3

INTRODUCTION

Aluminium is a neurotoxicant with no known biological function. Elevated

level of aluminium was demonstrated in patients with parkinsonism (10),

amyotrophic lateral sclerosis (28), senile dementia of Alzheimer's type

(5) and also in animal models (1,12). Aluminium can enter the food chain

as industrial development and usage of fertilizers have contributed to

acidification of agricultural areas and aquatic habitats (13,32). As long

as

acidification

of

the

environment

continues,

bioavailability

of

aluminium

will

continue

to

rise

(16).

The

Camelford

water

poisoning

accident (19) suggests that accidental exposure of general population to

aluminium salts can occur.

The biological response on exposure to a chemical can be biphasic. An

increase and decrease of any biological response observed with increase

in dosage of a test compound, is termed as

biphasic.

To

be

precise,

biphasic response is an increase in response at low dosage level and a

decrease in response at a high dose level. The biochemical and molecular

mechanism of aluminium neurotoxicity have been the subject of study under

elucidation. However, aluminium induced biphasic effect on

cholinergic

system has received less attention. This paper analyses aluminium induced

biphasic response on cholinergic system and their possible mechanism of

cause.