الفهرس 
INTRODUCTION AND AIM OF THE WORKOnly 14 pages are availabe for public view
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Abstract
Aluminum has been implicated in the etiology of several neurological diseases. Aluminum plays a causal role in some cases of Alzheimer’s disease .Aluminum induces its neurotoxicity via different mechanisms. Aluminum was observed to accumulate in all regions of the brain with maximum accumulation in the hippocampus.To investigate the effect of aluminum on the rat hippocampus, Forty Adult male albino rats weighing 150-200g were kept on normal diet and tap water ad libitum,. Rats were divided equally in four groups. Group one was the control group. Group two, three and four were given aluminum chloride (300 mglkg body weight orally daily) for one, two and four weeks consequently. The brain was removed intact and processed differently for, histological, histochemical, immunocytochemical and ultrastructural studies.
In hematoxylin-eosin sections degenerated neurons were
observed. The number of which were increased along the time course of treatment. There was also decrease in the neuronal populationespecially in CA2 and CA3 zones. Vacuolation of the neuropil was also observed.
The semithin sections stained with toluidine blue showed
neurons which were atrophied and densely stained with toluidine blue. Some neurons showed apoptotic changes characterized by formation of apoptotic bodies.
Silver impregnated sections revealed argyrophilic shrunken neurons that appeared with aluminum administration and increased in number along the time course of treatment. Neuritic plaques and neurofibrillary tangles were observed. They were similar to those appears in Alzheimer’s disease. Axons showed Wallerian-like degeneration.
Histochemical study for AChE it was found that the aluminum administration for one week caused an increase in AChE activity, while its administration for two and four weeks resulted in decreased AChE activity.
Immunocytochemical study showed upregulation of iNOS in the rat hippocampus along the time course of administration. The expression of COX-I was also increased. After Two weeks of administration some neurons showed translocation of COX-l expression from the cytoplasm to the nucleus. Immunocytochemical staining for COX-2 showed initial upregulation of COX-2 expression after one week, followed by down regulation after two and four weeks of administration.
At the ultrastructural level it was found that aluminum administration produced minimal effect at one week group. While its effect became more obvious at two and four weeks groups. Aluminum promoted granulovacuolar degeneration, mitochondrial degeneration, demyelination and deposition of lipofuscin. Degenerated shrunken dark neurons were always surrounded by swollen vacuolated astrocytes. Microglial like cell which showed the signs of activation were also found.