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Z Dabrowiecki

Publications and source records attributed to Z Dabrowiecki.

At least 19 recordsLinked to original sources
PubMed1986

Rabbit brain lipids during short-term hyperthermia.

Rabbits were subjected to 3 h of hyperthermia at 40 degrees C. The phospholipid content of the brain was unchanged, whereas the free fatty acids increased by about 73% over control levels. Hyperthermia also induced inhibition of fatty acid peroxidation processes. The last products of fatty acid peroxidation, the thiobarbituric acid reactive substances, diminished significantly during hyperthermia, whereas the level of the first intermediate of this pathway, the conjugated double bonds, remained unchanged. Simultaneously, the levels of lipid-soluble antioxidants decreased significantly. The content of free fatty acids, malondialdehyde, and lipid-soluble anti-oxidant returned toward control levels during 3 h of recovery. The content of gangliosides was 10-20% above control values in the groups of animals examined immediately and 3 h after hyperthermia. The ganglioside-specific enzymes, neuraminidase and sialyltransferase, both directed toward endogenous lipid substrates, were activated by hyperthermia, suggesting the stimulation of turnover of the gangliosides during the course of hyperthermia. Lipid alterations resulting from short-term hyperthermia may influence the physicochemical properties of neuronal membranes.

Animals↗
PubMed1986

Consequences of exposure of rats to hyperoxygenation for actomyosin-like protein from synaptosomes of brain.

This paper describes the changes caused by in vivo hyperoxygenation of rats in the brain synaptosomal actomyosin-like protein preparation. We demonstrate that this preparation is composed of protein and phospholipid components attached to each other. Upon hyperoxygenation, a peroxidation of phospholipids in the lipid component proceeds. Simultaneously, with the increase of malondialdehyde, conjugated double bonds, and fluorescence intensity levels, a decrease of protein -SH groups levels, and Mg2+-dependent ATPase activity is observed. The above changes reduce the ability of the protein to superprecipitate, which reflects a contractile reaction in vivo.

Actomyosin↗
PubMed1986

Changes in the metabolism and binding of GABA in the rat brain in thioacetamide-induced hepatogenic encephalopathy.

The GABA level, and the glutamic acid decarboxylase (GAD) and GABA-aminotransferase (GABA-T) activities were measured in the cortex and striatum of rats in which the early stages of hepatogenic encephalopathy (HE) had been induced by few intraperitoneal administrations of thioacetamide (TAA). Besides, the GABA binding to synaptic plasma membranes (SPM) isolated from whole brain hemispheres was examined. The first part of the study revealed significant changes both in the neurotransmitter level and in the enzyme activities; no correlation was observed, however, between the accumulation of GABA and the progression of the disease. In contrast, subsequent stages of HE in the TAA model were found to be characterized by a gradual decrease of both Bmax and KD values for GABA binding, which may reflect a gradual decrease in the number of binding sites, accompanied by sensitization of the remaining receptors. The results are discussed in view of the possible involvement of this inhibitory neurotransmitter in the pathogenesis of HE.

4-Aminobutyrate Transaminase↗
PubMed1985

The effects of ischemia and CDPamines on Na+, K+-ATPase and acetylcholinesterase activities in rat brain.

Cerebral ischemia produced a decrease in Na+, K+-ATPase activity in striatum and cortex; acetylcholinesterase activity was not affected in either region. Pretreatment of the animals with CDPcholine and CDPethanolamine did not prevent the decline in ATPase activity, suggesting that the accumulation of free fatty acids associated with ischemia is not responsible for these changes. Addition of exogenous diacylglycerols to the ATPase assay mixture produced an inhibition of the enzyme similar in magnitude to that observed in tissue samples from ischemic brain. These results support our hypothesis that the local accumulation of diacylglycerols following ischemia is involved in the observed changes in enzymatic activity.

Acetylcholinesterase↗
PubMed1983

Dopamine uptake in striatal synaptosomes exposed to peroxidation "in vitro".

The uptake of [3H]dopamine by synaptosomes from rat brain striatum was biphasic, the rapid phase requiring less than 1 min for completion and the slower phase occurring over a few minutes. This uptake of labeled dopamine was enhanced by prior exposure of the synaptosomes to Fe2+, which gives rise to peroxidation of the synaptosomal lipids. Both lipid peroxidation and enhancement of dopamine uptake were unaffected by the presence of inhibitors of monoamine oxidase but were blocked by inclusion of omicron-phenanthroline in the preincubation medium. It is concluded that lipid peroxidation may be involved in certain neuropsychiatric disorders such as seizures evoked by exposure to high oxygen pressures.

Animals↗
PubMed1983

Effects of CDPcholine and CDPethanolamine on the alterations in rat brain lipid metabolism induced by global ischemia.

The fast turnover pool of rat brain lipids was labeled by intracerebral injection of [3H]acetate. Cerebral ischemia for a duration of 5 min after decapitation caused a 2.2-fold increase in radioactivity in the free fatty acids and loss of more than 20% of the radioactivity from choline and ethanolamine glycerophospholipids. An intracerebral injection of 0.6 mumol each of cytidine diphosphocholine (CDPcholine) and cytidine diphosphoethanolamine (CDPethanolamine) prevented the loss of radioactivity from the glycerophospholipids and decreased the amount of radioactivity in the free fatty acids by 59% as compared with control values and 82% as compared with ischemia values. By GLC assays of the mass of the free fatty acids there was a threefold increase of free fatty acids in ischemic brains. Pretreatment of ischemic brains with CDPcholine and CDPethanolamine reduced the levels of unesterified fatty acids to 60% of the control values. Thus, a prior injection of cytidine nucleotides prevented the release of free fatty acids observed in ischemic brains.

Acetates↗
PubMed1979

Synthesis and content of ether-linked glycerophospholipids in the harderian gland of rabbits.

Although harderian glands are rich in neutral glycerolipids with ether bonds, less than 20% of the choline glycerophospholipids have ether bonds in the white and pink portions of the adult rabbit harderian gland. Only 6% of these are plasmalogens while 94% are alkylacyl glycerophosphocholines. The ethanolamine glycerophospholipids include 37% with ether bonds in both white and pink portions. In the white portion 96% are plasmalogens but only 19% are plasmalogens in the pink portion. The microsomal ethanolaminephosphotransferase (EC 2.7.8.1) is more active with diacylglycerols than with alkylacylglycerols. The microsomal cholinephosphotransferase (EC 2.7.8.2) is equally active with both diradylglycerols. Particularly with microsomes from the pink portion, the apparent Km values for CDPethanolamine and CDPcholine are ower in the presence of alkylacylglycerols than in the presence of diacylglycerols. The incorporation of radioactivity from CDP[14C]ethanolamine and CDP[14C]choline into ethanolamine and choline plasmalogens was increased several-fold by addition of alkylacylglycerols but was not increased substantially by addition of diacylglycerols.

Animals↗
PubMed1979

Effect of prostaglandin E2 and of indomethacin upon cerebral and pulmonary consequences of exposure to hyperbaric oxygen in rats.

There are few data in the literature suggesting that endogenous prostaglandins (PGs) might be involved in the pathomechanism of seizures. Since the mechanism of seizures inducted by exposure to oxygen high pressure (OHP) is not fully elucidated, this study was designed to investigate the effect of exogenous PG s and of indomethacin (a Pg synthesis inhibitor) upon the development and consequences of seizures in rats exposed to OHP (5 ata). In the animals pretreated with PGE2 (1 ng/kg s.c.) pre-seizure time was shortened, lung weight : body weight index increased and symptoms of respiratory failure potentiated, as compared with the control group. Indomethacin (5 mg/kg i.p) prevented the development of seizures and of pulmonary consequences of OHP exposure. Biochemical examination of brains has shown that velocity of free radical oxidation of lipids (reactions manifested by the breakdown of phospholipid fatty acids, mainly unsaturated ones) enhanced by OHP exposure, is further potentiated in rats pretreated with PGE2. Electron microscopic study has shown the alterations similar to those seen in brain ischemia and/or hypoxia, and the magnitude of changes was related to the intensity of symptoms evoked by OHP. The results show that cerebral and pulmonary consequences of OHP exposure are potentiated by exogenous PGE2 and prevented by inhibition of endogenous PG synthesis. This suggests that PGs and/or their active metabolites might be involved in the mechanism of oxygen toxicity during exposure to hyperbaric oxygen.

Animals↗
PubMed1977

Enzymic synthesis of ether types of choline and ethanolamine phosphoglycerides by microsomal fractions from rat brain and liver.

The formation of product by ethanolamine phosphotransferases (EC 2.7.8.1) and cholinephosphotransferases (EC 2.7.8.2) in microsomal fractions from brains and livers of mature rats is increased several fold by 1,2-diacyl-sn-glycerols. With the addition of 1-alkyl-2-acyl-sn-glycerols, we have found an 11-fold increase with brain microsomes and a 20-fold increase with lvier microsomes in the synthesis of choline ether lipids (1-alkyl-2-acyl- and 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphorylcholines). For the synthesis of ethanolamine ether lipids (1-alkyl-2-acyl and 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphorylethanolamines), the stimulation of alkylacylglycerols was 7-fold for brain microsomes and 18-fold for liver microsomes. The alkylacyl glycerols (8 mM) also inhibited the synthesis of diacyl phosphoglycerides by 44 to 65%, indicating that the same ethanolaminephosphotransferases and cholinephosphotransferases are utilized for the synthesis of alkylacyl phosphoglycerides and diacyl phosphoglycerides. A desaturation of the alkyl groups may take place in the same reaction mixture. The rate of incorporation of phosphorylcholine into alkenylacyl glycerophosphorylcholines (choline plasmalogens) with alkylacylglycerols, cytidine diphosphate choline, and liver microsomes was 15 nmoles per mg protein per hour. The in vitro synthesis of choline plasmalogens with alkylacylglycerols had not been observed previously. The corresponding rate of incorporation of phosphorylethanolamine into ethanolamine plasmalogens was 10 nmoles per mg protein per hour, a value greater than any of the previously reported values for ethanolamine plasmalogen formation from alkylacyl glycerophosphorylethanolamines.

Animals↗