The influence of hormonal preparations of FSH in a dose of 24 mg (480 IU) on levels of catecholamine (dopamine, norepinephrine and epinephrine) and the activity of their degradation enzyme monoamine oxidase (MAO) in the hypothalamic regions regulating the reproductive system of sheep (area preoptica, eminentia mediana, corpus mamillare) and pineal gland were investigated in the ocstrous period employing radiochemical methods. The administration of FSH resulted in significant (p<0.001) increases of dopamine levels in the area preoptica and corpus mamillare of the hypothalamus of sheep as compared to control groups with synchronized oestrus. Hormonal stimulation with FSH increased the levels of hypothalamic norepinephrine in the areas studied and these differences were significant in the eminentia mediana (p<0.05) and corpus mamillare (p<0.05). Significant (p<0.001) changes in epinephrine levels were found in the corpus mamillare and area preoptica (p<0.05). Our results indicate that the administration of FSH caused the most pronounced decrease of MAO activity in corpus mamillare (p<0.001). The pineal gland reacted to the hormonal preparation by decreased levels of norepinephrine and dopamine (p<0.001) and by an increase in MAO activity (p<0.01). We suggest that FSH administration affects catecholamine levels and the activity of monoamine oxidase in the studied areas of the brain of sheep by means of a feedback mechanism.
Monoamine oxidase (MAO, type A and B) and semicarbazide-sensitive amine oxidase (SSAO) metabolize biogenic amines, however, the impact of these enzymes in arteries from patients with type 2 diabetes remains poorly understood. We investigated the kinetic parameters of the enzymes to establish putative correlations with noradrenaline (NA) content and patient age in human mesenteric arteries from type 2 diabetic patients. The kinetic parameters were evaluated by radiochemical assay and NA content by high-performance liquid chromatography (HPLC). The activity of MAO-A and SSAO in type 2 diabetic vascular tissues was significantly lower compared to the activity obtained in non-diabetic tissues. In the correlation between MAO-A (Km) and NA content, we found a positive correlation for both the diabetic and non-diabetic group, but no correlation was established for patient age. In both groups, MAO-B (Vmax) showed a negative correlation with age. The results show that MAO-A and SSAO activities and NA content of type 2 diabetic tissues are lower compared to the non-diabetic tissues, while MAO-B activity remained unchanged. These remarks suggest that MAO-A and SSAO may play an import ant role in vascular tissue as well as in the vascular pathophysiology of type 2 diabetes., S. F. Nunes ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The effects of ionizing radiation on pineal melatonin and on key enzymes of its metabolism have been studied in our laboratory. After adaptation to an artificial light/dark cycle of 12:12 h, male Wistar rats were fractionally whole-body irradiated with a dose of 2.4 Gy of gamma-rays twice a week up to total doses of 4.8, 9.6 or 14.4 Gy. Irradiation and sham-irradiation were performed in the late afternoon. The rats were sacrificed at 24:00 to 01:00 h in darkness, 6 h, 3 or 5 days after the last exposure. Pineal and serum melatonin concentrations, pineal activities of serotonin N-acetyltransferase (NAT) and of monoamine oxidase (MAO) were determined. The NAT activities in the rats irradiated with 4.8 and 9.6 Gy decreased at some intervals without changes of melatonin concentration. Irradiation with a total dose of 14.4 Gy decreased NAT activity and the concentration of pineal and serum melatonin 6 h and 3 days after the last exposure. The activity of MAO, estimated only in the rats irradiated with the dose of 14.4 Gy, increased significantly 3 days after irradiation. The fractionated irradiation up to the dose of 14.4 Gy caused a transient decrease in pineal melatonin synthesis. This could be the consequence of preferential oxidative deamination of serotonin in comparison with its N-acetylation, leading to melatonin biosynthesis.