KUMAR7

Aluminium

exposure

resulted

in

significantly

(p<0.05-p<0.001)

increased LPO level in the brain regions (Table I). In olfactory lobe,

striatum,

spinal

cord

and

cortex

regions,

the

LPO

level

were

not

statistically different from the control group. In spinal cord and cortex

regions the LPO level were marginally reduced compared to the control.

The results reveal the regional differences in the brainAChE activity

and lipid peroxidizability.

DISCUSSION

involve

proteins of cholinergic transmission (Patocka, 1971; Yates et

al.,1980). Aluminium has been shown to be a non-competitive inhibitor of

AChE (Marquis and Black, 1984) and binds to the peripheral anionic site

of the enzyme (Marquis and Lerrick, 1982). It has been reported

that

mouse

neuroblastoma

cells

had

decreased

AChE

activity

when

grown

in

aluminium containing culture medium (Miller and Levine, 1974). As brain

aluminium accumulation increased with duration of exposure (Gulya et al.,

1990), the decrease in enzyme activity observed in the present study may

be due to direct neuronal toxicity resulting from the accumulation of

aluminium

in

the

brain

regions.

Bilkei-Gorzo

(1993)

have

reported

a

positive correlation on brain aluminium content and AChE activity. The

difference in AChE activity observed among brain regions in the present

study may be due to differences in the levels of aluminium accumulation.