KUMAR4

central

been

proposed

as

one

of

the

mechanisms

underlying

damage

to

nervous system (Otieza, 1993) and to aetiology of aluminium neurotoxicity

(Otieza, 1994). Aluminium alters the free state of lipid membranes and

induces membrane fusion and aggregation of phospholipid vesicles (Deleers

et al., 1987). Aluminium induced

changes

on

brain

LPO

are

scant

and

chronic toxic effect on brain regions LPO level are lacking. Since AChE

is a membrane

bound

enzyme

it

was

of

interest

to

find

if

aluminium

altered LPO level and the resultant changes if any on the AChE activity.

The present study therefore explores the effect of chronic exposure to

aluminium on the brain regions AChE activity and lipid peroxidazibility.

MATERIALS AND METHODS

Materials

Acetylthiocholine iodide, eserine sulfate, malonaldehyde, thiobarbituric

acid and bovine serum albumin were purchased from Sigma Chemical Co.,

(USA). All chemicals were analytical grade and commercially available.

Animals and treatment

Male

albino

rats

of

Wistar

strain

weighing

180-200

gm

were

maintained in temperature controlled room of 12 hr light/dark cycle with

free access to pellet food and tap water. Aluminium chloride was orally