Neural cells, damage

P. Saransaari, S. S. Oja (2000). Taurine and neural cell damage. Amino Acids 19 509-526. 

Stroke and, thus, contributes pivotally to significant losses in neurological functions. The major contributors of the apoptotic cell death are a family of cysteine proteases (caspases). They initiate apoptosis by cleaving key components of the neuronal infrastructure and activating the factors responsible for neural cell damage. 

Thereafter, a survey will be made of reports concerning neural cell damage following exposure to cadmium. Short reviews on the neurotoxicology of cadmium have recently been published by Tischner and Arvidson. ... 

Although the major part of the brain seems to be quite efficiently protected against the penetration of cadmium by the blood-brain barrier, there are certain regions of the CNS that are devoid of this barrier and autoradiographic studies indicate that cadmium may accumulate in such areas. Experimental studies are needed to determine whether the deposition of cadmium in these regions leads to neural cell damage. 

Adhesion molecules such as LI, neural cell adhesion molecule (N-CAM) and N-cadherin promote axonal regeneration by homophilic interactions between axons and Schwann cell surfaces (see Ch. 7). The expression of p75 (low affinity NGF receptor, Ch. 27) is also increased at the Schwann cell surface after injury. Extracellular matrix molecules, such as tenascin and proteoglycans, increase the regenerative potential of damaged peripheral nerves by binding to integrins on the axonal surface. 

The identity of factors released from damaged neurons to signal microglial cell activation may depend upon which type of neural cell is damaged, neuron versus glial, and on the the toxin or stimulus, glutamate versus /1-amyloid versus a-synuclein, and the nature of cellular death, apoptosis versus necrosis. Similarly, the molecular mechanisms and internal and external factors that modulate the dynamic aspects of acute and chronic inflammation in cell injury mediated by glutamate remain unclear. It also remains unclear to what extent inflammation is beneficial... 

The superoxide oxide radical interacts with nitric oxide to produce peroxynitrite at a rate which three times faster than the rate at which superoxide dismutase utilizes superoxide (Beckman, 1994). Peroxynitrite is capable of diffusing to distant places in neural cells where it induces lipid peroxidation and may be involved in synaptosomal and myelin damage (Van der Veen and Roberts, 1999). After protonation and decomposition, peroxynitrite produces more hydroxyl radicals. This mechanism of hydroxyl radical generation is not dependent on redox active metal ions and may be involved in initiating lipid and protein peroxidation in vivo (Warner et al., 2004). 

Ligand-operated Ca2+ channels (LOCCs), known also as ionotropic receptors, are important progressors of pathological Ca2+ entry, especially in the brain tissue. The best example of toxic plasmalemmal Ca2+ entry is represented by glutamate-induced excitotoxic death of neural cells (or glutamate excitotoxicity) in damaged... 

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