Nitric oxide (NO.) and the nitrosonium cation (NO+) reduce mitochondrial membrane potential and trigger apoptosis in neuronal PC12 cells.

Abstract

Nitric oxide and its redox related species exhibit both neuroprotective and neurotoxic effects. It has been suggested that the nitrosonium cation (NO') is neuroprotective towards NMDA toxicity, while the free radical nitric oxide (NO') is itself neurotoxic [I]. However, NO' releasers such as S-nitroso-N-acetyl penicillamine (SNAP) have also been shown to suppress the apoptotic death of neuronal PC12 cells following nerve growth factor (NGF) withdrawal [2]. In the present study we have investigated in detail the role of the two redox related species, NO' and NO', on neuronal apoptosis. We show that NO' and NO' will either prevent or trigger the apoptotic death of neuronal PC12 cells depending on the redox state of the cell, the concentration of donor species for NO' and NO' and the presence or absence of NGF in the culture medium. Neuronal PC 12 cells undergo apoptotic cell death following NGF withdrawal [3]. We first investigated the effects of low concentrations of NO' and NO' on the survival of PC12 cells