Role of Catalase in Oxidative Stress- And Age-Associated Degenerative Diseases

Ankita Nandi, Liang Jun Yan, Chandan Kumar Jana, Nilanjana Das

Research output: Contribution to journalArticle

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.

Original languageEnglish
Article number9613090
JournalOxidative Medicine and Cellular Longevity
Volume2019
DOIs
StatePublished - 1 Jan 2019

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Oxidative stress
Catalase
Oxidative Stress
Vitiligo
Antioxidants
Parkinson Disease
Acatalasia
Diabetes Mellitus
Alzheimer Disease
Defense Mechanisms
Enzymes
Medical problems
Bipolar Disorder
Vitamins
Nucleic Acids
Hydrogen Peroxide
Anemia
Schizophrenia
Proteins
Oxygen

Cite this

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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.",
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Role of Catalase in Oxidative Stress- And Age-Associated Degenerative Diseases. / Nandi, Ankita; Yan, Liang Jun; Jana, Chandan Kumar; Das, Nilanjana.

In: Oxidative Medicine and Cellular Longevity, Vol. 2019, 9613090, 01.01.2019.

Research output: Contribution to journalArticle

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