Protective effects of melatonin against apoptosis induced by oxidative stress in cultured cortical neurons and mixed glia

Protective effects of melatonin against apoptosis induced by oxidative stress in cultured cortical neurons and mixed glia

Shl Poster Abstracts PROTECTIVE STRESS EFFECTS IN CULTURED Jia-Yi Wang*, Dept. of Physiology, Hospital, protects HZ02 Defense organisms t...

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Shl

Poster Abstracts

PROTECTIVE STRESS

EFFECTS

IN CULTURED

Jia-Yi

Wang*,

Dept.

of Physiology,

Hospital,

protects

HZ02

Defense

organisms the neuronal

brain

the effects indicated

addition,

apoptosis

induced

by sublytic

inhibits thereby

Medical

oxidative

Center

INDUCED

BY

OXIDATIV~

GLIA

and Dept.

of

Psychiatry,

indirectly

lysis

(evidenced

injury

Tri-Service

of SNAP

effect

Besides

on astroglia.

in cultured

or glial

cells

cortical

plus H202 induced

and was prevented

oxidative

injury

possibly

melatonin

was also compared

DIURNAL

MELATONIN

Jiang*,

by

AND

and Jia-Yi

maintaining

cellular

GSH

Melatonin

deficiency

a direct

neurotoxicity.

(SNAP),

dependent

glia and

manner.

In

stains) was synergistically

by pretreatment

The

111

In the present study and mixed

sulfoximine

homeostasis.

Melatonin Moreover,

L-penicillamine nuclear

by buthionine

1998).

of melatonin

(BSO),

a drug which

the rate-limiting enzyme in glutathione (GStl) synthesis, gamma-glutamylcysteine depleting intracellular stores of the GSH. Our results suggest that melatonin

tlann-Kuang

General

neurons

in a concentration-

and fluorescent

diseases.

1997;

protein.

S-nitroso-N-acetyl-D,

fragmentation

the neurotoxicity

et al.,

and kainate.

a detrimental

compounds,

by Reiter

and wamyloid

to stroke

oxidative

of neurons

by DNA

concentrations

also counteracted

through

on the

that NO-releasing elicited

by kainate

in response

of melatonin

for several CNS degenerative

stress (reviewed

death induced

vulnerability

by themselves

Melatonin

APOPTOSIS MIXED

Jiang

to be responsible

from

death can be resulted

Our results

AND

Chen and Hann-Kuang

National

prevents

we compared

AGAINST

NEURONS

stress has been suggested

potentiates

neuronal

MELATONIN

Taiwan.

biological

melatonin fact,

Ching-Long

Taipei,

Oxidative

OF

CORTICAL

antioxidative

synthasc. prevents

the

potency

01

with other antioxidants.

CORTISOL

SECRETION

PROFILES

IN SCHIZOPHRENIC

PATIENTS

Wang

Department of Psychiatry, Tri-Service General Hospital: National Defense Medical Center, Taipei, Taiwan.

and Department

of Physiology

and Biophysics.

Although melatonin and/or cortisol secretions have been suggested as markers of both circadian and noradrenaline dysfunctions in psychiatric illnesses, especially in affective disorders, studies of melatonin and cortisol in schizophrenic patients are rare. In the present study, we evaluated the circadian proliles of melatonin and cortisol secretion in schizophrenic patients and control subjects. Twenty-four hour neuroendocrine screening was conducted on 21 medicated male paranoid schizophrenic inpatients (mean age, 27.3 ? 7.2 years) and 2 I age- and sex-matched controls: at 2-hour intervals from 0800 h to 2200 II, and at l-hour intervals from 2300 h to 0700 h. The standard dexamethasone suppression test was performed the next day to provide an index of hypothalamic-pituitary-adrenal axis (H-P-A) function. The results showed that the circadian rhythm of plasma melatonin secretion was disrupted in schizophrenics compared with controls, whereas the 24-hour profile of plasma cortisol was preserved. The melatonin to cottisol ratlo was significantly higher in control subjects than in schizophrenic patients. Results of the dexamethasone suppression tests indicated that there were no functional changes in the H-P-A axis in schizophrenic patients. Five drug-naive schizophrenic patients studied simultaneously, whose data were not included in the above analyses, had results consistent with those of the Inaintenance-medicated patients. These findings suggest the presence of abnormal melatonin metabolism in Taiwanese schizophrenics, which may possibly be related to the pathophysiological process itself. tlowever. broader pathogenetic aspects of these neuroendocrine interrelations remain to be elucidated