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M. Peet, MB, FRCPsych; J. D. E. Laugharne, MB, MRCPsych
Department of Psychiatry Northern General Hospital Herries Road Sheffield, England S5 7AU

D. F. Horrobin, DPhil
Kentville, Nova Scotia

G. P. Reynolds, PhD
Western Bank, Sheffield, England

Arch Gen Psychiatry. 1994;51(8):665-666.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

There is evidence of abnormalities of prostaglandin synthesis and action in schizophrenia; thus, there are reports of increased activity of phospholipase A₂,¹ increased plasma levels of prostaglandin E₂,² and subsensitivity of platelet prostaglandin receptors.³ The main precursor for prostaglandin synthesis is arachidonic acid, which is released from membrane phospholipid by phospholipase A₂. One possible consequence of increased phospholipase A₂ activity would be the depletion of arachidonic acid.

In the course of a study of membrane fatty acids, we measured⁴ red blood cell membrane arachidonic acid in a group of 23 hospitalized neuroleptic-treated schizophrenic patients (16 men and 7 women) aged 28 to 75 years (mean age, 55 years) and 16 control subjects matched for age and sex. We also measured the plasma levels of thiobarbituric acid reactive substances (TBARS) in the same blood samples. Thiobarbituric acid reactive substances are a measure of . . . [Full Text PDF of this Article]

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