KUMAR9

only in medulla oblongata and hypothalamus regions and there was only a

marginal increase (<20%) of LPO level in other brain regions studied.

Though aluminium exposure increased brain LPO level (Ohkawa, 1986; Chainy

et al.,1993; Oteiza, 1994), the present results show that the increase

were not high and not significantly different from control group in some

brain regions (Table I). Changes in the LPO level suggest that impact of

aluminium were overcome and the repair processes of the brain are able to

reduce the changes due to aluminium exposure.

AChE is a membrane bound enzyme and changes in AChE activity could

be mediated by the physical

state

of

the

membrane

(Mazzanti

et al.,

1986). The results of the present study suggest that AChE activity on

aluminium exposure was not influenced by changes in the LPO level of the

brain regions. In olfactory lobe, striatum and cortex though inhibition

of AChE activity was high, the LPO level was not significantly altered in

these regions. Thus aluminium induced changes in AChE activity and LPO

level

are

not

related

and

the

brain

regions

are

able

to

overcome

aluminium induced toxic effects. The study assumes importance as to the

neurotoxic

effect

of

aluminium

since

the

in vivotoxic

effect

are

different from

earlier reports. Further studies on the toxic effect of

aluminium for extended duration of exposure could probably reveal

mechanism of toxic action to explain the changes observed.

the