Oxidative stress cerebellum

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]. 

In mice, striatal dopamine was depleted in a dose-dependent manner following single intraperitoneal doses of 3-6 mg ochratoxin A/kg bw. Oxidative stress, oxidative DMA damage and a transient inhibition of oxidative DMA repair were also seen in the cerebellum, cortex, hippocampus, midbrain, caudate/putamen and pons/medulla (Sava et al., 2006). 

Rouach, H., Park, M.K., OrfaneUi, M.T., Janvier, B., and Nordmann, R. (1987). Ethanol-induced oxidative stress in the rat cerebellum. Alcohol Alcohol. 1 207-211. 

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