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S Antonopoulou

Publications and source records attributed to S Antonopoulou.

15 recordsLinked to original sources
PubMed2006

Effects of baseline serum levels of Se on markers of eccentric exercise-induced muscle injury.

Inflammation and oxidative stress have been implicated in the mechanism of eccentric exercise-induced muscle injury. This study examined whether baseline serum levels of selenium (Se), a trace element that participates in both antioxidant and anti-inflammatory systems, affects the overall response to injury. Thirteen males performed 36 maximal eccentric actions with the elbow flexors of the non-dominant arm on a motorized dynamometer. Venous blood samples were collected immediately before and after exercise at 2, 24, 48, 72 and 96 hours. Established indicators of muscle damage such as maximum isometric torque (MIT), range of motion (ROM), relaxed arm angle (RANG), flexed arm angle (FANG), arm circumference (CIRC), muscle soreness and serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) were determined at the same time points. Baseline serum levels of Se were also measured. Complementary data regarding assessment of Se status were retrieved by the use of a semi-quantitative food frequency questionnaire. All measures changed significantly (p<0.05) after exercise. The main finding of this study was that baseline Se serum levels were associated inversely with CK, LDH and FANG and positively with MIT and ROM (p<0.05). These data suggest that beyond overt Se deficiency, suboptimal Se status possibly worsens muscle functional decrements subsequent to eccentric muscle contractions.

Adult↗
PubMed2005

Dietary intake and biochemical risk factors for cardiovascular disease in two rural regions of Crete.

The aim of the present study was to identify any possible protective effects of wild greens on certain biochemical cardiovascular disease (CVD) risk factors in elderly women leaving in rural Crete. For the needs of the study a region with high consumption of wild greens (Avdou) and a region with low consumption (Anogia) were identified and a representative population from each area was recruited (n= 37 and n=35 respectively). Serum lipids and fibrinogen levels, total antioxidant capacity (TAC), soluble intercellular adhesion molucule-1 (sVCAM-1), soluble vascular adhesion molucule-1 (s-ICAM-1) and haematological factors were measured in both regions during winter and summer time when wild-green plants consumption is high and low, respectively. Regarding classic lipid risk factors for arteriosclerosis no significant different between the two regions were detected. TAC was found higher in Avdou compared to Anogia during winter screening, but null in both regions during summer. Fibrinogen was found higher in Avdou compared to Anogia while no differences between the two regions were detected for sVCAM-1 and s-ICAM-1 in both screenings. The significantly higher TAC and fibrinogen values detected in Avdou could be attributed to the higher wild green consumption in that region since recent data indicated that their content in vitamin C and E as well as flavonoids is particularly high.

Aged↗
PubMed2000

Separation of biologically active lipids from red wine.

A number of lines of evidence suggest that red wine exerts a protective effect against coronary heart disease, but the nature of the protective compounds is unclear and the mechanism is incompletely understood. In this study, total lipids of a Greek red wine were separated into neutral and polar lipids. Polar lipids were further separated into glyco- and phospholipids, which were fractionated by HPLC. Each lipid fraction was tested in vitro for its ability to inhibit platelet-activating factor (PAF) and thrombin-induced washed rabbit platelet aggregation and/or to cause platelet aggregation. A significant number of glyco- and phospholipids that exerted the above biological activities were detected. Structural data of an active phosphoglycolipid are also provided. trans-Resveratrol demonstrated also a dose-dependent inhibition of PAF-induced platelet aggregation along with the already reported inhibitory activity against thrombin and adenosine-5'-diphosphate. Because it has already been reported that PAF is involved in atheromatosis generation, the existence of PAF inhibitors in red wine may contribute to the protective role of red wine against atherosclerosis.

Animals↗
PubMed1998

Identification of a new endogenous platelet-activating factor-like molecule in gingival crevicular fluid.

Periodontal disease is an inflammatory disease and the major cause of tooth loss in adults. Bacteria and their products are the causative agents of this disease. Endogenous molecules mediate the inflammatory process and play a major role in its amplification and perpetuation as well as in the ensuing tissue destruction. The relationship between platelet-activating factor (PAF) and periodontal disease has not so far been examined thoroughly. We have isolated a phospholipid molecule with PAF-like activity from gingival crevicular fluid. This molecule, purified on HPLC, causes washed platelet aggregation with EC50 value 0.1 microM, based on phosphorus determination. It acts through PAF-receptors and is inactivated by PAF-acetylhydrolase. In addition, this phospholipid presents biological activity towards human platelets. The combination of the results obtained from the chemical and enzymic treatments, the biological assays as well as results from the electrospray analysis, leads to the conclusion that this phospholipid is a hydroxyl-PAF analogue with relative molecular mass 703. This PAF-like molecule may be implicated in periodontal disease.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1997

Synthesis of a new phosphoglycolipid with biological activity towards platelets.

Various synthetic as well as naturally occurring compounds have been found to exhibit platelet-activating factor (PAF)-like activity or to act as specific PAF inhibitors. In this work we have synthesized a new phosphoglycolipid, methyl 2,3,4-tri-O-acetyl-6-(1'-O-stearoyl-2'-O- acetyl-DL-glycero-3'-phosphoryl)-alpha-D-glucopyranoside ammonium salt, using a combination of known synthetic steps. This phosphoglycolipid was first purified on TLC (Rf 0.7, using chloroform/methanol/water, 65:25:4, v/v/v as solvent system). It was further purified onto a high performance liquid chromatography silica column with an elution system that contained acetonitrile and methanol (retention time 13.5 min). Its identification was based on chemical determinations and electrospray mass spectrometry analysis. The above compound induced washed platelet aggregation with an EC50 value at 2 x 10(-4) M. The aggregation curve was biphasic, the first wave of which was through the PAF way while the second one was through the ADP way. Treatment with acetylhydrolase resulted in a rapid decrease of the first wave of aggregation and in a slow decrease of the second wave. In lower concentrations, the phosphoglycolipid inhibited PAF- and thrombin-induced aggregation with IC50 values of the order of 10(-7) M. In conclusion, this phosphoglycolipid has a diverse biological activity. The PAF-like activity of this new lipid enforces the conception that PAF is a member of a large family consisting of lipid mediators.

Animals↗
PubMed1996

Blood cardiolipin in haemodialysis patients. Its implication in the biological action of platelet-activating factor.

Bovine heart cardiolipin specifically inhibits platelet aggregation induced by PAF in vitro. In the past we have reported that patients with primary glomerulonephritis have increased PAF levels in plasma (Iatrou et al., 1995b). In this work we investigate the existence of cardiolipin in the blood of end-stage renal patients due to primary glomerulonephritis and we study its implication in the biological study of PAF. Lipids from blood samples of end-stage renal patients were extracted, fractionated onto silicic acid column and onto High Performance Liquid Chromatography (HPLC) cation exchange column. PAF fraction was removed and phospholipids were separated from the rest lipid fraction with current counter distribution and furthermore fractionated onto HPLC silica column. The results show: 1. cardiolipin is present in the blood of end-stage renal patients. 2. Blood cardiolipin specifically inhibits PAF-induced aggregation in washed rabbit platelets. 3. Scatchard plot analysis of PAF binding, in the presence of unlabelled PAF and in the presence of cardiolipin, shows that rabbit platelets possess two different types of binding sites. One of which is saturable and of high affinity, kD = 0.103 +/- 0.03 nM (SEM, n = 3) with 337 +/- 94 binding sites per platelet for PAF and kD = 0.087 +/- 0.02 nM with 371 +/- 92.7 binding sites per platelet for cardiolipin while the other one has almost infinite binding capacity. 4. Blood cardiolipin competes [3H]PAF binding in rabbit platelets. This work shows that cardiolipin exists in the blood of end-stage renal patients and specifically inhibits PAF-induced aggregation as well as PAF binding in rabbit platelets. The possible implication of the biological actions of cardiolipin in the anticardiolipin-antiphospholipid syndrome is also discussed.

Cardiolipins↗
PubMed1996

Platelet-activating factor levels and PAF acetylhydrolase activities in patients with primary glomerulonephritis.

Platelet-activating factor (PAF) belongs to a new class of lipid chemical inflammatory mediators described as acetyl glyceryl ether phosphorylcholine. Although PAF has been implicated in kidney injury, its role in renal immune injury has not been clearly defined yet. We studied the levels of PAF in the plasma and urine and acetylhydrolase (AH) activities in serum and in renal tissue (cortex, C and medulla, M) in patients with primary glomerulonephritis (PGN). PAF levels in the plasma and urine and AH activity in serum of normal volunteers as well as AH activities in normal renal parenchyma (C and M) from nephrectomized patients (served as control) were also measured. Our results demonstrate increased PAF levels in the plasma and urine as well as increased AH activity in serum in patients with PGN in comparison to normal volunteers. AH activity in cortex of those patients was diminished compared to normal kidney tissue. We propose that the enhanced AH activity in serum in patients with PGN could be due to hyperproduction and low degradation of PAF in nephritic tissue which on one hand results in enhanced PAF levels in the plasma and in urine and on the other hand results in enhanced serum AH activity by virtue of substrate (PAF) availability. These data provide new knowledge in the homeostasis of PAF and its degrative enzyme in the setting of PGN.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1995

The influence of parathyroid hormone on platelet-activating factor (PAF) blood levels in hemodialysis patients.

PAF represents a new family of glycerophospholipids and possesses multiple biological activities including platelet aggregation. Production of PAF has been demonstrated in a number of different cell types and in response to various stimuli. In this work an attempt is made to study the effect of parathyroid hormone (PTH) on PAF production. In 13 hemodialysis patients with severe secondary hyperparathyroidism, PAF levels in blood as well as intact PTH (iPTH) and total calcium in serum (tCa), before and 10 days after parathyroidectomy (PTHx), were measured. Our results indicate that PAF levels in blood as well as iPTH and tCa were higher before PTHx than after [a) PAF before 1.10 x 10(-4) +/- 9 x 10(-5) gamma/ml and after 2 x 10(-5) +/- 1 x 10(-5) gamma/ml, p < 0.001; b) iPTH before 880 +/- 392.9 pm/ml and after 121.6 +/- 61.9 pm/ml, p < 0.001; c) tCa before 9.96 +/- 0.35 mg/dl and after 8.38 +/- 0.30 mg/dl, p < 0.001]. Using stepwise regression analysis it seems that PAF is dependent on calcium which is dependent mainly on iPTH. Since a) platelet dysfunction is among the factors which are incriminated for bleeding in uremia and b) PAF which induces platelet aggregation acts via specific receptors, we checked the response of platelets in terms of their ability to aggregate in vitro following increasing doses of exogenous PAF in 5 of the above patients in order to investigate whether the high levels of PAF before PTHx may desensitize platelets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The production of platelet-activating factor (PAF) during hemodialysis with cuprophane membrane. Does the calcium concentration in the dialysate play any role on it?

There is evidence that PAF may be produced during hemodialysis (HD) mainly when using cuprophane membrane (CU). It is also known that PAF production is dependent on the amount of extracellular calcium (ECa2+). In the present study, we investigated the production of PAF during HD with CU as well as the role of the Ca2+ in the dialysate with respect to PAF production. Five hemodialyzed patients were studied in two consecutive HD sessions (the first performed using dialysate without Ca2+ and the second with a Ca2+ concentration of 3.25 mEq/L) and at different times during the sessions the circulating PAF levels as well as the leukocyte and platelet counts were measured. The results demonstrated that a) PAF was indeed produced during HD with CU, b) the highest PAF levels in blood were observed between 5 and 15 minutes from the beginning of HD, at which time the lowest circulating leukocyte and platelet count were measured and c) PAF levels in blood were inversely proportional to the Ca2+ concentration in the dialysate (with the exceptional case of the 15 minutes), although we expected the opposite results.

Calcium↗
PubMed1994

Platelet-activating factor formation during oxidative modification of low-density lipoprotein when PAF-acetylhydrolase has been inactivated.

A PAF aggregating activity corresponding to 427 +/- 91, 668 +/- 111 and 1319 +/- 217 pg/mg protein was detected when LDL was preincubated at pH 3.5 or with 4 mM PMSF or both for 30 min (treatments that inactivate PAF-AH) and then oxidized with 20 microM Cu2+ at 37 degrees C for 24 h. This molecule was characterized as PAF by its chromatographic behavior on TLC and other established methods and was further characterized as 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (C16: PAF) by its retention time on reverse phase HPLC and by fast atom bombardment-mass spectroscopy. Native LDL incubated under non oxidizing conditions, even when PAF-AH has been inactivated, or oxidized in the absence of PAF-AH inactivating agents or after pretreatment with 0.5 mM pBPB, does not produce detectable amounts of PAF. The kinetics of PAF formation in relation to PAF-AH activity, show that the apparent rate of PAF formation as well as its total amount depends on both the existence of oxidative conditions and the remaining PAF-AH activity the first hours following the onset of oxidation. Peroxidation of the phosphatidylcholine (PC) content of native LDL produces PAF-like aggregating activity much lower than that produced when intact LDL is oxidized and is not inhibited by BN 52021 as effectively as PAF produced by LDL peroxidation. Our results provide evidence that C16: PAF is formed during LDL peroxidation when PAF-AH has been inactivated and it does not result as a product of peroxidation of the LDL-PC content.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1994

A simple and precise method for the routine determination of platelet-activating factor in blood and urine.

A simple and precise method is described for the measurement of platelet-activating factor (PAF) in blood and urine. The method involves the isolation of PAF from blood samples by two successive steps. In the first step, blood proteins are precipitated with ethanol and the "free" PAF, i.e., the PAF which is extractable with ethanol, is recovered. In the second step, "bound" PAF, i.e., PAF not extractable with ethanol, is extracted from the protein precipitate with chloroform/methanol/water. The extraction of PAF from urine samples requires only the ethanol extraction step. "Free" and "bound" PAF are then each fractionated by silicic acid column chromatography, and the methanol/water eluent containing PAF is then further fractionated by high-performance liquid chromatography using an isocratic solvent system of acetonitrile/methanol/water. PAF is then quantitated by measuring its ability to induce platelet aggregation in an aggregometer. Application of the method to blood and urine samples from twenty-three healthy volunteers revealed PAF levels in blood of 140-480 pg/mL (630-254.4 pg "free" PAF/mL and 64-225.6 pg "bound" PAF/mL), and of 1.2-4.0 pg PAF/mL in urine. The method overcomes various technical problems and was shown to be very precise. It should prove useful for monitoring PAF levels in various disease conditions.

Acetonitriles↗
PubMed1994

Platelet-activating factor acetylhydrolase (PAF-AH) in human kidney.

1. PAF-AH activity in human kidney (cortex and medulla) has been demonstrated and shares the following properties. 2. Does not require the presence of Ca2+ and appears to be different from phospholipase A2. 3. The pH optimum shows a peak at 7-7.4. 4. It is stable for 4 days at -30 degrees C. 5. It is mainly distributed in the microsomal fraction. 6. The apparent Km values of the enzymes of cortex and medulla are 0.553 and 0.207 microM, respectively and distinct from serum PAF-AH (1.439 microM). 7. The apparent molecular weight values are 60,000 and 25,000 for medulla and cortex, respectively and distinct from serum PAF-AH (94,000).

1-Alkyl-2-acetylglycerophosphocholine Esterase↗