Biomedical subjects

N Lukácová

Publications and source records attributed to N Lukácová.

At least 19 recordsLinked to original sources

PubMed2006

Neuronal nitric oxide synthase immunopositivity in motoneurons of the rabbit's spinal cord after transient ischemia/reperfusion injury.

1. Motoneurons in the spinal cord are especially vulnerable to ischemic injury and selectively destroyed after transient ischemia. To evaluate the role of nitric oxide (NO) in the pathophysiology of the spinal cord ischemia, the expression of neuronal nitric oxide synthase (nNOS) in the motoneurons of the lumbosacral spinal cord was examined in the rabbit model of transient abdominal aorta occlusion. 2. The aim of the present study was to find if there is any consensus between the duration of transient abdominal aorta occlusion, nNOS positivity of the motoneurons and neurological hind limb impairment. 3. According to the degree of neurological damage (i.e., from the group with almost no sign of damage to a group with fully developed paraplegia), the experimental animals were divided into three groups. The respective spinal cord segments of each experimental group were compared to the control group. 4. Spinal cord ischemia (15 min) was induced by Fogarty arterial embolectomy catheter occlusion of abdominal aorta with a reperfusion period of 7 days. On seventh day, the sections of lumbosacral segments were immunohistochemically treated and L1-L7, and S1-S2 segment sections were monitored using light microscopy.

Animals↗

PubMed2005

Experimental cauda equina compression induces HSP70 synthesis in dog.

The heat shock protein 70 (HSP70) is a key component of the stress response induced by various noxious conditions such as heat, oxygen stress, trauma and infection. In present study we have assessed the consequences of the compression of lower lumbar and sacral nerve roots caused by a multiple cauda equina constrictions (MCEC) on HSP70 immunoreactivity (HSP70-IR) in the dog. Our data indicate that constriction of central processes evokes HSP70 up-regulation in the spinal cord (L7, S1-Co3) as well as in the corresponding dorsal root ganglion cells (DRGs) (L7-S1) two days following injury. A limited number of bipolar or triangular HSP-IR neurons were found in the lateral collateral pathway (LCP) as well as in the pericentral region (lamina X) of the spinal cord. In contrast, a high number of HSP70 exhibiting motoneurons with fine processes appeared in the ventral horn (laminae VIII-IX) of lumbosacral segments. Concomitantly, close to them a few lightly HSP70-positive neuronal somata or cell bodies lacking the HSP70-IR occurred. In the DRGs, HSP70 expression was mildly up-regulated in small and medium-sized neurons and in satellite cells. On the contrary, DRGs from intact or sham-operated dogs did not reveal HSP70 specific neuronal staining. In conclusion, we have demonstrated that the MCEC in dogs mimicking the cauda equina syndrome in clinical settings evokes expression of HSP70 synthesis in specific neurons of the lumbo-sacro-coccygeal spinal cord segments and in small and medium sized neurons of corresponding DRGs. This suggests that HSP70 may play an active role in neuroprotective processes partly by maintaining intracellular protein integrity and preventing the neuronal degeneration in this experimental paradigm.

Animals↗

PubMed2003

Cauda equina syndrome and nitric oxide synthase immunoreactivity in the spinal cord of the dog.

The development of the cauda equina syndrome in the dog and the involvement of spinal nitric oxide synthase immunoreactivity (NOS-IR) and catalytic nitric oxide synthase (cNOS) activity were studied in a pain model caused by multiple cauda equina constrictions. Increased NOS-IR was found two days post-constriction in neurons of the deep dorsal horn and in large, mostly bipolar neurons located in the internal basal nucleus of Cajal seen along the medial border of the dorsal horn. Concomitantly, NOS-IR was detected in small neurons close to the medioventral border of the ventral horn. High NOS-IR appeared in a dense sacral vascular body close to the Lissauer tract in S1-S3 segments. Somatic and fiber-like NOS-IR appeared at five days post-constriction in the Lissauer tract and in the lateral and medial collateral pathways arising from the Lissauer tract. Both pathways were accompanied by a dense punctate NOS immunopositive staining. Simultaneously, the internal basal nucleus of Cajal and neuropil of this nucleus exhibited high NOS-IR. A significant decrease in the number of small NOS immunoreactive somata was noted in laminae I-II of L6-S2 segments at five days post-constriction while, at the same time, the number of NOS immunoreactive neurons located in laminae VIII and IX was significantly increased. Moreover, high immunopositivity in the sacral vascular body persisted along with a highly expressed NOS-IR staining of vessels supplying the dorsal sacral gray commissure and dorsal horn in S1-S3 segments. cNOS activity, based on a radioassay of compartmentalized gray and white matter regions of lower lumbar segments and non-compartmentalized gray and white matter of S1-S3 segments, proved to be highly variable for both post-constriction periods.

Animals↗

PubMed2001

Effect of spinal cord compression on cyclic 3',5'-guanosine monophosphate in the white matter columns of rabbit.

Changes in the level of cyclic 3',5'-guanosine monophosphate (cGMP) were studied one day after a surgically induced spinal cord constriction performed at the Th7 segment level in the dorsal, lateral and ventral white matter columns and in the non-compartmentalized white matter of Th5-Th6 segments, i.e., above the site of the spinal cord constriction and in Th8-Th9 segments, located below the spinal cord constriction. The midthoracic spinal cord constriction caused a significant decrease in the level of cGMP in the ventral column of Th5-Th6 segments and a significant increase in the lateral column of Th8-Th9 segments. The level of cGMP in the dorsal column, located either rostrally or caudally to the site of the spinal cord injury, remained unchanged. In addition, no significant changes in the level of cGMP were found in the non-compartmentalized white matter of Th5-Th6 and Th8-Th9 segments in response to constriction of the Th7 segment.

Animals↗

PubMed2001

Cauda equina syndrome.

Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome. The cauda equina nerve roots provide the sensory and motor innervation of most of the lower extremities, the pelvic floor and the sphincters. Therefore, in a fully developed cauda equina syndrome, multiple signs of sensory disorders may appear. These disorders include low-back pain, saddle anesthesia, bilateral sciatica, then motor weakness of the lower extremities or chronic paraplegia and, bladder dysfunction. Multiple etiologies can cause the cauda equina syndrome. Among them, non-neoplastic compressive etiologies such as herniated lumbosacral discs and spinal stenosis and spinal neoplasms play a significant role in the development of the cauda equina syndrome. Non-compressive etiologies of the cauda equina syndrome include ischemic insults, inflammatory conditions, spinal arachnoiditis and other infectious etiologies. The use of canine, porcine and rat models mimicking the cauda equina syndrome enabled discovery of the effects of the compression on nerve root neural and vascular anatomy, the impairment of impulse propagation and the changes of the neurotransmitters in the spinal cord after compression of cauda equina. The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments. Prominent changes of NADPH diaphorase exhibiting, Fos-like immunoreactive and heat shock protein HSP72 were detected in the lumbosacral segments in a short-and long-lasting compression of the cauda equina in the dog. Developments in the diagnosis and treatment of patients with back pain, sciatica and with a herniated lumbar disc are mentioned, including many treatment options available.

Animals↗

PubMed2001

The regional changes of the catalytic NOS activity in the spinal cord of the rabbit after repeated sublethal ischemia.

The regional distribution of catalytic NOS activity was studied in the lumbosacral segments of the spinal cord of the rabbit during single (8-min), twice (8-, 8-min) and thrice repeated (8-, 8-, 9-min) sublethal ischemia followed each time by 1 h of reperfusion. Single ischemia/reperfusion induced a significant increase of cNOS activity in almost all spinal cord regions, with the exception of non-significant increase in the dorsal horn. Sublethal ischemia repeated twice produced a significant decrease of enzyme activity in the intermediate zone and ventral horn and an increase in the white matter columns. Within thrice repeated ischemia, the activity of cNOS in the gray matter regions was similar to that found after a single ischemia/reperfusion. For all the animals subjected to single and twice repeated sublethal ischemic insults, there was no neurological impairment. Following thrice repeated ischemic insults, four out of five of the experimental animals recovered only partially and one was completely paraplegic. Our results do not indicate a cumulative effect of repeated sublethal ischemia on cNOS activity and, consequently, on NO production. The NO generated during thrice repeated ischemia/reperfusion appears to have a detrimental effect on the neurological outcome.

Animals↗

PubMed2000

Regional changes of cyclic 3',5'-guanosine monophosphate in the spinal cord of the rabbit following brief repeated ischemic insults.

The regional distribution of cyclic 3',5'-guanosine monophosphate was studied in the lumbosacral segments of the spinal cord of the rabbit under physiological conditions and following brief repeated sublethal ischemic insults. While the basal cGMP level in the gray matter was about 0.120 nmol cGMP/mg wet. wt., the level of cGMP in non-compartmentalized white matter was about half of this value. The highest level of cGMP in the compartmentalized gray matter was found in the dorsal horns, about 0.180 nmol cGMP/mg wet. wt., whereas the level of cGMP was greatly reduced in the ventral horns, reaching one half of the previous value. Multiple sublethal ischemic insults, repeated at 1-h intervals, caused a statistically significant decrease of cGMP in all gray matter regions. While the post-ischemic and post-reperfusion level of cGMP in the dorsal horns remained relatively high in comparison with the intermediate zone and ventral horns, the changes of cGMP level detected in the white matter columns differed considerably and resulted in a statistically significant cGMP increase in the dorsal and ventral columns and, vice versa, a statistically significant decrease of cGMP was found in the lateral columns.

Animals↗

PubMed2000

Effect of midthoracic spinal cord constriction on catalytic nitric oxide synthase activity in the white matter columns of rabbit.

The distribution and changes of catalytic nitric oxid synthase (cNOS) activity in the dorsal, lateral and ventral white matter columns at midthoracic level of the rabbit's spinal cord were studied in a model of surgically-induced spinal cord constriction performed at Th7 segment level and compared with the occurrence of nicotinamide adenine dinucleotide phosphate diaphorase expressing and neuronal nitric oxide synthase immunoreactive axons in the white matter of the control thoracic segments. Segmental and white-column dependent differences of cNOS activity were found in the dorsal (141.5 +/- 4.2 dpm/microm protein), lateral (87.3 +/- 11.5 dpm/microm protein) and ventral (117.1 +/- 7.6 dpm/microm protein) white matter columns in the Th5-Th6 segments and in the dorsal (103.3 +/- 15.5 dpm/microm protein), lateral (54.9 +/- 4.9 dpm/microm protein), and ventral (86.1 +/- 6.8 dpm/microm protein) white matter columns in the Th8-Th9 segments. A surgically-induced constriction of Th7 segment caused a disproportionate response of cNOS activity in the rostrally (Th5-Th6) and caudally (Th8-Th9) located segments in both lateral and ventral white matter columns. While a statistically significant decrease of cNOS activity was detected above the constriction site in the ventral columns, a considerable, statistically significant increase of cNOS activity was noted in the white lateral columns below the site of constriction. It is reasoned that the changes of cNOS activity may have adverse effects on nitric oxide (NO) production in the white matter close to the site of constriction injury, thus broadening the scope of the secondary mechanisms that play a role in neuronal trauma.

Animals↗

PubMed2000

Catalytic nitric oxide synthase activity in the white and gray matter regions of the spinal cord of rabbits.

The latest research reveals that nitric oxide as a gas messenger may diffuse into the surrounding extracellular fluid and act locally upon neighboring target cells. However, several observations raise the possibility that nitric oxide may also be released at a greater distance from the neuronal cell body. The catalytic nitric oxide synthase (cNOS) activity was therefore studied in the cervicothoracic and lumbosacral segments of the spinal cord of rabbits, including the white matter of dorsal columns (DC), lateral columns (LC) and ventral columns (VC), as well as the gray matter of dorsal horns (DH), intermediate zone (IZ) and ventral horns (VH). Lower cNOS activity was found in the white matter of both cervicothoracic (47%) and lumbosacral (30%) regions, whereas that detected in the gray matter of the lumbosacral part of the spinal cord was considerably higher (70%). Enzyme activity varied from 43.4 to 77.2 dpm/microg protein in the cervicothoracic segments of the gray matter in the descending order: DH>VH>IZ. Similar cNOS activity was found in the white matter of the cervicothoracic segments (42.1-62.8 dpm/microg protein). When the activity of cNOS was compared in the lumbosacral segments, the highest enzyme activity was found in DH of the gray matter (198.7 dpm/microg protein) and the lowest cNOS in DC (45.8 dpm/microg protein) of the white matter. It was concluded that the white matter of the spinal cord contains similar cNOS activity in comparison to the gray matter.

Animals↗

PubMed1999

Segmental and laminar distributions of nicotinamide adenine dinucleotide phosphate-diaphorase-expressing and neuronal nitric oxide synthase-immunoreactive neurons versus radioassay detection of catalytic nitric oxide synthase activity in the rabbit spinal cord.

The distributions of neuronal nitric oxide synthase-immunoreactive neurons and of nicotinamide adenine dinucleotide phosphate-diaphorase activity were studied in the C6, Th2, L1, L5, S2 and S3 segments and laminae in the rabbit spinal cord and compared with the catalytic nitric oxide synthase activity, determined by monitoring the conversion of [3H]arginine to [3H]citrulline in the same segments and laminae. Morphologically, a heterogeneous population of nicotinamide adenine dinucleotide phosphate-diaphorase-expressing and neuronal nitric oxide synthase-immunoreactive neurons was detected in the superficial and deep dorsal horn and the pericentral region in all segments studied, and in the intermediolateral cell column of the thoracic and lumbosacral segments. A disproportionate distribution of both neuronal categories which had a significantly higher number of nicotinamide adenine dinucleotide phosphate-diaphorase-expressing rather than neuronal nitric oxide synthase-immunoreactive cell bodies was found in all segments. The catalytic nitric oxide synthase activity was distributed unequally in the C6, Th2, L1, L5, S2 and S3 segments, with a comparatively low value in the Th2 segment (70 +/- 5.1 d.p.m./microg protein) in comparison with the S3 segment, where the highest level (140 +/- 5.5 d.p.m./microg protein) was found. A close correlation between the number of neuronal nitric oxide synthase-immunoreactive somata and catalytic nitric oxide synthase activity was revealed in the dorsal horn (laminae I-VI). Whereas a low number of neuronal nitric oxide synthase-immunoreactive somata in laminae VII-X was found in the L5, S2 and S3 segments, the values of catalytic nitric oxide synthase activity in the same laminae and segments were found to be exceedingly high. These findings indicate that the occurrence of many neuronal nitric oxide synthase-immunoreactive fibers (mainly axons), and dense, punctate, non-somatic neuronal nitric oxide synthase immunopositivity in the neuropil staining of the same laminae and segments, can substantially enhance catalytic nitric oxide synthase activity.

Animals↗

PubMed1998

Phospholipid composition in spinal cord regions after ischemia/reperfusion.

Ischemia-reperfusion induced changes in concentration of phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI) and sphingomyelin (SM) in the gray matter taken in toto, white matter, dorsal horns, intermediate zone and ventral horns of the rabbit's spinal cord were studied and compared with neurohistopathological changes. With the exception of PI concentration in the dorsal horns, ischemia of 25 min caused significant degradation of all phospholipids. While short-lasting recirculation (1 h) did not returned the levels of phospholipids to control values, postischemic recirculation for 3 h sharply increased the resynthesis of all phospholipids, but only the concentration of PE, PS, and PI in the dorsal horns and PC in the intermediate zone significantly improved and returned close to control values. Corresponding neurohistopathological changes resulting after the same reperfusion periods are given.

Anatomy, Cross-Sectional↗

PubMed1998

Lipid peroxidation and phospholipid composition in rat brain regions after ischemia and in early perfusion periods.

Lipid peroxidation products (LPPs) and phospholipid composition were studied in a model of four-vessel occlusion in rats in homogenates of cortex, striatum and hippocampus after 30 min forebrain ischemia and following 1, 5, 10, 15, 30 and 180 min of recirculation. Major modification of LPPs was found after shorter reperfusion time, 5 min in hippocampus and 15 min in cortex and striatum when compared to control, while a slight decrease in the level of LPPs in the striatum and hippocampus was detected after longer (30 and 180 min) intervals. However, significant decrease was found in the homogenates of cortex. The results obtained from enhanced iron-dependent peroxidation in homogenates of frontal and occipital cortex indicated marked susceptibility to lipid peroxidation in the tissue subjected to 30 min ischemia and after 15 min of recirculation. The level of DG + PA was significantly higher during ischemia in the striatum, while increased hydrolysis of PI and DG + PA concentrations in the cortex, PI and PE levels in the striatum and PE and PS in the hippocampus after 30 min of ischemia were found. After 15 min of reperfusion considerably higher degradation of almost all phospholipids was found within all brain regions studied. The irreversibility of changes in PS, PE and SM was noted in the hippocampus after longer reperfusion periods. Our results indicate that the correlation between the lipid peroxidat ion product formation and phospholipid hydrolysis does exist, and, moreover, early reperfusion period seems to be highly critical in the development of ischemia-reperfusion induced neuronal damage.

Animals↗

PubMed1998

[Changes in phospholipids after repeated induced sublethal spinal cord ischemia in rabbits].

BACKGROUND: Degradation of membrane bound phospholipids in CNS during ischaemia begins with extreme rapidity. Sublethal ischaemia influences ischaemic tolerance in the affected neurons and is stressful enough to induce neuronal changes such as postischaemic hypoperfusion, transient suppression of protein synthesis and induction of stress (HSP) proteins. It seems, that the nature of factors responsible for ischaemic tolerance may involve the activation of multiple different systems. MAIN PURPOSE: The aim of this study was to investigate the changes of phospholipids in gray matter regions of spinal cord following sublethal ischaemia repeated in long intervals of reperfusion. METHODS: Male rabbits, weight range 2.5-3.5 kg were used in the experiment. They were divided in following groups : 1. control animals; 2. animals subjected to 25 min ischaemia; 3. animals subjected to 25 min ischaemia and 3 h of reperfusion; 4. animals subjected to sublethal (8-8-9 min) ischaemia repeated in long-lasting (8-8-24 h) intervals of reperfusion. Phospholipids were separated by thin layer chromatography, lipidic phosphorus was assessed spectrophotometrically. RESULTS: Sublethal ischaemia repeated in long-lasting intervals of reperfusion increased the concentration of phospholipids to control levels in all gray matter regions. The resynthesis in the dorsal horns, of PC and PE in the ventral horns and of PC in the intermediate zone. CONCLUSIONS: An excessive renewal of phospholipids after sublethal ischaemia repeated in longer intervals of reperfusion was most pronounced in the eh dorsal horns of the spinal cord and can be the result of many defensive cellular mechanisms.

Animals↗

PubMed1997

Neuroprotective effect of graded postischemic reoxygenation in spinal cord ischemia in the rabbit.

Early ischemia/reperfusion-induced changes of four phospholipid compounds bound to the inner cell membrane leaflet, i.e., phosphatidic acid, inositol phospholipids, serine phospholipids, and ethanolamine plasmalogens, were studied in a model of spinal cord ischemia in the rabbit during normoxic and graded postischemic reoxygenation. Light and electron microscopic analysis after normoxic reoxygenation disclosed neuronal membrane argyrophilia of the interneuronal pool located in lamina VII of L4-L6 segments. The number of small neurons (10-25 microm in diameter) affected by somatodendritic argyrophilia was greatly reduced, and concomitantly the ultrastructure of the endoplasmic reticulum, mitochondria, and Golgi complexes remained almost undamaged when graded postischemic reoxygenation had been applied. A statistically significant increase of phosphatidylserine and ethanolamine plasmalogen levels, and a decrease of phosphatidic acid, were detected after a short-lasting graded postischemic reoxygenation. The formation of thiobarbituric acid-reactive substances was significantly reduced during 60 min of graded postischemic reoxygenation and remained close to control or ischemic levels. The present data indicate that graded postischemic reoxygenation, which is considered to be neuroprotective, can prevent neuronal argyrophilia and the development of reperfusion-induced alterations of organelles. Moreover, reoxygenation can positively modify ischemia-induced changes of some membrane-bound phospholipids.

Animals↗

PubMed1997

Regional distribution of phospholipids and polyphosphatidyl inositides in the rabbit's spinal cord.

The plasticity of the membrane phospholipids in general and stimulated phosphoinositides turnover in particular are the subjects in a variety of neural paradigms studying the molecular mechanisms of neuronal changes under normal and pathological conditions. The regional modifiability of phospholipids (SM, PC, PS, PI, PA + DG, PE), polyphosphatidylinositides (PI, PIP, PIP2) and diacylglycerol-dependent incorporation of CDP-choline into phosphatidylcholine in the gray matter, white matter, dorsal horns, intermediate zone and ventral horns of the rabbit's spinal cord was studied. We have found 1. a significant increase in the concentration of SM, PC, PS, DG + PA and PE in the white matter in comparison to the gray one, 2. the highest concentration of the outer membrane leaflet-bound phospholipids in the dorsal horns and the inner membrane phospholipids in the intermediate zone in comparison to the gray matter, 3. a substantial amount of labeled polyphosphatidylinositides (poly-PI(s)) in the spinal cord white matter with descending order PIP > PI > PIP2, 4. similar incorporation of myo-2-[3H]inositol into all poly-PI(s) in ventral horns and intermediate zone, but a different, lower incorporation into PI and PIP and higher into PIP2 in the dorsal horns, 5. higher diacylglycerol-dependent incorporation of CDP-choline into PC in the regionally undivided gray matter than in the white matter taken as a whole, 6. the high proportion of diacylglycerol-dependent incorporation of CDP-choline into PC in both the ventral and dorsal horns, whereas that in the intermediate zone remained low.

Animals↗

PubMed1996

Ischemia-reperfusion injury in the spinal cord of rabbits strongly enhances lipid peroxidation and modifies phospholipid profiles.

The effect of spinal cord ischemia (10, 20, and 40 min) and post-ischemic reperfusion (10, 30, and 60 min) on lipid peroxidation and phospholipids was investigated. Spinal cord ischemia was accompanied by lipolytic processes with significant changes in concentration of lipid peroxidation products (LPP). Reestablishment of the blood supply after 10 min ischemia was accompanied by significantly increased levels of thiobarbituric acid reactive substances (TBA-RS) after 10 and 30 min of reperfusion. Following 20 and 40 min ischemia a significant increase was observed at all reperfusion periods. Ischemia itself significantly reduced the concentration of phosphatidyl inositol (IP), phosphatidyl ethanolamine (EP) and ethanolamine plasmalogens (Epls). Significant changes were observed in concentration of phosphatidyl serine (SP) too, but only after 20 and 40 min of ischemia. The concentration of phosphatidic acid (PA) was significantly reduced only after 10 min of ischemia. The onset of reperfusion after ischemia was accompanied by a diverse pattern of changes in PA, IP, Epls and SP, while the concentration of EP remained at the above mentioned ischemic intervals.

Animals↗

PubMed1993

Effect of stobadine on lipid peroxidation and phospholipids in rabbit spinal cord after ischaemia.

Stobadine, a drug with the pyridoindol structure, was compared with thiopental and pentobarbital for its ability to inhibit stimulated peroxidation in homogenates of spinal cord in vitro. The antioxidative capacity of the drug exceeded that of barbiturates more than 100-fold. Stobadine was also shown to inhibit the increase in formation of TBA-RS in homogenates of rabbit spinal cord, subjected to 20 min ischaemia, to the level comparable with controls. Administration of the drug (6 mg kg-1) to animals 5 min before 20 min ischaemia had no effect on level of lipid peroxidation products in the spinal cord; however, it slowed down stimulated Fe(2+)-dependent peroxidation after in vitro incubation of the homogenates and increased the concentration of phosphatidylserine and ethanolamine plasmalogens, as compared with non-treated animals. Application of stobadine 2 min before the release of an aortic occlusion increased the antiradical capacity in homogenates of spinal cord and revealed an ameliorating effect on the composition of phospholipids.

Animals↗

PubMed1992

Effect of liposomes on lipid peroxidation and total phospholipids in rabbit ischemic spinal cord model.

The effect of spinal cord ischemia (induced by abdominal aorta ligation for 20 minutes) on lipid peroxidation and TPL composition was investigated and discussed in our previous articles. It is known, that partially reduced species of oxygen can be formed under aerobic conditions. For that reason, the effect of ligation release for 60 minutes was observed in experimental animals treated with the selected liposomes. Administration of CP, (CP+SA) and (CP+Chol) liposomes applied 30 minutes before 20 minutes ischemia revealed an ameliorating effect on in vivo and in vitro Fe-dependent peroxidation manifested by TBA-RS accumulation. Combined use of (CP+SA) liposomes with lipophylic form of stobadine (DP 1031) was not more effective. Application of CP liposomes directly before the ligation release slightly increased the antiradical capacity in spinal cord homogenates comparing with not-treated animals. Accumulation of TBA-RS was accompanied by TPL degradation during recirculation period but values of TPL after liposomal treatment were unaffected.

Animals↗