Effect of Oral Administration of Aluminum Chloride on the Hippocampus (Brain) of Wistar Rats
Objectives of the Study Include the Following
- To determine the relationship between drinking water containing Aluminium chloride and hippocampus damage of wistar rats by looking for histological changes in the
- To compare the haematological indices of the treated and control of wistar rats.
Aluminium chloride has its derivation from purified chlorine with molten aluminium. It is composed of Aluminium with molecular weight of 133.34 and formula (symbol) of AlCl3. Other names (synonymous) for this compound include Aluminium trichloride, Trichloroaluminum. It is whittish powder with melting point of 1940C and specific gravity of 2.44 while its boiling point sublimes with vapour density of 4.5. It is not combustible but react violently (decomposes) with water and heat will contribute to instability (Laschkarew, 1930).
Under the sales specification of AlCl3, its assay is 99.3% min with free Al of 100 ppm max and Fe (iron) of 100 ppm max. According to Li Runshen (1981), Aluminium chloride was used as a coagulant in Shenzhen water supply in China and found to have a coagulating effect as good as 2-3 times of traditional aluminium salt (Zhang, 1998). With its much lower price in comparison with organic coagulant, it has great advantages in improving water quality. It has the following characteristics:
- Floccus forms It needs a short time to react and settle down;
- It has a wide range of dosage and it is well suitable for variety of turbidity, alkalinity, organics in the water compared with Aluminium sulphate. It has a better coagulation effect even in lower –T<10. Li Runshen (1981).
There are some problems in application that coagulation does not effect expectantly. In a given condition of raw water physical and chemical properties, flocculent kind, purification, it is the key factor to get high water output with high quality water and low cost whether coagulant is used correctly (Zhang, 1998). Considering the practice of liquid Aluminium chloride used in Shenzhen (China), an experiment was carried out with different dosage, diluting times and different settlement time. It is expected that the result of the experiment will give reference for the water works to use Aluminium chloride in water treatment. (Wenbin et al., 2002).
Aluminium was found to be toxic to the nervous system of animals over 100 years ago. Injecting aluminium into the brains of sheep was reported in 1965 to result in changes in the brain that shrink: a “striking resemblance” to Alzheimer Disease (AD) in people. Dougall, (2004) stated that in 1973, brains of Alzheimer Disease (AD) patients were found to contain aluminium than people dying without this disease. About the same time, kidney patients on dialysis were found to suffer, sometimes fatal, brain damage (encephalopathy) from aluminium in their antacids (these antacids were used to bind phosphates in their intestines). More than 100 toxic of aluminium have been identified and many are damaging to the human brain (Mclachlan et al., 1991b).
The progressive deterioration in cognitive function associated with Alzheimer had been correlated with loss of cholinergic function and the degeneration of cholinergic neurons (Collerton, 1988; Francis et al., 1985; Smith and Swash, 1978; Whitehouse et al., 1985).
Aluminium is generally a recognized neurotoxin that is believed to be at the root cause of Alzheimer Disease (AD) and becomes more toxic when combined with a high cholesterol diet. They work together by means that have yet to be fully determined to create the senile plaques and ultimately the mental deterioration known as AD (Versieck and Cornelis, 1980). However, there are at least two recognized synergistic ways that these factors contribute to brain damage (Gonatas, 1967).
First, an acid-forming diet-one high in meat, poultry, eggs, and cheese-leads to increased senile and brain concentrations of aluminium. Second, aluminium enhances inflammation. The immune enhancing properties of aluminium discovered after immunization with diphtheria and tetanus vaccines in studies performed in the 1940s and 1950s and aluminium is used today to enhance the effectiveness of the inflammatory response of most vaccines given to adults and children. In the brain, aluminium enhances the inflammation that may result from the formation of senile plaques driven by cholesterol build up initial injury-this metal is known toxic to the nervous system-that starts the disease processes, leading to brain cell death, senile plaques neurofibillary tangles (Flaten and Odegard, 1989).
However, according to Dougall (2004), aluminium is present in our water, foods, medications and air. The healthy human body has effective barriers such as skin, lungs, and gastrointestinal tracts, against aluminium. Aluminium is not a nutrient-in other words and the body has no need for this metal and avoidance has no negative consequences (Sorenson et al., 1974; Fulton and Jeffery, 1990.).
All foods naturally contain aluminium, but some, such as tea, are partly high in this metal. Fortunately, most of the aluminium in natural plant foods is bound with other substances such as Silicon which prevents absorption of the aluminium into the body. The harmful (unbound, more absorbable) forms of aluminium enter our foods additives such as leaving agent and emulsion (Pennington, 1987).
MATERIAL AND METHODS
The subjects used in this research work were 50 female adult wister rats (Rattus Novegicus). The rats were purchased from the Faculty of Vet. Medicine A.B.U.Zaria with an average weight of between 150-200g at the beginning of the research work. They were kept in the animal house of Dept of Human Anatomy, Ahmadu Bello University, Zaria for three weeks under (normal) standard environmental conditions (22±10C, relative humidity of 60%, 12h-12h light-dark cycle with light on at 08:00h) with sufficient food, water and under a good ventilation in order for the animals (wistar rats) to acclamatized. The animals were all fed with grower’s mash obtained from Nassara Feeds, Kaduna. The nutritional composition of the feed is shown on Appendix I.
The result of the haematological indices are represented in Table 4.1.
Packed Cell Volume (PCV)
The result showed that the PCV mean value for group I was 40.67%, Group II was 42.67%, group III was 46.00%, group IV 46.33% and Group V 46.33%. There was statistical significant difference in the PCV value between the control and the treated groups at P<0.05 (Tables 4.1 and Figure 1).
This study showed degeneration of the pyramidal cells of the hippocampus due to exposure of the brain to aluminium. This may support a hypothetical statement by Yokel (1983) that Aluminium exposure has neuro-degenerating effect resulting in learning deficits in rats and also the documentation compiled by Frank (2006) which stated that in human aluminium inhibits learning.This result of this study may cause learning disability. There were also few neurofibrillary tangles in groups IV and V which suggested the possible effect of oral administration of aluminium chloride on the brain of the rats. This is in line with Muller-Hill and Beyreuther (1989) who suggested that aluminium might have a role in the aetio pathogenesis of Alzeheimer’s disease although based on circumstantial evidence.
According to Brodal (1992), the functions of certain learning and memory have been associated with different areas of the brain like the hippocampus and cerebellum. While the hippocampus is associated with memory of new words, faces, place and event, cerebellum has been associated with memory of learning new skills like playing an instrument etc.
SUMMARY, CONCLUSION AND RECOMMENDATION
Summary and Conclusion
Alzheimer’s disease is a neurodegenerative disorder characterized by a complex array of neuropathological biochemical and behavioural sequelae (Foltein and Whitehouse, 1983). It is a socioeconomic problem that has significant effects on a large percentage of an increasingly more aged populations.
Three microscopic abnormality characterized Alzheimer disease: they are neurofibrillary tangle, neurotic or senile plaque and granulovacuolar degeneration. All three may be present in small number in hippocampus of normal elderly patients and however, neurofibrllary tangle occupy the perikaryon of medium and large pyramidal cell (Robert and Terry, 1979).
The oral administration of Aluminium chloride in the experimental groups have shown some level of neurodegeneration (or granulovacuolar) on the hippocampus of the treated rats when compared with the control group I.
However, Aluminium has been linked with Alzheimer’s disease and this has led to concern about levels of aluminium in drinking water. Despite the fact that drinking water constitutes only a minor source of total dietary water aluminium intake; recent epidemiological studies have indicated a positive correlation between drinking water aluminium level and Alzheimer’s disease incidence (Cowling et al., 1991).
From careful observation of the photomicrograph of the slides, it can be concluded that oral administration of aluminium chloride has a neurodegenerating effect on the hippocampus and hence could suggest a link between exposure to aluminium and Alzheimer’s disease, which is in line with the observation of Cowling et al (1991).
Comparing the haematological indices of the control and experimental groups, it could also be concluded that oral administration of aluminium chloride result in increased white blood cells and neutrophil were statistically significant at P less than 5% (P<0.05); PVC was not statistically significant at P less than 5% (P<0.05) but at P less than 10%(P<0.10),the RBC was however was not significant statistically.
- From this experimental work, I therefore recommend that injection of Aluminium Chloride above 300mg in Human may not be safe.
- Public processed drinking water should be regulated so that the concentration of aluminium is very
- The regulatory body like National Agencies For Food, Drug, Administration and Control (NAFDAC) in Nigeria should encourage manufacturers to indicate the aluminium content of packages of all substances marketed for human consumption and contact, including processed foods, drinking fluid, cosmetics, toothpaste and pharmaceuticals.
- Abdel-Rehim M. S., El-Sokkary M. B. and El-Amir Y. (2004). Blood. Medical Physiology. Pp2-10.
- Baxter M., Burrel J. A. and Massey R. C. (1988). The Effect of fluoride on leaching of Aluminum Savcepians during cooking. Food Additive contam. 5:651-656
- Beal M. F., Mazurek, M. F. Ellison, D. W., Kowall, N. W., Solomon, P. R. and Pendlebury W. W. (1989). Neurochomical characteristics of aluminium induced neurfibrillary degeneration in rabbit. Neuroscience 2, 329 – 337
- Beavon J. B. G. (Jr.) (2004). Chemistry Contents, Aluminum chloride, Home page, 17 dean’s Yard London SWP3PB rod Beavone @westminister.org.u.k
- Birchall J. D. (1992). The interrelationship between silicon and aluminum in the biological effects of aluminum. In Aluminum in Biology and Medicine. Willey, Chichester (ciba found. Symp. 169; p 50-68)
- Birchall J. D. and Chappell J. S. (1989). Aluminium, water chemistry and Alzheimer’s diseases lancent 1:953
- Bishop N. J., Morley R., Day J. P. and Lucas A (1997). Engl Journal of Medicine. 336 (22): 1555-7-61
- Boutton A. A., Baker G. B. and Butterworth R. F. (1992). Animal models of neurological Diseases, 1 Neurodegenerative Diseases. (pg 33-40). The Humana Press Inc. 999 Riverview Drive, suite 208, Totowa, New Jersey 07512 USA.
- Bradbury P. (1992). Histological Methods. In: Hewer’s Textbook of Histology for Medical Students 9th Ed. ELBS pp 431-450
- Brodal S. (1992). The Central Nervous system: Structure and Function. Oxford University Press.
- Candy J. M., Oekley A. E., Klinowski J. et al (1986). Aluminosilicates and Senile Plaque formation in Alzheimer’s diseases Lancert 1: 354-357