(Q44035217)

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The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload.

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10 November 2019

The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload (English)

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10 November 2019

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10 November 2019

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H S Yin

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10 November 2019

Y Z Shen

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1 January 2002

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10 November 2019

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10 November 2019

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10 November 2019

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10 November 2019

707-716

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10 November 2019

Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid

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3-Nitropropionic acid neurotoxicity is attenuated in copper/zinc superoxide dismutase transgenic mice

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Partial inhibition of brain succinate dehydrogenase by 3-nitropropionic acid is sufficient to initiate striatal degeneration in rat.

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Dual responses of CNS mitochondria to elevated calcium

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3-Nitropropionic acid increases the intracellular Ca2+ in cultured astrocytes by reverse operation of the Na+-Ca2+ exchanger.

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Participation of par-4 in the degeneration of striatal neurons induced by metabolic compromise with 3-nitropropionic acid

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Cyclosporin A, but not FK 506, protects mitochondria and neurons against hypoglycemic damage and implicates the mitochondrial permeability transition in cell death.

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Astrocytes are more vulnerable than neurons to cellular Ca2+ overload induced by a mitochondrial toxin, 3-nitropropionic acid

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Doxorubicin treatment activates a Z-VAD-sensitive caspase, which causes deltapsim loss, caspase-9 activity, and apoptosis in Jurkat cells

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3-Nitropropionic acid exacerbates N-methyl-D-aspartate toxicity in striatal culture by multiple mechanisms.

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Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis

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Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: a type of hypoxic (energy deficient) brain damage.

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Mitochondrial regulation of store-operated calcium signaling in T lymphocytes

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Increased sensitivity to mitochondrial toxin-induced apoptosis in neural cells expressing mutant presenilin-1 is linked to perturbed calcium homeostasis and enhanced oxyradical production.

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Excitotoxicity is required for induction of oxidative stress and apoptosis in mouse striatum by the mitochondrial toxin, 3-nitropropionic acid

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Characteristics of the calcium-triggered mitochondrial permeability transition in nonsynaptic brain mitochondria: effect of cyclosporin A and ubiquinone O

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Mitochondrial control of apoptosis

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Pivotal role of mitochondrial calcium uptake in neural cell apoptosis and necrosis

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Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells

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Neuroprotective effect of lamotrigine and MK-801 on rat brain lesions induced by 3-nitropropionic acid: evaluation by magnetic resonance imaging and in vivo proton magnetic resonance spectroscopy

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Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death.

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Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis.

1 reference

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1 reference

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1 reference

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Identifiers

10.1016/S0306-4522(02)00097-0

1 reference

Europe PubMed Central

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10 November 2019

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10 November 2019

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