Edward G. Shaskan

Monoamine oxidase activity as a biological marker

Abstract Human blood platelet monoamine oxidase (MAO) has been proposed as a biological marker of vulnerability to a variety of psychiatric diseases. The functional significance of this association between peripheral enzyme activity and behaviour has been unclear. We have now developed a rationale for its clinical application and some thoughts for further experimentation.

Spiroperidol binding sites on mouse lymphoid cells. Effects of ascorbic acid and psychotropic drugs

Since highly differentiated cells of mammalian immune systems reportedly have binding sites for a variety of neurohumoral agents, we investigated parameters related to possible existence of dopamine receptors on murine lymphoid cells. Using a dopamine antagonist, [3H]spiroperidol, we found evidence for displaceable binding on mouse spleen cells. Total and displaceable (10 microM haloperidol) binding of spiroperidol was markedly enhanced by the absence of ascorbic acid in the incubation medium. Displaceable binding of a dopamine receptor agonist [( 3H]ADTN) could not be found on lymphoid cells either in the presence or absence of ascorbic acid. In the absence of ascorbate, displaceable spiroperidol binding to mouse spleen cells revealed partially saturable, but complex, kinetics and we calculated positive cooperativity at low ligand concentrations.

Elevated endogenous breath acetaldehyde levels among abusers of alcohol and cigarettes

Endogenous (fasting) breath acetaldehyde levels were assessed as a discriminator between alcoholic and non-alcoholic subjects. The influence of smoking as a potential confounding variable on breath acetaldehyde was determined. Individuals with a history of smoking and/or drinking had higher endogenous breath acetaldehyde levels as compared to controls. Mean acetaldehyde levels revealed an additive (noninteractive) pattern associated with combined abuse of these substances. The similarity in acetaldehyde levels between alcoholic non-smokers and non-alcoholic smokers limits the usefulness of endogenous breath acetaldehyde for the purpose of early diagnosis of alcoholism. Results support hypotheses that elevations in acetaldehyde could be a common factor in disease associated with alcohol and cigarette abuse.

Endogenous breath acetaldehyde levels among alcoholic and non-alcoholic probands: Effect of alcohol use and smoking

The effects of possible confounding factors on endogenous breath acetaldehyde levels were examined in alcoholic and non-alcoholic subjects. Demographic characteristics, family history for alcoholism, smoking and drinking history, and breath acetaldehyde levels were assessed. Differences in endogenous breath acetaldehyde levels could not be attributed to age, sex, or having a family history positive for alcoholism. Individuals who smoke or abuse alcohol had higher endogenous breath acetaldehyde levels than persons who did not.

Dietary ascorbic acid deficiency in guinea pigs: No effect on ethanol preference, spiroperidol binding, or monoamine oxidase activity

Ascorbic acid levels are commonly reported to be decreased in alcoholics. Although this deficiency could be due to dietary factors, there is evidence that ascorbic acid may be involved in the metabolism and acute effects of ethanol, possibly related to the pathogenesis of alcoholism. Therefore, we examined ethanol preference in guinea pigs receiving an ascorbate deficient vs a normal diet. Brain and spleen ascorbic acid levels were dramatically decreased, but ethanol preference was not altered by the acute dietary deficiency of this vitamin. In addition, an acute stressor (cold water swim), alone or in combination with ascorbate deficiency, had no effect on ethanol preference. At termination of the experiment, two measures of brain aminergic function (MAO activity and 3H-spiroperidol binding), purportedly altered by ethanol or ascorbic acid or both, were not associated with tissue ascorbate levels.

Elevation of serum prostagladin E levels following electrical stimulation of the midbrain

Serum prostaglandin E (PGE) levels were measured in rats immediately following electrical stimulation of the mesencephalic periaqueductal gray (PAG) region and the nucleus raphe magnus (NRM) and compared to controls. An additional group received aspirin prior to PAG stimulation. A significant increase in serum PGE levels was found after stimulation of the PAG, but not the NRM. Aspirin inhibited the stimulation-induced increases in PGE.