There is a considerable inconsistency in terms of the association between alcoholism and alterations in monoamine oxidase (MAO) activity. The main objectives of this study were to investigate the changes in platelet MAO-B activity throughout the alcohol withdrawal period and whether or not MAO-B activity differed between patients with high- and low-aggression tendency. We assayed platelet MAO-B levels spectrophotometrically in 22 male inpatients with alcohol dependence in their first and fourth weeks of withdrawal and in 20 healthy controls. Patients were divided into two high- and low-aggression subgroups according to scores obtained in a Brown-Goodwin Assessment for Life History of Aggression. Our data revealed that the significantly lower platelet MAO-B activity observed during the first week of alcohol withdrawal in patients, compared to controls, did not continue in the fourth week, and that there was no relationship between aggressiveness and MAO activity. These results suggest that low platelet MAO activity may be a state marker of alcohol withdrawal period or a result of high alcohol consumption rather than a trait marker of alcoholism.

It is known that the first step in the de novo synthesis of tetrahydrobiopterin from GTP is the conversion of GTP to dihydroneopterin triphosphate. Recent evidence supports the conclusion that beyond this first step, the pterin intermediates in the pathway are all at the tetrahydro level of reduction. We have now shown that partially purified fractions from rat liver, rat brain and bovine adrenal medulla catalyze the conversion of dihydroneopterin triphosphate to tetrahydrobiopterin, as well as to the putative intermediates in the pathway, 6-pyruvoyl-tetrahydropterin and 6-lactoyl-tetrahydropterin. Results of both enzymatic and chemical studies support the assigned structures for the latter two tetrahydropterins. We have also purified extensively from brain an enzyme, distinct from sepiapterin reductase, that catalyzes the TPNH-dependent reduction of 6-pyruvoyl-tetrahydropterin to 6-lactoyl-tetrahydropterin. The role of this reductase in tetrahydrobiopterin synthesis has not yet been established.

1. In this study, the authors sought to test the hypothesis that Li (lithium) treatment can induce alterations in PRL (prolactin) secretion in euthymic bipolar patients compared to controls and that short and long-term administration can lead to prolactin changes different from each other. 2. Twenty euthymic bipolar male patients on long-term lithium carbonate treatment for more than 6 months and 15 euthymic male bipolar patients on short-term Li treatment for shorter than 6 months who met DSM-IV criteria for bipolar affective disorder were included in the study. Seventeen age-matched healthy control males were chosen among the hospital staff. The mean +/- SD duration of Li use was 68.93+/-46.31 months in the long-term lithium-treated group and 4+/-3.42 months in the short-term lithium-treated group. 3. Serum PRL values in the long-term Li-treated group were significantly lower than those of the control group, while there was no significant difference in PRL values between the short-term Li-treated group and the control group. 4. Our study documents that short-term (<6 months) Li treatment does not induce any significant changes in PRL release in bipolar patients compared to normal control subjects while long-term Li treatment (>6 months) leads to lower PRL release compared to the controls. Furthermore, PRL has wide intra-interindividual and circadian variations Li-PRL relationship seems to be very complex and probably depends on various interactions among dopamine, serotonin and PRL. Therefore, further studies are needed to confirm the data.

Endogenous opioid peptides are thought to participate in the phenomena of alcohol tolerance and withdrawal. Since in the pituitary gland, beta-endorphin (beta-EP) and adrenocorticotropic hormone (ACTH) are produced from the same precursor molecule, pro-opiomelanocortin, it may be expected that alterations in plasma ACTH and cortisol levels should parallel changes in plasma beta-EP levels during alcohol withdrawal. The aim of the present study was to investigate the alterations of beta-EP, ACTH and cortisol secretion patterns in alcohol-dependent patients with heavy intake in the early withdrawal period and, if any, whether these changes remained stable on long-term withdrawal. Twenty-two hospitalized male patients (mean age +/- SD: 43.45 +/- 9.22 years, mean daily amount of alcohol +/- SD: 421.59 +/- 116.57 g) who were diagnosed to have alcohol withdrawal and 20 age-matched healthy men (mean age +/- SD: 38.35 +/- 7.63 years) were included in the study. Morning and night levels of plasma beta-EP, ACTH and cortisol were measured in the patients during the early (first week) and late (fourth week) withdrawal periods following alcohol cessation, and only once in the control subjects. It was found that both morning beta-EP and morning ACTH levels were reduced during both early and late withdrawals, whereas cortisol levels were increased in early withdrawal and normalized towards the late withdrawal period. The finding that beta-EP deficiency continued despite withdrawal symptoms subsiding in patients suggests that their beta-EP deficiency is independent of the withdrawal syndrome and that reduced beta-EP activity may be a trait contributing to alcohol craving.

It has been proposed that new atypical antipsychotics cause minimal prolactin (PRL) elevation compared to traditional antipsychotic agents because they spare dopamine blockade within the brain's tuberoinfundibular tract. The aim of this study was to compare the effects of olanzapine and haloperidol on PRL secretion in male schizophrenic patients. Twenty-nine male schizophrenic inpatients were included in the study. Fifteen of them were given olanzapine in a fixed dose of 10 mg/day PO and 14 of them were given haloperidol in a fixed dose of 10 mg/day PO for 6 weeks after a 2-week drug washout period. Fifteen age-matched healthy control subjects were used as control group. PRL levels were measured both before and after the 6-week treatment period in the patients. At the end of the 6th week, the PRL values observed with olanzapine treatment were significantly less than those observed with haloperidol, but not different from those of the controls. There was a significant positive correlation between the PRL values and the severity of extrapyramidal side effects in only the haloperidol group after the six week's treatment period. Our data indicate that short-term olanzapine treatment at doses of 10 mg/day PO causes minimal elevations in PRL secretion in male schizophrenic patients in contrast to haloperidol. This finding is consistent with the previous reports and may be attributed to olanzapine's differential effects on dopamine neurotransmission.

The pycolylamine derivative, 3,5-ethoxy-4-aminomethylpyridine (B24) is a novel amine oxidase inhibitor with selectivity for semicarbazide-sensitive amine oxidase enzymes (SSAO). If selective enough it could be of use in studies of the relative importance of tissue bound SSAO and other amine oxidase enzymes, such as plasma SSAO (BAO), monoamine oxidase (MAO) and diamine oxidase (DAO) in the inactivation of endogenous and exogenous amines. The inhibition of the SSAO of brown adipose tissue of the rat by B24 was mixed and time dependent, with an IC50 value against 10 μM benzylamine of 0.3 μM B24 was also potent on pig plasma BAO, where its effect was also mixed but fully reversible by dialysis, with an IC50 of 0.17 μM. These values contrast with a Ki of 800 μM for rat liver mitochondrial MAO-A and an IC50 of greater than 1 mM for the deamination of 2-phenylethylamine (mainly MAO-B). DAO and lysyl oxidase were also very insensitive to inhibition by B24. Addition of B24 to the fluid perfusing the isolated mesenteric arterial bed of the rat significantly reduced the deamination of both benzylamine and tyramine, indicating that it was able to inhibit SSAO in situ. It appears that B24 is a selective inhibitor of both tissue bound and plasma SSAO, which should be an important aid in clarifying the physiological rôles of the various SSAO enzymes.