Apoptosis cyanide-induced

Cyanide-induced cell death involves the selective activation of apoptosis or necrosis in different nemonal populations. Mills et al (1999) reported that cyanide-induced cell death occurred via apoptosis in the cortical region of a mouse brain and via necrosis in the substantia nigra. Similarly, Prabhakaran et al (2002) reported that cyanide-induced cell death occurred via apoptosis in primary cortical cells and via necrosis in primary mesencephalic cells. While exposure to potassium cyanide (400 pM) increased the formation of ROS in both cell types, the rates of formation and the nature of ROS varied. For example, catalase and superoxide dismutase decreased the formation of ROS in cortical cells but not in mesencephalic cells. These findings suggest that the selective vulnerabihty of these neuronal populations to cyanide may be related to differences in their susceptibility to oxidative stress. 

Li, L., Prahhakaran, K., Shou, Y., Borowitz, J.L., Isom, G.E. (2002). Oxidative stress and cyclooxygenase-2 induction mediate cyanide-induced apoptosis of cortical cells. Toxicol. Appl. Pharmacol. 185 55-63. 

Shou Y, Li L, Prabhakaran K et al. (2003). p45 Mitogen-activated protein kinase contributes to Bax translocation and cytochrome c release in cyanide-induced apoptosis. Toxicol Sci, 75, 99-107. 

Gunasekar, PG., Borowitz, J.L., and Isom, G.E., Cyanide-induced apoptosis involves NMDA receptor-mediated oxidative stress and NF-, B linked activation of caspase-3 protease, submitted for publication. 

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