Suramin inhibits β-bungarotoxin-induced activation of N-methyl-d-aspartate receptors and cytotoxicity in primary neurons

Tseng, Wen-Pei; Lin‐Shiau, Shoei‐Yn

doi:10.1016/s0041-008x(03)00102-9

Cited by 2 publications

(1 citation statement)

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“…Furthermore, the role of caspase activation in neuronal death in CGNs treated with -BuTX was analyzed. The present results revealed a dramatic increase in caspase-3 activity, in line with similar observations of Tseng and Lin-Shiau (2003c). Glycyrrhizin, aristolochic acid, and DMPO reduced the activation of caspase-3 induced by -BuTX.…”

Section: Discussionsupporting

confidence: 92%

Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Chen

2005

J. Neurobiol.

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The aim of this study was to investigate the mechanism of the cytotoxic effect of beta-bungarotoxin (beta-BuTX), a presynaptic neurotoxin, on rat cerebellar granule neurons (CGNs). The maturation of CGNs is characterized by the prominent dense neurite networks that became fragmented after treatment with beta-BuTX, and this cytotoxic effect of beta-BuTX on CGNs was in a dose- and time-dependant manner. The cytotoxic effect of beta-BuTX was found to be more potent than other toxins, such as alpha-BuTX, cardiotoxin, melittin, and Naja naja atra venom phospholipase A(2). Meanwhile, undifferentiated neuroblastoma neuronal cell lines, IMR-32 and SK-N-MC, and astrocytes were found to be resistant to beta-BuTX. These results indicated that only the mature CGNs were sensitive to beta-BuTX insults. None of the following chemicals: antioxidants, K(+)-channel activator, K(+)-channel antagonists, intracellular Ca(2+) chelator, Ca(2+)-channel blockers, NMDA receptor antagonists, and nitric oxide synthase inhibitor tested, were able to reduce beta-BuTX-induced cytotoxicity. However, secretory type phospholipase A(2) inhibitors (glycyrrhizin and aristolochic acid) and a free radical scavenger (5,5-dimethyl pyrroline N-oxide, DMPO) could attenuate not only beta-BuTX-induced cytotoxicity but also ROS production and caspase-3 activation. These data suggest that phospholipase A(2) activity of beta-BuTX may be responsible for free radical generation and caspase-3 activation that accounts for the observed cytotoxic effect. It is proposed that the CGNs can be a useful tool for studying interactions of the molecules on neuronal plasma membrane with beta-BuTX that mediates the specific cytotoxicity.

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Section: Discussionsupporting

confidence: 92%

Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Chen

2005

J. Neurobiol.

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Pyrrolizidine alkaloid clivorine induces apoptosis in human normal liver L-02 cells and reduces the expression of p53 protein

Zhang

Sheng

et al. 2005

Toxicology in Vitro

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Suramin inhibits β-bungarotoxin-induced activation of N-methyl-d-aspartate receptors and cytotoxicity in primary neurons

Cited by 2 publications

References 50 publications

Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Pyrrolizidine alkaloid clivorine induces apoptosis in human normal liver L-02 cells and reduces the expression of p53 protein

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Suramin inhibits β-bungarotoxin-induced activation of N-methyl-d-aspartate receptors and cytotoxicity in primary neurons

Cited by 2 publications

References 50 publications

Phospholipase A2 activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Phospholipase A2 activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Pyrrolizidine alkaloid clivorine induces apoptosis in human normal liver L-02 cells and reduces the expression of p53 protein

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Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons

Phospholipase A₂ activity of β‐bungarotoxin is essential for induction of cytotoxicity on cerebellar granule neurons