ArticleBritish journal of pharmacology2000
Veratridine induces apoptotic death in bovine chromaffin cells through superoxide production.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Screening of natural compounds library for protection against endoplasmic reticulum stress in corneal endothelial cells.Frontiers in ophthalmology · 2026Article
- Synthesis and Neuroprotective Properties of N-SubstitutedACS omega · 2019Article
- Development of a rapid and economic in vivo electrocardiogram platform for cardiovascular drug assay and electrophysiology research in adult zebrafish.Scientific reports · 2018Article
- Chromaffin cells as a model to evaluate mechanisms of cell death and neuroprotective compounds.Pflugers Archiv : European journal of physiology · 2018Review
- A plant alkaloid, veratridine, potentiates cancer chemosensitivity by UBXN2A-dependent inhibition of an oncoprotein, mortalin-2.Oncotarget · 2015Article
- The endoplasmic reticulum stress and the HIF-1 signalling pathways are involved in the neuronal damage caused by chemical hypoxia.British journal of pharmacology · 2015Article
- Transient receptor potential melastatin 4 and cell death.Pflugers Archiv : European journal of physiology · 2012Review
- Aliskiren prevents the toxic effects of peritoneal dialysis fluids during chronic dialysis in rats.PloS one · 2012Article
- Mechanism of pyrethroid pesticide-induced apoptosis: role of calpain and the ER stress pathway.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Bcl-x(L) blocks a mitochondrial inner membrane channel and prevents Ca2+ overload-mediated cell death.PloS one · 2011Article
- Acetaminophen induces apoptosis in rat cortical neurons.PloS one · 2010Article
- Neuroprotective activity of 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (PAN-811), a cancer therapeutic agent.CNS drug reviews · 2006Review
- Potential roles of electrogenic ion transport and plasma membrane depolarization in apoptosis.The Journal of membrane biology · 2006Review
- Reactive oxygen species induce swelling and cytochrome c release but not transmembrane depolarization in isolated rat brain mitochondria.British journal of pharmacology · 2003Article
- Superoxide anions mediate veratridine-induced cytochrome c release and caspase activity in bovine chromaffin cells.British journal of pharmacology · 2002Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms involved in veratridine-induced chromaffin cell death have been explored. We have found that exposure to veratridine (30 microM, 1 h) produces a delayed cellular death that reaches 55% of the cells 24 h after veratridine exposure. This death has the features of apoptosis as DNA fragmentation can be observed. Calcium ions play an important role in veratridine-induced chromaffin cell death because the cell permeant Ca(2+) chelator BAPTA-AM and extracellular Ca(2+) removal completely prevented veratridine-induced toxicity. Following veratridine treatment, there is a decrease in mitochondrial function and an increase in superoxide anion production. Veratridine-induced increase in superoxide production was blocked by tetrodotoxin (TTX; 10 microM), extracellular Ca(2+) removal and the mitochondrial permeability transition pore blocker cyclosporine A (10 microM). Veratridine-induced death was prevented by different antioxidant treatments including catalase (100 IU ml(-1)), N-acetyl cysteine (100 microM), allopurinol (100 microM) or vitamin E (50 microM). Veratridine-induced DNA fragmentation was prevented by TTX (10 microM). Veratridine produced a time-dependent increase in caspase activity that was prevented by Ca(2+) removal and TTX (10 microM). In addition, calpain and caspases inhibitors partially prevented veratridine-induced death. These results indicate that chromaffin cells share with neurons the molecular machinery involved in apoptotic death and might be considered a good model to study neuronal death during neurodegeneration.
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