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Oxidative stress and its significant roles in neurodegenerative diseases and cancer.

Thanan R, Oikawa S, Hiraku Y, Ohnishi S, Ma N, Pinlaor S, Yongvanit P, Kawanishi S, Murata M - Int J Mol Sci (2014)

Bottom Line: Accumulating evidence indicates that oxidative damage to biomolecules including lipids, proteins and DNA, contributes to these diseases.Our recent studies identifying and characterizing carbonylated proteins reveal oxidative damage to heat shock proteins in neurodegenerative disease models and inflammation-related cancer, suggesting dysfunction in their antioxidative properties.Immunohistochemical analyses showed co-localization of oxidative/nitrative DNA lesions and stemness markers in the cells of inflammation-related cancers.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. mrsomchaip@yahoo.com.

ABSTRACT
Reactive oxygen and nitrogen species have been implicated in diverse pathophysiological conditions, including inflammation, neurodegenerative diseases and cancer. Accumulating evidence indicates that oxidative damage to biomolecules including lipids, proteins and DNA, contributes to these diseases. Previous studies suggest roles of lipid peroxidation and oxysterols in the development of neurodegenerative diseases and inflammation-related cancer. Our recent studies identifying and characterizing carbonylated proteins reveal oxidative damage to heat shock proteins in neurodegenerative disease models and inflammation-related cancer, suggesting dysfunction in their antioxidative properties. In neurodegenerative diseases, DNA damage may not only play a role in the induction of apoptosis, but also may inhibit cellular division via telomere shortening. Immunohistochemical analyses showed co-localization of oxidative/nitrative DNA lesions and stemness markers in the cells of inflammation-related cancers. Here, we review oxidative stress and its significant roles in neurodegenerative diseases and cancer.

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Roles of oxidative stress in neurodegenerative diseases and cancer.
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ijms-16-00193-f005: Roles of oxidative stress in neurodegenerative diseases and cancer.

Mentions: Aging is a multifactorial process derived from an interaction between genetic and environmental factors. Aging is accompanied by an up-regulation of inflammatory responses, and inflammatory changes are common to many age-related diseases such as neurodegenerative diseases and cancer [140]. Environmental factors can cause metabolic changes in humans that either increase the production of ROS/RNS or decrease the antioxidant production with increased lipid peroxidation, protein and DNA oxidation [141]. Oxidative stress induces the formation of lipid peroxidation leading to prolongation of oxidative stress via the propagating chain reaction [142]. Oxidized proteins accumulate in cells via aggregations, protein aggregates cause more mitochondrial damage, and damaged mitochondria can further induce protein damage [143]. Moreover, reactive species damage DNA, which may lead to aberrant cell cycle entry, and further to differential regulation of common genes such as p53 and Wnt in neurodegenerative diseases and cancer [144]. As shown in Figure 5 (distinct pathway), the striking differences between post-mitotic neurons and regular mitotic cells provide insight into the inverse association between cancer and neurodegeneration, that is, apoptosis of neural cells (up-regulation of p53 and down-regulation of Wnt) and proliferation of cancer cells (down-regulation of p53 and up-regulation of Wnt) [144]. Additionally, tissue injury can activate normally quiescent adult liver stem cells that thereby become a potential target cell population in many cancers. When several carcinogenic events such as mutation and epigenetic changes occur in stem cells under oxidative stress, the cells may acquire the properties of cancer stem cells. Nevertheless, age- and environment-related inflammation and oxidative stress may be a common initiating event for both neurodegeneration and carcinogenesis, as shown in Figure 5 (common pathway). Overall, the common pathway could be a target for developing chemopreventive and therapeutic strategies against oxidative stress in neurodegenerative diseases and cancer.


Oxidative stress and its significant roles in neurodegenerative diseases and cancer.

Thanan R, Oikawa S, Hiraku Y, Ohnishi S, Ma N, Pinlaor S, Yongvanit P, Kawanishi S, Murata M - Int J Mol Sci (2014)

Roles of oxidative stress in neurodegenerative diseases and cancer.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4307243&req=5

ijms-16-00193-f005: Roles of oxidative stress in neurodegenerative diseases and cancer.
Mentions: Aging is a multifactorial process derived from an interaction between genetic and environmental factors. Aging is accompanied by an up-regulation of inflammatory responses, and inflammatory changes are common to many age-related diseases such as neurodegenerative diseases and cancer [140]. Environmental factors can cause metabolic changes in humans that either increase the production of ROS/RNS or decrease the antioxidant production with increased lipid peroxidation, protein and DNA oxidation [141]. Oxidative stress induces the formation of lipid peroxidation leading to prolongation of oxidative stress via the propagating chain reaction [142]. Oxidized proteins accumulate in cells via aggregations, protein aggregates cause more mitochondrial damage, and damaged mitochondria can further induce protein damage [143]. Moreover, reactive species damage DNA, which may lead to aberrant cell cycle entry, and further to differential regulation of common genes such as p53 and Wnt in neurodegenerative diseases and cancer [144]. As shown in Figure 5 (distinct pathway), the striking differences between post-mitotic neurons and regular mitotic cells provide insight into the inverse association between cancer and neurodegeneration, that is, apoptosis of neural cells (up-regulation of p53 and down-regulation of Wnt) and proliferation of cancer cells (down-regulation of p53 and up-regulation of Wnt) [144]. Additionally, tissue injury can activate normally quiescent adult liver stem cells that thereby become a potential target cell population in many cancers. When several carcinogenic events such as mutation and epigenetic changes occur in stem cells under oxidative stress, the cells may acquire the properties of cancer stem cells. Nevertheless, age- and environment-related inflammation and oxidative stress may be a common initiating event for both neurodegeneration and carcinogenesis, as shown in Figure 5 (common pathway). Overall, the common pathway could be a target for developing chemopreventive and therapeutic strategies against oxidative stress in neurodegenerative diseases and cancer.

Bottom Line: Accumulating evidence indicates that oxidative damage to biomolecules including lipids, proteins and DNA, contributes to these diseases.Our recent studies identifying and characterizing carbonylated proteins reveal oxidative damage to heat shock proteins in neurodegenerative disease models and inflammation-related cancer, suggesting dysfunction in their antioxidative properties.Immunohistochemical analyses showed co-localization of oxidative/nitrative DNA lesions and stemness markers in the cells of inflammation-related cancers.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand. mrsomchaip@yahoo.com.

ABSTRACT
Reactive oxygen and nitrogen species have been implicated in diverse pathophysiological conditions, including inflammation, neurodegenerative diseases and cancer. Accumulating evidence indicates that oxidative damage to biomolecules including lipids, proteins and DNA, contributes to these diseases. Previous studies suggest roles of lipid peroxidation and oxysterols in the development of neurodegenerative diseases and inflammation-related cancer. Our recent studies identifying and characterizing carbonylated proteins reveal oxidative damage to heat shock proteins in neurodegenerative disease models and inflammation-related cancer, suggesting dysfunction in their antioxidative properties. In neurodegenerative diseases, DNA damage may not only play a role in the induction of apoptosis, but also may inhibit cellular division via telomere shortening. Immunohistochemical analyses showed co-localization of oxidative/nitrative DNA lesions and stemness markers in the cells of inflammation-related cancers. Here, we review oxidative stress and its significant roles in neurodegenerative diseases and cancer.

Show MeSH
Related in: MedlinePlus