Platelet monoamine oxidase, plasma benzylamine oxidase and liver mixed function oxidase in cirrhotic patients

Because it has been suggested that an accumulation of false neurochemical transmitters plays a part in the cardiovascular and neurological complications of cirrhosis it appeared worthwhile to study the level of monoamine oxidase in the liver and platelets of cirrhotic patients. In fact a decrease of such activities might explain the increase of false neurotransmitters observed in cirrhotic patients. Other enzyme were also tested: the plasma benzylamine oxidase activity and the liver mixed function oxidases. 13 cases of severe cirrhosis (B, C according to Child classification) and 10 cases of less severe cirrhosis (A according to Child classification) were studied in comparison to patients affected by cholelithiasis. A defect in the level of monoamine oxidase activity of platelets and liver was observed in some cirrhotic patients together with a decrease of the level of the liver mixed function oxidases.     

Platelet monoamine oxidase activity in subgroups of schizophrenic disorders

This article summarizes findings from a series of studies that examined platelet monoamine oxidase (MAO) activity in patients with nonaffective schizophrenic disorders and schizophrenia-related depressions. The findings indicate that mean platelet MAO activity was not different from control values in the subgroup of nonaffective schizophrenic disorders without auditory hallucinations (that is, the S-1 subgroup). However, mean platelet MAO activity was reduced in the subgroup of nonaffective schizophrenic disorders characterized by the presence of auditory hallucinations often occurring in conjunction with paranoid features (that is, the S-2 subgroup). Moreover, we found that mean platelet MAO activity was increased in schizophrenia-related depressions characterized by histories of chronic asocial, eccentric, or bizarre behavior.     

Genotype dependence of monoamine oxidase in inbred strains of mice

MAO activity was found to be influenced by the genotype or strain of mouse up to 20 days of age. The strain differences observed may derive from different rates of brain development. A number of neurological mutations comprizing three pathological classes had no effect on MAO.     

Ontogenesis of monoamine oxidase in the thyroid gland of rats

Mongolian gerbils (Meriones unguiculatus) were exposed to Mycobacterium paratuberculosis by intraperitoneal and oral routes. Fourteen weeks after exposure, the gerbils were necropsied and tissues were cultured and examined microscopically. Results of the study showed that gerbils can be infected with M paratuberculosis but are not suitable for studies of paratuberculosis.     

Critical evaluation of measurement of platelet monoamine oxidase in man

Some biochemical characteristics such as substrate specificity, substrate affinity and inhibitor sensitivity of monoamine oxidase of human blood platelets were investigated. Tyramine, tryptamine and beta-phenylethylamine were used as substrates. The apparent Michaelis constants, maximal velocity rates and I50 for the inhibitor tranylcypromine were determined. The data were analyzed according to Lineweaver-Burk and Dixon. The influence of amitriptyline, a prototype of tricyclic antidepressants, on the selected variables (Km, V, I50), was studied. The parameters investigated showed remarkably low interindividual differences when healthy volunteers were tested. The inhibitor activity of amitriptyline towards platelet monoamine oxidase depends on the substrate used. Amitriptyline concentrations which showed a pronounced effect on the enzyme characteristics are significantly higher than plasma levels of the drug found under therapeutic conditions.     

Therapeutic doses of cyproheptadine do not inhibit monoamine oxidase in man

Cypro, a serotonin and histamine antagonist, has been shown to be a moderately potent reversible inhibitor of tissue monoamine oxidase (MAO) obtained from hamsters and rabbits. In the present study, Cypro inhibits MAO obtained from human platelets with the same potency as harmine (Ki = 5 x 10(-5) M). However, when ten normal volunteers received conventional therapeutic doses of Cypro (16 mg/day) for two days, there was no alteration in their urinary excretion of tryptamine, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxymandelic acid, epinephrine, or norepinephrine. We conclude that, when used in conventional clinical doses, Cypro does not inhibit MAO in man.