Neurons, apoptotic death compounds

Central among the toxic responses to oxidative stress is the induction of apop-totic death (Curtin et al, 2002 Fleury et al, 2002 Polster and Fkskum, 2004 Ryter et al, 2007). While it is clear that it can be an initiator as well as a signaling event within the apoptotic process, the specific mechanisms underlying these remain uncertain. Likely, these responses could be related to the damage of cellular components e.g. DNA, lipids, and polysaccharides. One potential pathway by which ethanol-mediated oxidative stress may elicit apoptosis of neurons is associated with the oxidation of polyunsaturated fatty acids within mitochondria (Ramachandran et al, 2001, 2003). Among the variety of oxidation products of these fatty acids are toxic/pro-apoptotic aldehydes, the most potent being 4-hydrox-ynonenal (Esterbauer et al, 1990 Uchida et al., 1993). This compound readily induces apoptotic death of neurons (Lovell and Markesbery, 2006 Dwivedi et al., 2007) and is produced in neurons secondary to ethanol-related oxidative stress (Ramachandran et al, 2001, 2003)... 

Apoptotic/necrotic transformation of excitable cells. Effects of dipeptides directed to support stability of cellular structures increase the reliability of cellular functions under normal conditions and especially during oxidative stress, which accompanies effect of several extreme factors. It was found in experiments on individual neurons that carnosine prevents cell death induced by excitotoxic compounds, N-methyl-D-aspartic acid (NMDA) or kainate [93-95] or experimental hypoxia/reoxigenation [96]. Apoptosis induced by exposure of cerebellum neurons to kainic acid (see Table 6), was arrested if the cells were pre-incubated with carnosine or anserine and simultaneously heavy necrotic processes were substitute by light (reversible) necrosis. At the same time, N-acetylcamosine or homocaraosine did not reveal protecting action [94,95]. 

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