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Biomedical subjects

L F Major

Publications and source records attributed to L F Major.

46 records · Page 3Linked to original sources
PubMed1978

Platelet and plasma amine oxidase activity in alcoholic individuals.

Platelet and plasma amine oxidase activity was determined in a group of 99 healthy male (active duty military) alcoholics referred for hospital treatment who had been abstinent from alcohol for 2-10 days, and compared with that of a control military group. Platelet MAO activity was slightly but significantly lower in the alcoholic group. Both groups were significantly lower in MAO activity compared to a group of 42 non-military controls. In the alcoholic group there was no correlation between platelet MAO and severity or chronicity of drinking, nor was there evidence of iron deficiency to account for the lowered MAO activity. When the alcoholic and military control groups were split at the median, the first degree relatives of both the 'low' MAO alcoholics and the 'low' MAO military controls had a higher incidence of alcoholism than did the relatives of both 'high' MAO subgroups. No personal or family history data of alcohol-related problems were available on the non-military control group.

Adult↗
PubMed1978

Effects of disulfiram and pyridoxine on serum cholesterol.

Disulfiram, 500 mg/day, raised serum cholesterol levels in alcoholic persons from a mean of 193 +/- 16.4 mg/dl to 227.2 +/- 17.2 mg/dl after 3 weeks and 264 +/- 40 mg/dl after 6 weeks. This increase was not seen in a group taking pyridoxine 50 mg/day in addition to disulfiram 500 mg/day. In contrast to the disulfiram and disulfiram-pyridoxine treatment groups, control groups receiving pyridoxine alone, or no drug, had a 33 mg/dl reduction in serum cholesterol during the first 3 weeks of abstinence, a finding consistent with other evidence showing a rapid decrease in serum lipids on abstinence from alcohol. Patients taking disulfiram 250 mg/day, with or without pyridoxine, did not have this expected decrease in serum cholesterol. Since increased serum cholesterol is one of the risk factors in a coronary heart disease, chronic disulfirm therapy may increase the incidence of arteriosclerotic cardiovascular disease, as has been the case with chronic exposure to carbon disulfide, a principal metabolite of disulfiram.

Alcoholism↗
PubMed1978

Dopamine-beta-hydroxylase in the cerebrospinal fluid of psychiatric patients.

The activity of dopamine-beta-hydroxylase (DBH) in cerebrospinal fluid (CSF) from 59 psychiatric patients has been analyzed by a highly sensitive radio-enzymatic assay. There was no sex difference in DBH, but there was a significant positive correlation with age. Probenecid administration had no effect on CSF DBH. DBH in CSF correlated positively (r = 0.60) with the plasma enzyme. Among patients hospitalized for major depressive disorder, unipolar or bipolar, schizo-affective disorder, schizophrenia, alcoholism, or personality disorders there were no significant between-group differences. Among the patients with bipolar affective disorder, DBH activity from manic patients was significantly lower than that from depressed or euthymic patients. The results are discussed with reference to the theory that the amount of DBH in CSF may serve as an indicator of central noradrenergic activity.

Adolescent↗
PubMed1977

Increased sympathetic nervous system activity in alcoholic patients treated with disulfiram.

The authors measured plasma levels of norepinephrine (NE) and dopamine beta-hydroxylase (DBH), pulse rates, and blood pressures of 81 hospitalized alcoholic patients. Treatment with 500 mg/day of disulfiram (but not 250 mg/day or placebo) resulted in small but significant increases in plasma NE and in blood pressure. The 500-mg dose did not appreciably inhibit DBH. Patients receiving high doses of disulfiram should have their blood pressure monitored and their dose decreased to 250 mg/day when possible.

Adult↗
PubMed1977

Cerebrospinal fluid homovanillic acid in male alcoholics: effects of disulfiram.

It is well know that if an individual maintained on disulfiram (Antabuse) ingests alcohol, excess acetaldehyde is formed, resulting in a toxic reaction. In addition to this toxic interaction with alcohol (the basis of its use as a deterrent), there are both behavioral and biochemical observations to suggest that disulfiram alone has a direct effect on the CNS. The possibility that some of disulfiram's effects are related to alterations in biogenic amine metabolism led to the present study of cerebrospinal fluid amine metabolites in a group of male alcoholics. In this group, disulfiram treatment was associated with a significant reduction in homovanillic acid, the major metabolite of dopamine, while no change was noted in 5-hydroxyindoleacetic acid, the major metabolite of serotonin. Prior to disulfiram, patients with withdrawal symptoms had significantly lower homovanillic acid than those without such symptoms.

Adult↗
PubMedDate not supplied

Human brain: aldehyde dehydrogenase activity and isozyme distribution in different areas.

Three human post-mortem brains were dissected into seventeen areas and assayed for aldehyde dehydrogenase (EC 1.2.1.3) activity employing two assay systems: one at 68 microM and another at 13.6 mM propionaldehyde. The levels of activity with 68 microM propionaldehyde were significantly higher in cerebellum and putamen. The same brain areas were also examined by isoelectric focusing. By this procedure two distinct bands of aldehyde dehydrogenase activity (the cytoplasmic E1 and mitochondrial E2) could be readily visualized in cerebellum and putamen while other brain areas contained mainly the mitochondrial E2 isozyme.

Aged↗
PubMedDate not supplied

Trace element levels in human alcoholic brain.

Copper, magnesium, zinc and manganese levels in the temporal cortex of human alcoholic and control brains were measured by atomic absorption spectrophotometry using both the flame and graphite furnace. All of the 21 alcoholics were male with a mean age of 54.1 years; the 19 male controls had a mean age of 60.2 years. The only statistically significant change in ion levels was an increase in manganese concentration (expressed both as microgram/g wet weight and ng/mg protein) in the alcoholic group when compared to the control group. Five of the alcoholics had malignancies, while 16 of the controls had systemic malignancies. Covariance analysis showed there was no effect of age on the level of manganese in the temporal cortex.

Adult↗
PubMedDate not supplied

Elevated cerebrospinal fluid histidine in alcohol withdrawal.

Cerebrospinal fluid (CSF) histidine concentration was significantly elevated in seven patients early in the alcohol withdrawal syndrome (206.3 +/- 74.4 (SEM) nanomols/ml CSF). When these same patients were restudied an average of six days later when alcohol withdrawal was clinically resolved, their mean CSF histidine concentration continued to be significantly elevated (164.7 +/- 24.7) when compared to normal (12.0 +/- 0.5 nanomols/ml CSF). Other amino acids (aspartic acid, serine, alanine, methionine, leucine, tyrosine, phenylalanine, lysine and arginine) showed no definite changes from normal, and no change during the course of alcohol withdrawal. Possible reasons for these high concentrations and the extreme variability (especially early in alcohol withdrawal) are discussed.

Adult↗
PubMedDate not supplied

Brain and liver monoamine oxidase type A and type B activity in alcoholics and controls.

Monoamine oxidase activity in human postmortem brain and liver samples was measured in a group of patients with a prior history of alcoholism and compared to a control group with no prior history of alcoholism. Liver samples from patients with a prior history of alcoholism showed significantly lower monoamine oxidase activity with both phenylethylamine and serotonin as substrates. Postmortem brain samples, however, were not different in the two groups.

Adult↗