الفهرس 
INTRODUCTION AND REVIEW OF LITERATUREOnly 14 pages are availabe for public view
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Abstract
Due to the increasing use of MSG as a food additive and due to the serious effects of this
substance on the human health, this study aims to study the histopathological, histochemical and
cytological changes in the liver, kidney, cerebellum and spinal cord of adult male white albino
rats.
Experimental animals (130 to 150 g) were divided into seven groups. First group is the control
group. Second, third and fourth groups were given doses 5, 10 and 20 mg MSG I 100 g. b. wt. for 2
weeks. Fifth, sixth and seventh groups were given doses 5, 10 and 20 mg MSG I 100 g. b. wt. for 6
weeks. The last group was left for the test of recovery. At the end of the study, specimens of the
liver, kidney, cerebellum and spinal cord were taken and fixed by Bouin, Formol saline and Dafano
fixatives for microscopic examination.
Changes which observed in the liver of treated rats included congestion in blood sinusoid,
vacuolation in the cytoplasm of the hepatocytes, with degenerative nuclei, congestion and dilation
of the central vein as well as aggregations of lymphocytes and fibroblasts. Also, amyloid
deposition can be detected. These
changes may be attributed to hepatitis and liver lesions. The
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vacuolation of hepatocytes interpreted as a kind of cellular
defensive mechanism against injurious substances. The cellular degeneration of the cytoplasm
and nuclei might be attributed to the
liberation of acid hydrolases which is released from the destructed lysosomes to facilitate the
process of autolysis. Accumulation of fibroblasts together with inflammatory lesions observed in
the current study as congestion of blood sinusoids and blood vessels were reported as chronic
inflammatory diseases which explain the presence of fibrosis around the portal tract. In addition,
the cytological studies showed changes in number and density of the Golgi granules in the
hepatocytes.
Histochemically, the current study showed a disturbance in polysaccharides and protein .contents of
the liver tissue. The variation in polysaccharides of the liver tissue may be regarded as a
result of the release of the insulin and glucagons which are inducted by MSG whi<;h stimulate the
glutamate receptors (GlutRs) in the pancreasleading to the release of its hormones.
Changes which observed in the kidney of treated rats included proliferation and. damage of the
glomerular tufts associated with hemorrhage and vacuolation as well as dilatation of the urinary
spaces. The renaltubules showed a wide lumen lined with shrunken cells having flattened or
elongated nuclei. These alterations could be interpreted as nephrotoxic changes induced by MSG
which induced by the release of glutamate metabolites like ammonia. The interstitial hemorrhage and
amyloid deposition in the rat kidney ’tubules may be due to the hypersensitivity to MSG.
Such damage and alterations may be attributed to the increase of lipid peroxidation products in
rats which in tum enhance incidence of degeneration changes. The cytological studies showed changes
in the number and density of the Golgi granules in the renal tubules, especially in the distal
tubules.
The histochemical .changes included a slight decrease in
carbohydrates and a slight increase in protein contents in cortex and medulla of the kidneys of
treated rats. These changes may be due to glomerulonephritis which led to disturbance in the
reabsorption of glucose and protein molecules by renal tubules.
The histopathological changes of MSG on the cerebellar · cortex of treated rats included
the increased affinity of the cytoplasm of the Purkinje cells to Haematoxylin (basic
stain), abnormalities in cell shape of Purkinje cells and abnormalities of the nerve fiber
orientation. In addition to the previous changes, dark neurons and pyknotic nuclei appeared in the
cerebellar cortex of treated rats as a sign of cell death or injury. These alterations could be
interpreted as a result of the penetration of glutamate to the blood bran barrier which in tum
overexcites the GlutRs on neurons and causes their damage or injury. In addition, there was a
decrease in the . number and density of Golgi granules in the Purkinje cells of the
cerebellar cortex.
Histochemically, the current study showed some variations in protein contents of the cerebellar
cortex. The slight increase noticed in high doses may be due to the high tendency of the nervous
tissue to accumulate glutamate in it. The decrease in Nissl bodies might be due to cell injury
caused by over stimulation of glutamate receptors on neurons.
Changes which observed in the spinal cord of treated rats included the increased affinity of cell
bodies of neurons to the basic stains and the appearance of a small number of dark pyknotic cells
in high doses. Also, there was an increase in the nerve fibers. These changes may be exerted by the
neurotoxic effect of MSG because excessive glutamate overexcites GlutRs which in turn causes the
injury and death of neurons.
Histochemical studies showed that there was a slight decrease in protein and Nissl bodies in the
neurons of the spinal cord of treated animals. This.is might be due to the assumption that
glutamate hardly penetrates the blood spinal cord barrier.