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Journal of the Anatomical Society of India

Effects of Copper Chloride Toxicity On Corpus Striatum Of Rat Brain - A Histological Study

Author(s): Tariq Zaidi, M; Faruqi, N.A; Abidi, S.H.M.

Vol. 51, No. 1 (2002-01 - 2002-06)

Department of Anatomy, Jawaharlal Nehru Medical College, Aligarh Muslim University Aligarh INDIA

Abstract

Copper is an essential trace element. Due to its functions as a coenzyme, its accumulation is harmful. The present study was carried out to determine the effects of copper chloride on corpus striatum in albino rats, Twelve adults albino rats of either sex were divided into control and experimental groups of animal each. The experimental group received copper chloride 100 mg of body weight orally daily for one month, The corpus striatum was fixed in 10% formaline and processed for paraffin embedding. The 10 micron thick sections were stained with Haematoxylene and Eosin, thionin and Kluver Barrera. The tissue examined under light microscope. showed degenerative changes in the appearance of concentric spaces around the nerve fibers bundles. Components of corpus striatum showed differential effects of copper toxicity, which may be due to their variable vascularity and cellularity.

Key words: Corpus striatum, caudate putamen complex, Globus pallidus.

Introduction:

Copper is an essential trace metal for mammals, because it is an important constituent of a number of enzymes. In brain the natural distribution of copper is unequal and both of its deficiency as well as excess in blood and cerebrospinal fluid are known to damage the central nervous system (Maeda et al, 1997; Lai & Blass, 1984; Howel 1977). Histological studies are considered to be reliable method to detect neuronal changes due to toxicities. (Larargues et al, 1995). Clinical observations of patient suffering from copper toxicity (Wilson's disease) are indicative of involvement of corpus striatum. Larargues, et al, 1995). Report available on microscopic observations of neuronal damages in corpus striatum is inadequate. The present study was undertaken to confirm and supplement the previous findings.

Material and Methods:

Adult rats (2 months of age) of both sexes in 120 ± 5 g were obtained from central animal house J.N.M.C. Aligarh. These were fed on soaked gram and water ad libitum. The animals were also given yeast tablets to make up the nutritional deficiency. The rats were divided into two groups of 6 animals each. First group served as a control while second group acted as experimental. Copper chloride was dissolved to distiled water (1 gm / 100 ml) and administered to the rats of experimental group in a daily oral dose of 100 mg / kg with the help of tuberculin syringe for a period of one month. A portion of cerebrum anterior to optic chaisma was obtained from the rats of both control and experimental groups. The brain tissue was processed to obtain thin sections, which were stained with haematoxylene and Eosin, Thionnin, Triple staining Kluve Barrera). These sections were observed microscopically to find out histopathological changes in the copper chloride treated animals.

Results:

1. Caudate putamen complex The degenerative changes were maximal in caudate putamen complex. Such changes varied from a moth-eaten appearance to complete softening and cavity formation (Fig. 1) as compared to normal (Fig. 2). There was clumping of degenerated cells & loosening of nerve fibers with appearance of concentric spaces around the bundle of nerve fibers (Fig. 3) Thus there was an over all spongification of caudate putamen complex.

II. Globus pallidus The degenerative changes were less marked in globus pallidus, which showed atrophy, & necrosis of nerve cells and proliferation of neuroglial cells. There was no cavitation, but loosening of nerve fibers with appearance of concentric spaces around it (Fig. 4) was commonly observed. The above observations indicate that the basal ganglia in the albino rat is vulnerable to copper toxicity. The toxicity of copper mainly affects the caudate putamen complex of basal ganglia.

Discussion:

Copper belongs to second B group of the D block of trasitional elements of the periodic table. It is an essential nutrient but its over dose is harmful and causes poisoning when ingested in toxic amount or for sufficiently long period. Its toxic effect involves a variety of body systems. Much emphasis has been placed on their effect on the central nervous system due to an apparent relation with the extrapyramidal symptoms in cases of coper toxicity. (Lai, & Blass, 1984). It causes cell injury by damage to lysosomal membranes leading to release of copper in the cytoplasm of the cell. (Lindquist, 1968). Similarity of ataxic signs of lambs to those of the extrapyramidal motor disease such as Parkinson's disease suggests that the dopaminergic system may be affected. (O. Dell, 1976). The concentration of copper in the brain of ataxic lambs with or without copper supplementation was measured which showed that copper supplementation greatly increases the dopamine level in the brain of ataxic lambs. In Globus pallidus the degenerative changes were less marked because of the decreased concentration of nerve cells and increase in the nerve fibers and decrease vascularity. (Williams et al, 1995). More over preferential toxicity in the different components of basal ganglia may be due to selective accumulation of copper.

References:

  1. Howel, J.M. Gopinath (1977) : Copper toxicity sheep - The effect of repeated intervenous injection of copper sulphate. Research Vet. Science. 22(1): 86-94.
  2. Lai, J.C. and Blass, J.P. (1984): Neurotoxic effect of copper, Inhibition of glycolysis and glycolytic enzymes. Neurochemical Research. 1 (12): 1699-710.
  3. Larargues, G.P.: Shapcott, D. et al (1995): Accumulation of manganese and copper in pallidium of cirrhotic patient - Role in the pathogensis of hepatic encephalopathy. Metabolism Brand disease. 10(4): 353-356.
  4. Lindquist, R.R. (1968): The effect of Copper on rat liver lysosome. Amerian Journal of Pathology 53: 903-927.
  5. Maeda, H, Sato, M. et al (1997): Brain imaging in patiant with heapatic cirrhosis - Relationship between high intensity signal in basal ganglia on T1 weighted images and elemental concentration of copper in brain. Neuroradiology 39(8) : 546-50.
  6. O. Dell, B.L. : Biochemistry and Physiology of copper in vertebrates, Trace element in normal health disease, vol. -1 (A.S. Prasad ed.) Academic Press, New York, p.391-413. (1976)
  7. Williams, P.L., Bannister, L.H., Berry, M.M.; Collins P; Dyson M; Dussek, J.E.; & Ferguson, M.W.J.: Gray's Anatomy Churchil Livingstone New York, London, 38th ed., p-1192-93 (1995)

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Fig. 1. Photomicrograph of the caudate putamen complex of an albino rat exposed to copper chloride showing degeneration, vacuolation, spongification & cavity formation (Kluveer Barrera Stain, X 400)

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Fig. 2. Photomicrograph of the globus pallidus of an albino rat exposed to normal diet. (H & E Stain, x400)

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Fig. 3. Photomicrograph of the caudate putamen complex of an albino rat exposed to copper chloride showing degeration of nerve fibres with appearance of concentric spaces around the nerve fibre bundles. (H & E, x400)

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Fig. 4. Photomicrograph of the junction of caudate putamen complex (cp) & globus pallidus (GP) of an albino rat exposed to copper chloride showing increased degeneration with cavitation (c) in caudate putamen complex in comparison to globus pallidus (Kluver Barrera staining x 400)

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