced, the nuclei were transformed into acid fast positive bodies. The latter could be described as intracellular inclusion bodies and appeared by light microscopy in haematoxylin stained sections as homogenous acidophilic masses surrounded in some cases with basophilic nuclear membrane.
Regarding the lead nephropathic the microscopic changes of the renal parencyma were expressed in all group and commenced twenty four hour, post - adminstration and persisted till the end of the experiment. The alterations did not vary significantly as regard to the rout of adminstration of the two lead compounds. However they could be related to the concentration used and this perhaps could be refered to
the amount given per animal. The ‘nephropathic alteration
noticed included vascular hyperemia as well as regressive
metabolic changes in the renal epithelium.
Lead encephalopathic lesions in our experiments were minimal and icluded congestion of the brain capillaries as well as minute erythrocytic extravasations associated with accidental neuronal degeneratiön’ and microglial activation.
Lead cardiomyopathic lesions included hyperemia,
vascular damage regressive metabolic changes reached to cardiomyomalcic foci.
In our findings non specific lung lesions included
congestion, emphysema, bronchial epithelial hyperplasia were noticed.