Oxidative damage to DNA, p53 gene expression and p53 protein level in the process of aging in rat brain

Dorszewska, Jolanta; Adamczewska-Goncerzewicz, Z

doi:10.1016/j.resp.2003.10.005

Cited by 33 publications

(22 citation statements)

References 49 publications

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“…These results indicate that aging is coupled to an increase in cerebellar oxidative damage for a broad array of molecules. In confirmation of previous work, aging was associated with an increase in cerebellar markers of lipid [21] and DNA oxidation [4,8,30]. In addition, the currents study provides the first evidence that RNA oxidation increases in the cerebellum with advanced age.…”

Section: Discussionsupporting

confidence: 91%

Comparison of lifelong and late life exercise on oxidative stress in the cerebellum

Cui

Hofer

Rani

et al. 2009

Neurobiology of Aging

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Aging was associated with increased oxidation of DNA, RNA, and lipids in the cerebellum of male rats. DNA and lipid oxidation was reduced by lifelong (94 weeks) voluntary exercise on a running wheel. A reduction in cerebellar lipid oxidation, but not RNA or DNA oxidation, was observed following 3 months of moderate exercise or dietary supplementation of vitamin E, initiated at 18 months of age. The level of lipid oxidation correlated with measures of forelimb grip strength. The results indicate that lifelong exercise attenuates multiple molecular markers of age-related oxidative damage in the cerebellum. In addition, modest exercise initiated late in life can have a beneficial effect on lipid oxidation and motor function.

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Section: Discussionsupporting

confidence: 91%

Comparison of lifelong and late life exercise on oxidative stress in the cerebellum

Cui

Hofer

Rani

et al. 2009

Neurobiology of Aging

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“…The increased expression of GFAP, indicative of reactive astrocytosis, in Ercc1 mutant mice is also seen in the brains normally aging rats, mice, and humans (O'Callaghan and Miller, 1991;Nichols et al, 1993;Takahashi et al, 2006). In addition, the increased p53 expression we found is observed in normal aging rat brain (Chung et al, 2000;Dorszewska and Adamczewska-Goncerzewicz, 2004). Together, these results show that (neuronal) DNA damage results in brain pathology that shares characteristics with normal aging.…”

Section: Discussionsupporting

confidence: 66%

“…Several studies show that aging is accompanied by accumulation of neuronal DNA damage in rodents and humans (Sohal et al, 1994;Hamilton et al, 2001;Dorszewska and Adamczewska-Goncerzewicz, 2004;Gedik et al, 2005). Furthermore, the brain is particularly vulnerable to oxidative stress since it exhibits very high oxygen metabolism, has abundant lipid content and relatively low levels of antioxidants compared to other organs (Cai et al, 1996;Leutner et al, 2001;Serrano and Klann, 2004;Møller et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Accelerated Age-Related Cognitive Decline and Neurodegeneration, Caused by Deficient DNA Repair

Borgesius

Waard²,

Pluijm³

et al. 2011

J. Neurosci.

109

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Age-related cognitive decline and neurodegenerative diseases are a growing challenge for our societies with their aging populations. Accumulation of DNA damage has been proposed to contribute to these impairments, but direct proof that DNA damage results in impaired neuronal plasticity and memory is lacking. Here we take advantage of Ercc1 ⌬/Ϫ mutant mice, which are impaired in DNA nucleotide excision repair, interstrand crosslink repair, and double-strand break repair. We show that these mice exhibit an agedependent decrease in neuronal plasticity and progressive neuronal pathology, suggestive of neurodegenerative processes. A similar phenotype is observed in mice where the mutation is restricted to excitatory forebrain neurons. Moreover, these neuron-specific mutants develop a learning impairment. Together, these results suggest a causal relationship between unrepaired, accumulating DNA damage, and age-dependent cognitive decline and neurodegeneration. Hence, accumulated DNA damage could therefore be an important factor in the onset and progression of age-related cognitive decline and neurodegenerative diseases.

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“…The p53 protein does not lead to repair cells with damaged DNA or does not direct them to the path of apoptosis. The efect of these functional changes is increased susceptibility to infections, autoimmune diseases and cancers, including malignancies [1,2]. The pathogenesis of tumors associated with the p53 protein is contained in this book.…”

Section: Aging and Old Age Diseasesmentioning

confidence: 99%

“…Simultaneously, ROS may lead to the damage of macromolecular compounds, such as lipids, proteins, and DNA [2,3]. ROS may also play an important role in the modulation of transcription factors activation, gene expression, and various life processes of a cell.…”

Section: Introductionmentioning

confidence: 99%

Introductory Chapter: Molecular Basis of Senescence

Dorszewska¹,

Kozubski²

2017

Senescence - Physiology or Pathology

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Oxidative damage to DNA, p53 gene expression and p53 protein level in the process of aging in rat brain

Cited by 33 publications

References 49 publications

Comparison of lifelong and late life exercise on oxidative stress in the cerebellum

Comparison of lifelong and late life exercise on oxidative stress in the cerebellum

Accelerated Age-Related Cognitive Decline and Neurodegeneration, Caused by Deficient DNA Repair

Introductory Chapter: Molecular Basis of Senescence

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