Prolactin and polyamine catabolism: specific effect on polyamine oxidase activity in rat thymus.

Much evidence suggests that prolactin has an immunoregulatory function and that its effects on cells of the immune system depend on the level and specific forms of the receptors present on the target cells. The effect of administration of prolactin on polyamine catabolism was investigated in thymus of male intact rats by measuring the activities of spermidine/spermine N(1)-acetyltransferase and polyamine oxidase, because of the relationships between polyamines (especially putrescine) and the immune system. The administration of prolactin to rats resulted in the rapid induction of spermidine/spermine N(1)-acetyltransferase activity in the thymus (1.6-times the level of control rats, within 4 h), and in a marked decrease in polyamine oxidase activity at 24 h. The changes in enzyme activities were accompanied by an increase in putrescine concentration and a decrease in spermidine and spermine concentrations. In the spleen, prolactin increased SAT activity only 24 h after administration and was ineffective on PAO activity.

Polyamine oxidase activity in lymphoid tissues of glucocorticoid-treated rats.

Glucocorticoids are known to negatively affect lymphoid tissues, in which they cause programmed cell death. Polyamine depletion, which occurs in glucocorticoid-treated animals by inhibition of biosynthesis and induction of acetylation, may represent a signal to thymocytes for progression into the apoptotic program. Since catalysis of polyamines by the catabolic pathway produces hydrogen peroxide as a by-product, it has been suggested that the apoptotic process may be, in part, due to oxidative stress as a result of hydrogen peroxide production. In order to verify whether polyamine oxidase (EC 1.5.3.11) may play a role in the process, we examined the activity of the enzyme in the thymus and spleen of glucocorticoid-treated rats. We administered dexamethasone (4 mg/kg) or two different doses of corticosterone (4 mg/kg or 30 mg/kg) to rats, which were killed 8 or 24 hr after hormone injection. We found that corticosterone and dexamethasone affected polyamine oxidase activity in both tissues, with an opposite dose-dependent effect of the natural hormone in the thymus. The decrease and increase in polyamine oxidase after the two doses of corticosterone were correlated with the absence and the occurrence of DNA fragmentation, respectively. Moreover, corticosterone affected polyamine oxidase activity earlier (8 hr) than dexamethasone (24 hr), but the synthetic hormone was more efficient than the natural hormone in thymic polyamine depletion. The polyamine oxidase response may represent an important event in lymphoid tissues after glucocorticoid treatment, suggesting a role of the enzyme in the catabolic effects exerted by the two hormones.

Gender-related differences in polyamine oxidase activity in rat tissues.

Variations in level of polyamines and their related enzymes are frequently observed in response to some treatments which affect in a different way male and female. The possibility of a gender-related difference in the oxidation of polyamines was investigated in rats by measuring the activity of polyamine oxidase, a ubiquitous enzyme of vertebrate tissues, which transforms spermine into spermidine and spermidine into putrescine. The study was carried out on thymus, spleen, kidney and liver of young rats of both sexes, and female rats showed a lower polyamine oxidase activity than male rats in all the tissues. We also found higher values of spermidine acetylation in female than male rats in thymus and liver. Owing to these gender-related differences, a higher spermidine N-acetyltransferase/polyamine oxidase ratio was found in female than in male rats. A second gender-related difference was a higher spermidine/spermine ratio in female than in male, the only exception being the thymus. These basal differences possibly account for the gender-related differences of polyamine metabolic enzyme activities in response to some treatments, including drugs or hormones.

Changes in hepatic polyamine catabolism in elderly rats.

AIMS/BACKGROUND: Given the important role of polyamines (putrescine, spermidine, spermine) in the modulation of macromolecular syntheses, gene expression and proteolysis, alterations in their metabolic pathways could be relevant during senescence. Since the few existing data address mainly polyamine biosynthesis, we studied the oxidative catabolism of polyamines in the liver of rats 3-36 months of age. METHODS: Polyamine oxidase activity was fluorimetrically measured using N1-acetylspermine as substrate. Spermidine/spermine N1-acetyltransferase and diamine oxidase were measured by radiochemical methods using labeled acetyl-coenzyme A and putrescine, respectively, as substrate. Polyamines were separated by HPLC and fluorimetrically quantified after post-column derivatization with o-phthaldialdehyde. RESULTS: Spermidine/spermine N1-acetyltransferase activity increased in 36-month-old rats and polyamine oxidase activity in 24- and 36-month-old rats. A decline in spermine and increases in spermidine and putrescine in elderly rats suggested an activation of the interconversion pathway of higher into lower polyamines. The activity of diamine oxidase, which degrades putrescine, was enhanced starting from 12 months of age. CONCLUSION: In the liver of aged rats, an increase in the catabolic enzymes leads to a reconversion of the higher polyamines to putrescine. This increased catabolism may represent an important age-related change and may contribute to impairment of the expression of growth-related genes in senescence.

Aging and polyamine acetylation in rat kidney.

The acetylation of polyamines was investigated in rat kidney as a function of age. The activity of cytosolic spermidine/spermine N1-acetyltransferase, the rate-limiting enzyme in polyamine interconversion, increased from 3 to 36 months of age. The activity of cytosolic spermidine N8-acetyltransferase, an enzyme probably related to polyamine excretion, also increased. The activity of polyamine oxidase, which catalyzes the oxidative cleavage of polyamine N1-acetyl derivatives into putrescine, decreased until 24 months, when an accumulation of N1-acetylspermidine occurred. Subsequently, at 36 months, polyamine oxidase activity returned toward high values, in concomitance with the disappearance of N1-acetylspermidine, an increase in spermidine and putrescine, and a decline in spermine was observed. Our results show that in rat kidney during aging there is an activation of the acetylation and interconversion of higher polyamines into putrescine, which is considered an alternative pathway of spermidine and putrescine formation.

[Respiratory and cardiac activity during sleep at high altitude (4650 m. above sea level)]. / Attivita' respiratoria e cardiaca nel sonno in alta quota (4650 m. s.l.m.).

In this study, the relationship between the cardiac rhythm and ventilatory rhythm, during the sleep, at high altitude (4560 s.l.- Peruvian Andes) has been evaluated in native acclimated, and long-term resident people. The experimental observation has been performed from 11.00 p.m. to 7.00 a m. (when the barometric pressure was 430 mmHg, pO2 was 90 mmHg and paO2 was 71 mmHg) by using an eight channel polygraph for EEG, usefully modified for ECG and pneumographic recordings. In agreement with the observations of other Authors, a periodic breathing was recorded when the theta rhythm (low amplitude waves, characteristic of the second stage of the sleep) appeared in the EEG. During the REM stage of the sleep, the respiration becomes irregular, without periodicity in the ventilatory rhythm. Any statistical difference was not observed between European and Andinian subjects. During the N-REM phases of the sleep, the cardiac activity was often clearly dissociated from respiratory cycles. This finding suggests that, during the 2 and 4 phases of the sleep, in our experimental conditions, the cardio-inhibitory and cardio-acceleratory centers seem to lose the correlation with the regulatory centers of the breathing.

Effect of sudden reductions of the arterial blood pressure on the mean diastolic coronary resistance.

At the beginning of a 10 sec arterial haemorrhage, vascular elasticity induces an increase of mean diastolic coronary resistance. Then, the increase is counteracted by the relaxation of the vascular musculature, which causes a coronary hyperaemia when, after the haemorrhage is arrested, the vascular wall is stretched by a sudden though slight increase of blood pressure.