Role of Catalase in Oxidative Stress- and Age-Associated Degenerative Diseases.
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TLDR
The direct and indirect involvement of deficiency and/or modification of catalase in the pathogenesis of some important diseases such as diabetes mellitus, Alzheimer's disease, Parkinson’s disease, vitiligo, and acatalasemia is described.Abstract:
Reactive species produced in the cell during normal cellular metabolism can chemically react with cellular biomolecules such as nucleic acids, proteins, and lipids, thereby causing their oxidative modifications leading to alterations in their compositions and potential damage to their cellular activities. Fortunately, cells have evolved several antioxidant defense mechanisms (as metabolites, vitamins, and enzymes) to neutralize or mitigate the harmful effect of reactive species and/or their byproducts. Any perturbation in the balance in the level of antioxidants and the reactive species results in a physiological condition called "oxidative stress." A catalase is one of the crucial antioxidant enzymes that mitigates oxidative stress to a considerable extent by destroying cellular hydrogen peroxide to produce water and oxygen. Deficiency or malfunction of catalase is postulated to be related to the pathogenesis of many age-associated degenerative diseases like diabetes mellitus, hypertension, anemia, vitiligo, Alzheimer's disease, Parkinson's disease, bipolar disorder, cancer, and schizophrenia. Therefore, efforts are being undertaken in many laboratories to explore its use as a potential drug for the treatment of such diseases. This paper describes the direct and indirect involvement of deficiency and/or modification of catalase in the pathogenesis of some important diseases such as diabetes mellitus, Alzheimer's disease, Parkinson's disease, vitiligo, and acatalasemia. Details on the efforts exploring the potential treatment of these diseases using a catalase as a protein therapeutic agent have also been described.read more
Citations
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References
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TL;DR: The present study provided additional support for the concept of an intermediate state of catalase, through which NADPH serves to prevent the formation (rather than increase the removal) of compound II.
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Lifespan Extension and Rescue of Spongiform Encephalopathy in Superoxide Dismutase 2 Nullizygous Mice Treated with Superoxide Dismutase–Catalase Mimetics
Simon Melov,Susan R. Doctrow,Julie A. Schneider,Joanna Haberson,Manisha Patel,Pinar Coskun,Karl Huffman,Douglas C. Wallace,Bernard Malfroy +8 more
TL;DR: It is shown that treatment of sod2 nullizygous mice with synthetic superoxide dismutase (SOD)–catalase mimetics extends their lifespan by threefold, rescues the spongiform encephalopathy, and attenuates mitochondrial defects.
Journal ArticleDOI
A common functional C-T substitution polymorphism in the promoter region of the human catalase gene influences transcription factor binding, reporter gene transcription and is correlated to blood catalase levels.
TL;DR: It was found that catalase levels were significantly higher in donors carrying the T allele in comparison to donors homozygous for the C allele, the first common genetic variant in a fundamental oxidative stress protection gene with a defined phenotype reported here.
Journal ArticleDOI
Predominant role of catalase in the disposal of hydrogen peroxide within human erythrocytes
Gian Franco Gaetani,Anna Maria Ferraris,Michela Rolfo,Rosa Mangerini,Sara Arena,Henry N. Kirkman +5 more
TL;DR: The present results raise the possibility that the major function of glutathione peroxidase may be the disposal of organic peroxides rather than the removal of hydrogen peroxide.
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