Biomedical subjects

L Struzyńska

Publications and source records attributed to L Struzyńska.

8 recordsLinked to original sources

PubMed2000

Acute lead intoxication in vivo affects myelin membrane morphology and CNPase activity.

The aim of the present study was to assess the sensitivity of central nervous system myelin to acute Pb-toxicity in an animal model, that imitates lead toxicity in occupationally exposed workers, or in occasional incidents of poisoning. Our results indicated that in vivo acute lead intoxication affected both the morphology of myelin and enzymatic activity of the myelin marker, CNPase (2'3'-cyclic nucleotide 3'-phosphodiesterase). The multilayered structure of myelin sheaths was regionally disturbed, with loosely arranged membranes or ovoid-shaped swollen fragments. The activity of CNPase was diminished and Michaelis-Menten kinetics showed a decreased affinity and lower velocity of the enzyme. These data suggest that the disturbances in CNPase activity may contribute, in some extent, to the changes in myelin morphology observed in acute Pb-intoxication.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed2000

The protective role of astroglia in the early period of experimental lead toxicity in the rat.

Although the clinical manifestations of lead (Pb) neurotoxicity are documented, the subcellular mechanisms of its action are still an open question. The purpose of this study was to assess the function of nerve ending particles after acute lead exposure and to investigate whether it exerts a toxic effect on astroglial functions. The studies were performed using the rodent model of acute lead toxicity. Cellular fractions were used in biochemical measurements--synaptosomes and glial plasmalemmal vesicles (GPV). Since a procedure for the isolation of the fraction of astroglial origin has been developed, it becomes possible to investigate lead-astroglia interactions after in vivo exposure. It is of importance because most of the studies concerning lead toxicity were performed using astroglial culture systems. It was found that the uptake of glutamate (Glu) to the synaptosomes was lowered and KCl-dependent release was increased, suggesting the impairment of glutamatergic transmission leading to the elevation of extracellular amino acid concentration. In contrast, glutamate uptake to the GPV fraction was significantly elevated. The activity of the marker enzyme--glutamine synthetase (GS) was also significantly increased in the GPV fraction. The activation of glial functions suggest a regulatory role for these cells in the early period of acute lead toxicity.

Acute Disease↗

PubMed1997

Lead-induced abnormalities in blood-brain barrier permeability in experimental chronic toxicity.

The aim of this paper was to determine whether prolonged drinking of lead acetate-containing water by adult rats, which imitates environmental exposure to lead (Pb), affects some morphological and biochemical properties of rat brain microvessels. We noted a significant increase of lead level in capillaries and synaptosomes obtained from brains of rats under chronic toxicity conditions. Intravenously injected horseradish peroxidase (HRP) was used to evaluate the functional state of the blood-brain barrier (BBB). The results indicate that, systematically administered at low doses, lead induces BBB dysfunction. The changes, revealed in light microscopy and confirmed by electron microscopic studies, are typical for "leaky" microvessels, reported for variety of neuropathological conditions associated with BBB damage. Enhanced pinocytotic activity of the endothelial cells and the opening of interendothelial tight junctions, together with enormous phagocytizing action of the pericytes, are the most characteristic ultrastructural features noted. The presence of specific type of perivascular cells containing droplets of lipids in the cytoplasm, together with changes in phospholipid profile in brain capillaries, suggest that altered lipid composition of membranes may, at least in part, be responsible for changes in observed membrane permeability.

Animals↗

PubMed1997

Acute lead toxicity and energy metabolism in rat brain synaptosomes.

Although the neurotoxic effects of lead (Pb) are well documented, the subcellular mechanisms of its action in the central nervous system are not fully understood. The present work examined some parameters of energy metabolism in nerve endings of the brains of adult rats exposed to Pb. We applied the model of acute Pb toxicity in vivo, imitating the acute action of lead observed in occupationally exposed workers or in occasional incidents of poisoning. The measurement of Pb levels in the synaptosomal fraction exhibited its significant accumulation under applied conditions. Oxygen consumption increased in synaptosomes from Pb-treated rats whereas the activity of cytochrome c oxidase did not change. The intrasynaptosomal levels of ATP and CrP were significantly elevated, as was the activity of creatine kinase, suggesting the activation of the CrP/CK system. On the other hand, the activity of the synaptosomal Na+,K(+)-ATP-ase decreased. We suggest that under acute Pb toxicity conditions the mobilization of CrP/CK system may take place to protect the cell against the effects of decreased Na+,K(+)-ATP-ase activity.

Animals↗

PubMed1996

Effect of acute and chronic lead exposure on the level of sulfhydryl groups in rat brain.

Lead is known to be a potent neurotoxic agent. The interactions of lead with proteins are considered to be at least one of the mechanisms due to which lead exerts its toxicity. In the present work we demonstrate that acute and chronic models of exposure to lead affected the level of total and protein-bound SH groups in homogenates and synaptosomes obtained from rat brains. The concentrations of SH groups were lowered significantly (P < 0.05) in both types of poisoning. Different classes of cellular proteins were considered to play a role in high affinity binding of lead to these ligands.

Animals↗

PubMed1996

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes?

The aim of the experiments presented here was to discern whether prolonged consumption of leaden water, that imitates environmental exposure, affects some energetic parameters in nerve endings of adult rat brains. Our results indicated that during chronic lead intoxication the oxidation chain of synaptic mitochondria remains intact. The oxygen consumption by synaptosomes and activity of cytochrom oxidase in synaptic and pericarionic mitochondria obtained from intoxicated rats did not change in comparison to those from the control samples. Compared with the control samples, the concentration of ATP decreased and the concentration of creatine phosphate (CrP) increased drastically in fractions obtained from Pb2+ intoxicated animals with simultaneously increased activity of creatine kinase (CK). It seems likely that, the CrP/Cr/CK system constitutes a satisfactory regulatory mechanism for chronic Pb2+ toxicity effects on energy metabolism in nerve endings of the adult rats.

Adenosine Triphosphate↗

PubMed1994

The effect of lead on dopamine, GABA and histidine spontaneous and KCl-dependent releases from rat brain synaptosomes.

The effect of lead on the release of [14C]GABA, [3H]dopamine and [14C]histidine (as a precursor of histamine) was studied in synaptosomes obtained from chronically lead-treated rats and in synaptosomes with in vitro lead added. In vivo treatment of rats with lead acetate results in a decrease in the K(+)-depolarization-dependent release of GABA and dopamine and histidine. Lead given in vitro itself (independently of depolarizing condition) stimulated the release of previously accumulated neurotransmitters in synaptosomes (GABA and dopamine). This effect depends on lead acetate concentration. On the other hand lead, in different concentrations, did not cause changes in the histidine release. The results show that lead can attack the synaptic neurotransmission in two ways: by depressing the Ca-KCl-evoked release of GABA, dopamine and histidine and by a selective stimulation of a spontaneous release (independent of depolarization conditions) of GABA and dopamine but not histidine.

Animals↗

PubMedDate not supplied

Does lead provoke the peroxidation process in rat brain synaptosomes?

Up to now there has been no information concerning the effect of lead on the peroxidation process in brain nerve endings. We have examined whether lead acetate (in chronic and acute models of toxicity in vivo and in vitro) affected the level of free radicals in synaptosomes obtained from rat brain. Simultaneously, we have checked the effect of peroxidation of Pb2+ on brain homogenates and microsomal fraction. Our results indicated that the lead level in synaptosomal fraction obtained from lead-treated rats was much higher than in controls. We did not observe induction of spontaneous and Fe(3+)-dependent peroxidation either in synaptosomes or in homogenates and brain microsomes after chronic and acute lead administration to the rats. Lead itself also did not enhance both processes when added in vitro to the control brain synaptosomes in micromolar concentrations. The lack of the lead effect on the peroxidation process in subcellular fractions of brain was rather surprising, because lead is known to be the accelerator of Fe(3+)-dependent peroxidation processes in liver. Additionally, livers from rats under the same toxicity conditions were examined. We have found that lead did not provoke spontaneous peroxidation in liver, but contrary to brain fractions, it drastically increased iron-dependent peroxidation in liver homogenates and microsomes. The lack of the effect of lead on inducing peroxidation processes in brain is probably the consequence of the brain having stronger protective mechanisms against its toxicity than the liver.

Acute Disease↗