Lipid peroxidation induced by iron complex in rat brain: An in vivo model

PharmacologicaI Research Communications. VoL 20, Supplement I. 1988

155

LIPID PEROXIDATION INDUCED BY IRON COHPLEX IN RAT BRAIN= AN iN VlVO HODEL Ciu£fi

H.,

Zilletti

Niccolai

G. 0

G.,

Luzzi S.,

Franchi N i c h e l i

V, le 6. B. Horgagni, Key words:

and C l i n i c a l

iron complex,

(hemorrhagic or the

Pharmacology - U n i v e r s i t y o f Florence

peroxidatJont

lipid

in

severa)

ischemic c o r t i c a l

decompartmentalization

£oliowed

HDA, l i p o ~ u s c i n e - l i K e compounds

pathological

conditions

intracerebral

infarction,

peroxidation

o£

lipid

~ractions

both in v i t r o

and in v i v o .

in

(Payan et a l . ,

components o~

tissues

and

discharges,

electrical

peroxidation,

lipid

acute b r a i n disease (Triggs and Willmore,

i n j e c t i o n s o£ iron complexes,

the ~ree metal, used

(Huller,

w i t h the p r o t e i n

rats

below the exposed dura. (200

saccharose

solution

pg

solution.

abnormality

and

an

p e r o x i d a t i v e e£fect

o~

hydroxide-carbohydrate

ligand

replaced

(apo~erritin)

small

hole was made into the r i g h t

to the bregw~;

ca~varium,

T r e a t e d animals received 3.3 mg whereas

controls

were

o~

iron-

injected

pl at the same c o n c e n t r a t i o n and pH were K i l l e d

animals

the i n j e c t i o n was performed

oY

with

the

iron

7

days

by d e c a p i t a t i o n 2 hours or

Samples ~rom the i n j e c t e d and the c o n t r o l a t e r a l

peroxidation

animals did not show

any

apparent

or

c o n v u l s i v e symptomatology,

neither

nor

during the f o l l o w i n g days.

Intracortical

0031-6989/88/20S10155-2/$03.00/0

inmediately

were

products

t973) and o f TBA r e a c t a n t compounds (Ohkawa et a l , , control

hemi-

plane at the level o f corpus callosum,

~or the d e t e r m i n a t i o n o~ ~luorescent l i p i d

Treated

injection,

10

cut along a h o r i z o n t a l

( F l e t c h e r et a l . ,

mimicking

(250-300 g) were placed in

Fe) in 10 p l ,

Animals

the i n j e c t i o n .

processed

and

tff74).

Wistar

saccharate

spheres,

injected

behaviourai

a polynuclear ~erric

...~nposterior and 3 nm l a t e r a l

a~ter

subcellular

lesion.

s t e r e o t a x i c apparatus and a d r i l l e d

complex

and

in order to o b t a i n a slow development o~ the b r a i n

Anaesthetized

nm

is

release

complex, s i m i l a r t o ~ e r r i t i n ,

1.6

Iron

believed to g r a d u a l l y

the i r o n - s a c c h a r a t e ,

by c a r b o h y d r a t e

tissue

1984).

aim o f our research was to study the l i p i d

intracortical

the

Ferrous and ~ e r r i c c h l o r i d e

a b n o r m a l i t i e s associated w i t h

CNS

autoxidative

into r a t b r a i n c o r t e x caused ~ocal e p i l e p t i f o r m

The

the

t970).

undergoing u n i v a l e n t redox r e a c t i o n s ,

enzymatic

o~

hematoma, e t c . )

o~ iron compounds present

the r e l e a s e o# the ~ree metal

by

Known to c a t a l i z e ,

t

and

65 - 50~34 Firenze - t e l 055/441133-431364

common ~actor

A

We

S.

L.

Department o~ P r e c l i n i c a l

is

6entilini

t979).

behavioural after

the

a d m i n i s t r a t i o n o~

© 1988 The Italian Pharmacological Society

156

Pharmadologica/ Research Communications. Vol. 20. Supplement I, 1988

a)

2

b)

Tf. I

E 0 n

1.5

E

uJ

30

O~

20

!

=sic i£=.e

_J ii

.:.:.:. ~

++

4O

Ul

0.5

.Ll.e+

;.'.::

+ • •

10

@

:!!i-,

eoiBee !

o,.e=! •.P£+2i I ore;.;.

E

Pl++ql '°.%', '+2,,:'

Ililili b+• - • ' .

c

;6)

L

Cgl 17) o.e=il

L

R

R

E C1O N T R O L L :

(9) JCI71 ':':':"

left

~

emlsphere

R:

TREATED

Injected

right

emlsphere

Fig. t. MDA (a) and l i p i d - s o l u b l e f l u o r e s c e n c e (b) levels homogenates o f r a t b r a i n c o r t e x 7 days a f t e r the i n t r a c o r t i c a l In brackets number o f e x p e r i m e n t s , Data are means ~ SEM. . : p
and o f

days

after

developing

lipofuscine-]iKe

the

injection.

of

lipid-soluble

significant

(Fig.

1) seven

change~

no s i g n i f i c a n t

fluorescence

in

increase o f malonaldehyde

compounds in t h e b r a i n t i s s u e

On the c o n t r a r y j

observed injection.

and HDA were found

~

in h

the after

treatment. In

conclusion,

the

intracortical

induces

lipid

peroxidation

to

slow

and

be

pathological further

its

investigating this

Fiectcher

Dillard

is

Therefore+ the r o l e o f

drugs a f f e c t i n g B.L•,

in the r e g i o n o f

development

symptom.

administration

iron

saccharate

This process appears

injection•

not

of

accompanied

by

any

t h i s model r e p r e s e n t s an u s e f u l iron-induced

evident tool

brain

lipid

peroxidation

(t973).

Anal,

Biochem.

for and

process,

C.d. arid Tappel A.L.

Payan H.+ Toga N. and B e r a r d - B a d i e r H U l l e r A• (1974).

Arzneim.

Ohkawa H.. Ohlshi

N, and Yagi K.

T r i g g s W.J. and W i i l n ~ r e

H.

(t970)•

Epilepsia

tip

80-94.

Forsch• 24: 880-883.

L.J.

(1979).

{1984).

J.

Anal.

Biochem• 95:

Neurochem.

351-358.

4~2: 976-980,

52:

t-9•