Currently there is sufficient documentation to place oxidative and nitrative processes in the center of the pathogenic mechanism that leads to neuronal loss.
Therefore, HOCl as an oxidant related to both oxidative and nitrative procceses deserves more attention in the study of neurodegenerative diseases. The current study provides insight into the involvement of molecular targets such as calpains, cathepsin proteases, and many other apoptotic genes in HOCl-mediated neuronal apoptosis. Their participation in the neurotoxicity of HOCl enables them to be targeted for multiple disorders which HOCl is found associated. However, some of their functions have not yet been reported in neurodegenerative disorders such as Nr4a1. Further studies of their normal function, role in disease pathogenesis, and contribution to other pathways, are required in order to increase the success rate of newly identified pharmacological compounds. Potential defences against the toxicity of HOCl for instance the induction of
pathway, and HSPs and repression of cell cycle proteins as well as ATP-dependent processes have also been discovered via microarray analysis. However, all these responses are considerably low in neurons. Given that, strategies to boost the defensive gene expression would be useful in reducing neuronal vulnerability to oxidative stress.
Overall, our study have provided the first insight into the role of this oxidant in neuronal cell death, which in turn may present valuable information to the understanding of the development of neurodegenerative diseases such as AD and the identification of cellular defensive mechanisms as revealed by microarray may ultimately serve to elucidate robust therapeutic strategies against neurodegenerative disorders and allow clinical research to mature from ‘‘promise’’ to ‘‘practice’.
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