Ganglioside-dependent factor, inhibiting lipid peroxidation in rat brain synaptosomes

Tyurin, Vladimir A.; Tyurina, Yulia Y.; Аврова, Н. Ф.

doi:10.1016/0197-0186(92)90055-v

Cited by 29 publications

(25 citation statements)

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“…Gangliosides were extracted from brain tissues as described by Folch et al [15]; preparations were purified and ganglioside GM 1 was isolated on silica gel columns [33]. The purity of the resulting GM 1 preparation amounted to 98-99%, as demonstrated by HPTLP (Merck, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…The quality of preparations was assessed by electron microscopy and by using the voltage-dependent fluorescent probe dis-C3-(5) [33].…”

Section: Methodsmentioning

confidence: 99%

“…Deciphering of the mechanisms of glutamate neurotoxicity is also made difficult by the fact that they can differ according to the stage of development and local types of nerve cells [22,23,28,37]. A literature search yielded no systematic studies of the effects of glutamate and antioxidants on a variety of parameters characterizing calcium ion metabolism in nerve cells.Understanding of the mechanisms of the protective actions of gangliosides and endogenous glycosphingolipids of neuron membranes [2], which can inhibit free-radical reactions [3,5,21,33], should be aided by comparing their actions with the effects of antioxidants. We were unable to find data on the effects of gangliosides 0097-0549/00/3005-0535525.00 9…”

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confidence: 99%

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The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes

Аврова

Shestak

Захарова

et al. 2000

Neurosci Behav Physiol

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Glutamate is shown to induce increases in intracellular Ca2+ concentrations ([Ca2+]i), increases in 45Ca2+ influx, decreases in the activity of Na+,K+-ATPase activity, and activation of the Na+/Ca2+ exchanger in rat cerebral cortex synaptosomes. NMDA receptor antagonists virtually prevented these effects. Preincubation of synaptosomes with alpha-tocopherol, superoxide dismutase, and ganglioside GM1 normalized [Ca2+]i, 45Ca2+ influx, and Na+,K+-ATPase activity in rat cerebral cortex synaptosomes exposed to glutamate. Glutamate and GM1 activated the Na+/K+ exchanger, and their effects were additive. Calcium ions entering cerebral cortex nerve cells via NMDA receptors during exposure to high glutamate concentrations appeared to be only the trigger for the processes activating free-radical reactions. Activation of these reactions led to increases in Ca2+ influx into cells, decreases in Na+,K+-ATPase activity, and significant increases in [Ca2+]i, though this could be prevented by antioxidants and gangliosides.

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Section: Methodsmentioning

confidence: 99%

“…The quality of preparations was assessed by electron microscopy and by using the voltage-dependent fluorescent probe dis-C3-(5) [33].…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes

Аврова

Shestak

Захарова

et al. 2000

Neurosci Behav Physiol

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“…The increase in [Ca2+]i after exposure to toxic glutamate concentrations can result from increased membrane permeability due to accumulation of lipid peroxidation products [ 14]. Glutamate-induced stimulation of 45Ca2+ entry is significantly inhibited by cz-tocopherol and SOD [1], therefore the effect of gangliosides can be associated with inhibition of free radical reactions activated by glutamate [2,15]. Activation of Na+/Ca 2+ exchanger in rat brain synaptosomes by glutamate and GMt can also have a protective effect, since its inactivation significantly promotes neuronal death in culture [3].…”

Section: Methodsmentioning

confidence: 99%

“…GM~ ganglioside was isolated on silica gel columns [15]. Gangliosides were isolated from bovine brain as described elsewhere [7].…”

Section: Methodsmentioning

confidence: 99%

Gangliosides stabilize ionic homeostasis in rat cortical synaptosomes exposed to toxic concentrations of glutamate

et al. 2000

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Glutamate significantly increased intracellular calcium concentration, enhanced 45Ca2+ entry, and activated Na+/Ca 2 § exchanger in synaptosomes from rat cerebral cortex. Preincubation with GMI ganglioside reduced the glutamate-induced increase in intracellular calcium and 45Ca2+ entry. Gangliosides and glutamate stimulated Na+/Ca 2 § exchanger showing additive effects.Key Words: GM 1 ganglioside," glutamate; calcium; cerebral cortex synaptosomes Neuronal damage in ischemia, brain trauma, and some neurological diseases is largely determined by toxic effects of high concentrations of glutamate released into the intercellular space [2,3,12]. Excitotoxin-induced disturbance in intracellular calcium ([Ca2+]i) homeostasis is considered to be the major cause of neuronal death under these conditions [4].Activation of N-methyl-D-aspartate receptors triggering this process is a necessary but not sufficient condition for sustained elevation of [Ca:+]i. An important role in the development of pathological processes initiated by excitotoxins is played by activation of free radical reactions [1,13] and other processes stimulating Ca 2+ entry and inactivating the system stabilizing calcium homeostasis.Gangliosides, the most complex animal glicosphingolipids, improve viability of cultured nervous cells exposed to glutamate [3,6] and significantly decrease [Ca 2+] ~, which seems to underlie their neuroprotective activity [12]. However, the mechanism of this effect remains unclear. We found no reports on the effects of gangliosides on glutamate-induced activation of Ca 2+ entry or activity of Na+/Ca 2+ exchanger.Our aim was to study the mechanism of stabilizing effect of gangliosides on Ca 2+ homeostasis dis- MATERIALS AND METHODSSynaptosomes isolated from the brain of male Wistar rats (150-180 g) as described elsewhere [9] were resuspended in buffer A containing (in mM): 135 NaC1, 1.2 MgSO4, 2.0 KC1. 10 glucose, and 20 tris-HC1 (pH=7.4), centrifuged at 15,000g for 15 min, and resuspended again in buffer A (4-5 mg/ml protein concentration).[Ca2+]i was measured with Fura-2M (Sigma), a fluorescent calcium probe. Synaptosomes (1 ml) were mixed with 1 ml buffer A containing 0.5% BSA (flee from fatty acids) and 8 gM Fura-2M dissolved in 0.4% DMSO and incubated for 40 min at 30~ [16]. Preincubation with 50 nM GM~ ganglioside was performed simultaneously with Fura-2M loading, which was stopped by adding 20-fold volume of buffer A followed by 15-min centrifugation at 12,000g. The sediment was resuspended in MgSQ-free buffer B containing (in mM): 135 NaC1. 2.0 KC1, 1.0 CaC 89 10 glucose. and 20 tris-HC1 (pH=7.4) and incubated with glutamate and other test compounds for 15 min at 30~ Fluorescence was measured on a MPF-2A fluorimeter (Hitachi) at 340 and 380 nm excitation and 510 nm 9 0007-4888/00/0001-36525.00

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The Effect of Glutamate, Antioxid Ants, and Gangliosides on Na+,K+-Atpase Activity in Rat Brain Cortex Synaptosomes

et al. 1997

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Ganglioside-dependent factor, inhibiting lipid peroxidation in rat brain synaptosomes

Cited by 29 publications

References 20 publications

The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes

The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes

Gangliosides stabilize ionic homeostasis in rat cortical synaptosomes exposed to toxic concentrations of glutamate

The Effect of Glutamate, Antioxid Ants, and Gangliosides on Na+,K+-Atpase Activity in Rat Brain Cortex Synaptosomes

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