Abstract |
Nitric oxide (NO) donors, sodium nitroprusside and NOC 7, caused pheochromocytoma (PC12) cell death in a concentration and time-dependent manner. This cytotoxicity was blocked by the NO trapping agent, oxyhemoglobin. A membrane permeable cGMP analogue had no cytotoxicity in a reasonable concentration. Moreover, the selective inhibitor of cGMP-dependent protein kinase, KT5823, had no effect on NOC 7 cytotoxicity. These results suggest that NO caused PC12 cell death but not through the cGMP pathway. Additionally, this NO-induced PC12 cell death is not accompanied by DNA fragmentation. Nerve growth factor ( NGF), which is able to rescue PC12 cells from serum deprivation, failed to protect PC12 cells from NO-induced cell death by acute treatment. However, PC12 cells differentiated by NGF treatment for more than 3 days did not die after NO exposure. The differentiated PC12 cells, but not undifferentiated cells, expressed NO synthase (NOS). NGF-differentiated PC12 cells acquired the resistance to NO, by a mechanism not yet identified, accompanied by the expression of NOS.
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Authors | K Wada, N Okada, T Yamamura, S Koizumi |
Journal | Neurochemistry international
(Neurochem Int)
Vol. 29
Issue 5
Pg. 461-7
(Nov 1996)
ISSN: 0197-0186 [Print] England |
PMID | 8939456
(Publication Type: Journal Article)
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Chemical References |
- (1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-3-aminopropyl)-3-methyl-1-triazene
- Culture Media, Serum-Free
- Nerve Growth Factors
- Triazenes
- Nitric Oxide
- Nitric Oxide Synthase
- Cyclic GMP
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Topics |
- Animals
- Cell Differentiation
(drug effects)
- Cell Nucleus
(drug effects)
- Cell Survival
(drug effects)
- Culture Media, Serum-Free
- Cyclic GMP
(physiology)
- DNA Fragmentation
- Drug Resistance
- Nerve Growth Factors
(pharmacology)
- Neurons
(cytology, drug effects)
- Nitric Oxide
(toxicity)
- Nitric Oxide Synthase
(analysis)
- PC12 Cells
- Rats
- Sympathetic Nervous System
(cytology, drug effects)
- Triazenes
(toxicity)
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