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Review
. 2018 Dec 17;7(12):274.
doi: 10.3390/cells7120274.

The Role of Mitochondria in Reactive Oxygen Species Generation and Its Implications for Neurodegenerative Diseases

Affiliations
Review

The Role of Mitochondria in Reactive Oxygen Species Generation and Its Implications for Neurodegenerative Diseases

Saima Kausar et al. Cells. .

Abstract

Mitochondria are dynamic cellular organelles that consistently migrate, fuse, and divide to modulate their number, size, and shape. In addition, they produce ATP, reactive oxygen species, and also have a biological role in antioxidant activities and Ca2+ buffering. Mitochondria are thought to play a crucial biological role in most neurodegenerative disorders. Neurons, being high-energy-demanding cells, are closely related to the maintenance, dynamics, and functions of mitochondria. Thus, impairment of mitochondrial activities is associated with neurodegenerative diseases, pointing to the significance of mitochondrial functions in normal cell physiology. In recent years, considerable progress has been made in our knowledge of mitochondrial functions, which has raised interest in defining the involvement of mitochondrial dysfunction in neurodegenerative diseases. Here, we summarize the existing knowledge of the mitochondrial function in reactive oxygen species generation and its involvement in the development of neurodegenerative diseases.

Keywords: electron transport chain; mitochondria; neurodegenerative diseases; oxidative damage.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The major sites for the production of reactive oxygen species in a mitochondrion.
Figure 2
Figure 2
The causes of oxidative stress in neurodegenerative diseases.

References

    1. Chan D.C. Mitochondria: Dynamic organelles in disease, aging and development. Cell. 2000;125:141–152. doi: 10.1016/j.cell.2006.06.010. - DOI - PubMed
    1. Sun Y.X., Wang L., Wei G.Q., Qian C., Dai L.S., Sun Y., Abbas M.N., Zhu B.J., Liu C.L. Characterization of the complete mitochondrial genome of Leucoma salicis (Lepidoptera: Lymantriidae) and comparison with other lepidopteran insects. Sci. Rep. 2016;6:39153. doi: 10.1038/srep39153. - DOI - PMC - PubMed
    1. Picard M., Taivassalo T., Gouspillou G., Hepple R.T. Mitochondria: Isolation, structure and function. J. Physiol. 2011;589:4413–4421. doi: 10.1113/jphysiol.2011.212712. - DOI - PMC - PubMed
    1. Duchen M.R. Mitochondria in health and disease: Perspectives on a new mitochondrial biology. Mol. Aspects Med. 2004;25:365–451. doi: 10.1016/j.mam.2004.03.001. - DOI - PubMed
    1. Pryde K.R., Hirst J. Superoxide is produced by the reduced flavin in mitochondrial complex I: A single, unified mechanism that applies during both forward and reverse electron transfer. J. Biol. Chem. 2011;286:18056–18065. doi: 10.1074/jbc.M110.186841. - DOI - PMC - PubMed

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