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

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Dabrowska-Bouta B., Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
233-236
EN
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 obtainded from rat brains. The concentrations of SH groups were lowered significantly (P less then 0.05) in both types of poisoning. Different classes of cellural proteins were considered to play a role in high affinity binding of lead to these ligands.
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Acute lead toxicity and energy metabolism in rat brain synaptosomes

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Struzynska L., Dabrowska-Bouta B., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1997
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vol. 57
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issue 4
275-281
EN
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 mobiliaztion of CrP/CK system may take place to protect the cell against the effects of decreased Na+,K+ ATP ase activity. ATP ase
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Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

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Rafalowska U., Struzynska L., Dabrowska-Bouta B., Lenkiewicz A.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
611-617
EN
RThe aim of the experiment 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 brain.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 conrtol samples.Compared with the control samples, the concentration of ATP decreased and the concentration of creatine phosphate (CrP) increased drasticly in fractions obtained from Pb2+ intoxicated animals with simultaneously increased activity of creatine kinase (CK).It seems likely that, the CrP/Cr/CK system constituens a satisfactory regulatory mechanism for chronic Pb2+ toxicity on energy metabolism in nerve endings of the adult rats.
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