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F Stastný

Publications and source records attributed to F Stastný.

At least 37 records · Page 2Linked to original sources

Changes in the activity of gamma-glutamyl transpeptidase induced by kainic acid and surgical lesions of the hippocampal formation in young rats.

To study possible functional involvement of gamma-glutamyl transpeptidase (GGT) in glutamate transmitter metabolism we lesioned putative glutamatergic structures of the rat hippocampal formation by intracerebroventricular (i.c.v.) injection of kainic acid (KA) or by surgical CA3 axotomy. Unilateral injection of KA into the left lateral cerebral ventricle of 30-day-old rats resulted in decreased GGT activity in hippocampal areas CA3, Ca1 ipsilaterally, and in the contralateral area CA1, four hours after the induction of the chemical lesion. Four days after the injection, the enzyme activity was decreased in all hippocampal areas with the exception of the contralateral dentate gyrus. Four days after bilateral i.c.v. injection of KA, lower GGT levels were found than was seen after bilateral surgical lesion of the CA3 pyramidal cell axons (Schaffer's collaterals). The surgical lesion was followed by a decrease of GGT only in the stratum pyramidale and stratum radiatum of area CA1. In contrast to the effects in 30-day-old rats, unilateral i.c.v. injection of KA on postnatal day 12 did not alter the GGT activity in any studied hippocampal area presumably because of incomplete maturation of structures required for KA vulnerability.

Age Factors↗

Changes in the activity of gamma-glutamyl transpeptidase in brain microvessels, astroglial cells and synaptosomes derived from rats with hepatic encephalopathy.

Prolonged thioacetamide treatment increased gamma-glutamyl transpeptidase (GGT) activity in the rat liver and induced neurological symptoms of hepatic encephalopathy (HE). The enzyme activity measured without an amino acid or peptide acceptor was increased in cortical capillaries and synaptosomes, but remained unchanged in astroglia isolated from the brains of hyperammonemic rats. In the presence of L-glutamine the activity of GGT was stimulated by about 60% in astroglial cells while in the capillaries and synaptosomes the amino acid stimulation was less pronounced. Glycylglycine also stimulated the GGT activity in the astroglia more (4-fold) than in cortical capillaries or synaptosomes (3-fold). Similar stimulatory effects of these gamma-glutamyl moiety acceptors on the GGT activity were observed in capillaries, glial cells and synaptosomes derived from the brains of rats with HE. These results indicate that GGT may be involved in the excessive accumulation of large neutral amino acids (and some peptides) in the brain of rats with HE.

Animals↗

Development of gamma-glutamyl transpeptidase activity in primary cultures of neurones and glial cells derived from the cerebral hemispheres of chick embryos.

The development of gamma-glutamyl transpeptidase (GGT) activity in neurones and glial cells was studied in primary cell cultures derived from the cerebral hemispheres of chick embryos. GGT activity was found in both basic types of nervous tissue cells. It was always higher in glial cell cultures, where it was up to 2.3-fold the values in neurone-enriched cultures. If the culture medium contained foetal calf serum, the GGT activity of both types of nerve cells was higher than in the presence of inactivated calf serum. Comparison with the in vivo situation showed that the level of GGT activity in nerve cell cultures was significantly lower. Between the seventh day of embryogenesis and the third day of postnatal development of the nerve cells, there were marked differences between the GGT activity of cells maintained under in vitro conditions and cells of the same age in brain tissue homogenate. GGT activity in cerebral hemisphere homogenates from a 17-day-old embryos amounted to 4-fold the activity in a primary glial cell culture and to 16-fold the value in a neurone-enriched culture from hemispheres at the same stage of development.

Animals↗

Plasma xanthine oxidase activity correlates with the resistance to severe hypoxia in different species.

A rapid polarographic method of measuring the O-form of xanthine oxidase (XOD) is described. Activities of this enzyme and oxypurine concentrations were measured in the plasma and cerebrospinal fluid (CSF) of 1, 12, 25 and 60-day-old rats. In the CSF, the highest oxypurine concentration was found in the group of 12-day-old rats (34.07 +/- 12.37 mumol.l-1), and it remained nearly at the same level in groups of older animals. Oxypurines in the plasma, on the contrary, are polarographically measurable on the first day of life; in groups of older rats their concentration is below the sensitivity of the method (5 mumol.l-1). This was explained by the development of XOD activity in the plasma, which increased from 8.17 +/- 2.80 to 99.46 +/- 13.85 nkat.l-1 during the first 60 days of postnatal life. The higher the normal plasma XOD activity, the shorter was the survival time of the species during interrupted hypobaric hypoxia. Adult guinea-pigs and hamsters have no measurable XOD activity in the plasma; adult rats and mice have 99.46 +/- 13.85 and 259.69 +/- 58.23 nkat.l-1, respectively. The survival time of these animals at 10,500 m was measured following exposure to an altitude of 8,000 m for 30 min and 15 minute normoxia. Guinea-pigs survived 100.8 +/- 13.84 min, hamsters 54.25 +/- 11.33, rats 25.2 +/- 5.37 and mice 3.33 +/- 1.00 min.

Animals↗

Effect of short-term or intermittent hypobaric hypoxia on plasma lipids in young rats.

Changes in the level of plasma lipids (cholesterol, fatty acids and lipoproteins) were followed in young rats exposed once or repeatedly to hypobaric hypoxia. A single exposure to hypoxia increased the level of LDL lipoproteins but did not influence the concentration of cholesterol and fatty acids in 18-day-old rats. Repeated exposure to hypobaric hypoxia caused a statistically significant increase in the concentration of cholesterol, fatty acids, chylomicra, low density beta-lipoproteins (LDL) and very-low-density beta-lipoproteins (VLDL) in 18-day-old rats, while the level of high-density alpha-lipoproteins (HDL) decreased. In animals that had been repeatedly exposed to hypoxia in their youth, a significant decrease of the LDL lipoprotein fraction was observed at the age of 108 days.

Aging↗

A morphometric study of cortisol-induced changes in the development of neuronal process outgrowth in the corticoid zone of the embryonic chick telencephalon.

The development of dendritic arborization was analysed and quantitative data (number of stem dendrites, their segments and total length of dendritic tree) were obtained. Early administration of cortisol (on day 11) inhibited all three dendritic parameters of small stellate neurones situated in the corticoid zone of the telencephalon in 19-day-old chick embryos, but in large stellate neurones the number of dendritic segments and their total length were only impaired. Late administration of this hormone (on day 17) did not influence the development of the dendritic network of large neurones, but it affected the number of segments and total dendritic length of small neurones. These results suggest that the number of stem dendrites is set in first, followed by elongation and ramification of the fibres. The main effect of cortisol on the neuronal differentiation is the inhibition of dendritic outgrowth with a dependence on period when dendrites, their branches and dendritic spines develop most rapidly.

Animals↗

Effects of short-term and prolonged aerogenic hypoxia on gamma-glutamyl transpeptidase activity in the brain, liver, and biological fluids of young rats.

Posthypoxic fluctuations in the levels of two excitatory amino acids, glutamate and aspartate, may be related to changes in mechanism(s) which are responsible for their reuptake. As gamma-glutamyl transpeptidase (GGT) plays a role in mediating the uptake of glutamate and aspartate into various compartments of the brain, we studied changes in the activity of this enzyme in main regions of the brain in young and adult rats. We found a posthypoxic increase in bound GGT activity in some brain regions of 18-day-old animals after acute exposure, but no changes were observed after prolonged altitude hypoxia, with the exception of a decrease in cortical GGT activity. In contrast, acute hypoxia decreased GGT activity in the cortical capillaries to 59%, but prolonged hypoxic exposure was ineffective. However, the activity of soluble GGT in the cerebrospinal fluid of both groups of rats was several-times elevated in comparison with controls. At the same time, bound GGT activity was increased in the liver after acute or prolonged altitude hypoxia. The soluble GGT activity in plasma was only increased after prolonged exposure. Ninety days after prolonged hypoxic exposure the bound GGT activity was reduced in all brain regions to about 60-70% of controls (significantly higher in females than in males) as long-term developmental sequel from early postnatal hypoxia.

Altitude↗

Gamma-glutamyl transpeptidase activity in isolated cells and in various regions of the mouse brain during early development and aging.

Differences in the distribution of gamma-glutamyl transpeptidase (GGT) activity during early and late postnatal development of the mouse brain were studied at the cellular and regional level. From the 7th to the 25th day of brain development, GGT activity rose evenly in the neuronal perikarya, glial cells and in the neuropil. At 25 days and 5 weeks of age, a 1.5-fold enrichment was observed in nerve cell bodies and in neuroglia as compared with the neuropil and the original cell suspension. During the same period, an abrupt increase in GGT activity was observed in brain capillaries, and between the 10th day and the 5th week, this was 1.5-5 times higher than the enzyme activity in cellular elements and in the neuropil. This increase in enzyme activity in brain capillaries continued up to the age of 12 months, when it was succeeded by a decrease in GGT activity to the level found at 3 months. GGT activity in the choroid plexi rose significantly (more than double) between the age of 5 weeks and 18 months and was a whole order higher than GGT activity in 10 other regions of the mouse brain, whose development displayed no pronounced changes in the activity of the enzyme. A single dose of dexamethasone, or adrenalectomy, were used to demonstrate any participation by steroid hormones in the regulation of GGT activity in the brain tissue. Of the two techniques, only adrenalectomy led to a statistically significant decrease in activity in brain and liver tissue, while the apparent increase in GGT activity after a single dose of dexamethasone was not statistically significant.

Aging↗

Developmental formation and cortisol regulation of gamma-glutamyl transpeptidase in brain and spinal cord of chick embryo.

The developmentally conditioned changes in gamma-glutamyl transpeptidase (GGT) activity in chick embryonic hemispheres, optic lobes, cerebellum, brain stem and in lumbar and brachial enlargements of the spinal cord were studied. A marked increase in GGT activity was found in all tissues between embryonic day 11 and hatching. The application of cortisol enhanced GGT activity particularly on embryonic days 15 and 17. This effect of cortisol was reversed by the concomitant administration of actinomycin D or cycloheximide. The results are discussed in relation to the potential metabolic and transport role of GGT and its regulation in the developing chick embryonic brain.

Animals↗

Cortisol regulation of gamma-glutamyl transpeptidase in liver, choroid plexus, blood plasma and cerebrospinal fluid of developing chick embryo.

A relationship between membrane-bound gamma-glutamyl transpeptidase (GGT) in liver and choroid plexus and the soluble GGT in blood plasma and cerebrospinal fluids is indicated by a decrease of the former activity in the organs and a concomitant increase of the latter in the body fluids of the embryonic chick between day 11 and hatching. Starting on day 15, the administration of cortisol caused a marked increase in the activity of soluble GGT in blood plasma and cerebrospinal fluid which might be related to an increase of the membrane-bound activity of this enzyme by the glucocorticoid in liver, brain and choroid plexus during the same developmental period. However, before day 15 cortisol reduced GGT activity in the liver and choroid plexus suggesting a biphasic effect of the steroid on the activity of membrane-bound GGT.

Animals↗