Platelet monoamine oxidase activity in Down's syndrome

The activity of platelet monoamine oxidase in Down's syndrome cases was significantly lower than that of controls. This difference was found for both males and females, and with tyramine, tryptamine and β-phenethylamine as substrate. The K_m values of the monoamine oxidase towards tryptamine as substrate from controls and Down's syndrome patients were similar.     

Platelet monoamine oxidase activity and cigarette smoking

Platelet MAO activity and plasma thiocyanate concentrations were determined in 72 normal volunteers (22 non-smokers and 50 smokers). Thiocyanate concentrations were used as an index of exposure to cigarette smoke. A significant negative correlation between MAO and thiocyanate concentration was observed for the group (rs = 0.35; P less than 0.005). When examined by sex, the correlation was significant for females but not for males. Mean MAO activity was significantly lower for female smokers than for female non-smokers. For males, no significant differences in MAO activity were observed between smokers and non-smokers. It is possible that smoking causes inhibition of MAO by a direct effect or by indirect effects such as altering hormone levels. Alternatively women with a low MAO activity have a greater innate tendency to smoke.     

Platelet monoamine oxidase activity in schlzophrenic families-kinetic aspects

Monoamine oxidase activity (MAO) was determined in platelets in samples from a North-Swedish pedigree with a high frequency of schizophrenia. The MAO assay was performed with phenethylamine as substrate and with two concentrations of oxygen (0.06 and 0.12 mM). A tendency to lowered V_max and increased apparent K_m values was observed among the schizophrenic subjects, although there were no statistically significant differences in apparent K_m and V_max values between schizophrenics and their non-schizophrenic relatives.     

Platelet monoamine oxidase activity during the course of a schizophreniform psychosis.

A case is reported in which platelet monoamine oxidase (MAO) activity fluctuated in the course of a schizophreniform psychosis in a way which suggests a direct relationship between low levels of MAO activity and the psychosis.     

Platelet monoamine oxidase activity during surgical intervention under condition of hypothermic perfusion

Platelet and plasma monoamine oxidase activity was determined at early stages of hypothermic perfusion and circulatory arrest. Monoamine oxidase activity decreased more drastically and restored more slowly against the background of deep (14°C) compared to moderate hypothermia (25–29°C). The decrease in platelet monoamine oxidase activity was accompanied by its increase in the plasma, which attests to mechanical (in tubes) and toxic damage to platelets. The latter is associated with increased partial O₂ pressure in the plasma during hypothermia, which promotes the formation of reactive oxygen species. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 129, No. 4, pp. 393–395, April, 2000     

Methylation of DNA in megaloblastic anaemia.

Methylation of cytosine residues in DNA samples, collected before and serially after cobalamin treatment from patients with cobalamin deficiency, was studied using restriction endonucleases Hpa II and Msp I and an epsilon globin gene probe. There was no evidence of hypomethylation in any of the samples. It was concluded that although hypomethylation of metabolites such as choline occurs, that of DNA is preserved in megaloblastic anaemia.     

Plasma lactate dehydrogenase in megaloblastic anaemia

Raised plasma lactate dehydrogenase (LDH) values were found in 26 patients with marked megaloblastic anaemia due either to vitamin B₁₂ or folic-acid deficiency or a combination of these factors.     

Acidosis and severe megaloblastic anaemia

Ten patients with severe megaloblastic anaemia were studied to investigate whether the causative metabolic defects might predispose them to lactic or other acidosis. One patient had compensated acidosis with hyperlactataemia before treatment but there were obvious causes other than anaemia. No other patient developed an acidosis. Neither anaemia per se nor the metabolic defects of vitamin B₁₂ or folic acid deficiency are likely to cause clinically significant lactic acidosis or hyperlactataemia.     

Platelet monoamine oxidase activity and life stress as predictors of psychopathology and coping in a community sample

The present study, using a diathesis-stress model, attempted to confirm prior findings with platelet monoamine oxidase (MAO) activity and stress in a middle-aged, non-clinic population. One hundred and seventy-eight adult males from a statewide community club were tested for platelet MAO activity and stressful life events and were also given a variety of psychological measures of both psychopathology and psychosocial coping. The data were examined both for correlations across the total sample and for a comparison of high-risk groups (top and bottom 15% of MAO activity) with a middle MAO group. Low platelet MAO activity was related to a higher incidence of contact with mental health professionals, and more frequent use of alcohol and cigarette smoking. High MAO activity was related to higher levels of anxiety and somatization. High levels of stress were related to increased psychosocial problems reported for female and family members, higher scores on two schizophrenia-related MMPI scales (schizophrenia and paranoia subscales), but fewer idiosyncratic associations, elevated hypomanic, depression, and anxiety scores, increased alcohol use, and increased use of prescribed antianxiety and sedative medication. Neither MAO nor stress were related to current levels of psychosocial coping. Moreover, no interaction effects were uncovered for MAO activity and stress combined.     

Platelet monoamine oxidase in a pedigree with schizophrenia: an interlaboratory project

Conflicting reports on the association between platelet MAO activity and schizophrenia prompted a critical review and determinations on identical samples at one laboratory in Sweden and one in the USA. Samples originated from eight schizophrenics and 27 relatives belonging to a large pedigree, thus ensuring biological homogeneity.
In the USA laboratory, a significantly lower MAO activity was found in the schizophrenics when benzylamine or β–phenylethylamine was used as substrate (but not with trypt–amine), while a similar result was obtained in the Swedish laboratory when tryptamine was used (but not with benzylamine or (β–phenylethylamine). Comparisons between materials examined in different laboratories do not seem meaningful until differences in methodologies have been clarified. At present there is neither proof nor disproof of MAO being a "genetic marker" for vulnerability to the schizophrenic disorder.     

Lymphocyte subpopulations in patients with hydroxocobalamin responsive megaloblastic anaemia.

Lymphocyte subpopulations and intrinsic factor and gastric parietal cell antibodies have been measured in 23 patients with megaloblastic anaemia who responded to treatment with hydroxocobalamin. The ratio of helper (OKT4) to suppressor (OKT8) lymphocytes was significantly increased in patients with intrinsic factor antibody compared with those who lacked the antibody. No such correlation was found for gastric parietal cell antibody. Alterations in the lymphocyte helper to suppressor (OKT4:OKT8) ratio may be associated with pernicious anaemia.     

Reversible absorptive defects in anticonvulsant megaloblastic anaemia

Two cases of anticonvulsant megaloblastic anaemia are described, showing features of unusual interest. Though both cases were apparently deficient in folic acid, the Figlu tests were negative. One patient had an extremely low serum B(12) concentration apparently associated with defective B(12) absorption due to deficiency of intrinsic factor, and both showed impaired intestinal absorption of D-xylose. There was, however, no evidence of permanent gastro-intestinal dysfunction, and the absorptive defects disappeared completely after treatment with folic acid.Possible reasons for the findings are discussed. It is suggested that absorptive defects produced by the drugs may play some part in initiating anticonvulsant megaloblastic anaemia, and that once deficiencies of haemopoietic factors are established, a vicious circle may be set up owing to the effects of these deficiencies on the gastro-intestinal tract.     

Altered platelet monoamine oxidase activity in affective disorders

Platelet MAO activity was found to be elevated in primary depressive illness, and the severity to correlate positively with MAO activity. The reactive depression subgroup's mean platelet MAO activity was not significantly different from that of the controls. The endogenous group's unipolar and bipolar subgroups had significantly different platelet MAO activity, respectively high and low. The differences in MAO activity between unipolar and bipolar patients appeared to persist in the well state, but not after lithium carbonate therapy. These differences in MAO activity were apparent with the substrate tyramine but not with benzylamine. Altered MAO activity in patients with affective disorders may be determined through genetic mechanisms.     

Chondrocytic monoamine oxidase activity in the development of natural murine osteoarthritis.

Most of the male STR/ORT mice develop osteoarthritis (OA) involving the medial tibial plateau. A peculiarity of two chondroprotective drugs is the presence of a nitrogen atom so that cleavage of the molecule could generate a molecule that might act as an inhibitor of monoamine oxidase (MAO). Direct examination showed abnormal localization of MAO in the potentially osteoarthritic cartilage indicating possible abnormal response to catecholamines. In normal cartilage, the direct effect of excessive concentration of adrenaline caused considerable oedema, as measured by microscopic interferometry. It is therefore suggested that the excess of water found in the matrix of osteoarthritic cartilage may be related to disturbance of the MAO activity.