DNA repair gene OGG1 polymorphism and its relation with oxidative DNA damage in patients with Alzheimer’s disease

Dinçer, Yıldız; Akkaya, Çağlayan; Mutlu, Tuba; Yavuzer, Serap; Erkol, Gökhan; Bozluolçay, Melda; Güven, Mehmet

doi:10.1016/j.neulet.2019.134362

Cited by 19 publications

(18 citation statements)

References 27 publications

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“…The OGG1 gene is located on the long arm of chromosome 3 (3p26.2) and consists of 11 exons and 10 introns [9,12,23]. The enzyme encoded by this gene is 8-oxoguanine DNA glycosylase, which acts directly on the BER pathway by catalyzing the repair of oxidative stress-induced damage to guanine [4,15,24]. The oxidation products of guanine are mostly 8-hydroxy deoxyguanosine (8-OHDG) and 8-oxoguanine [24][25][26].…”

Section: State Of Knowledgementioning

confidence: 99%

“…The enzyme encoded by this gene is 8-oxoguanine DNA glycosylase, which acts directly on the BER pathway by catalyzing the repair of oxidative stress-induced damage to guanine [4,15,24]. The oxidation products of guanine are mostly 8-hydroxy deoxyguanosine (8-OHDG) and 8-oxoguanine [24][25][26]. These oxidized guanine compounds are first detected by 8-oxoguanine DNA glycosylase that catalyzes the excision of the damaged base by cutting the glycosidic bond between the modified base and the sugar fraction, generating an abasic site (AP), which facilitates the subsequent addition of an unmodified base (Fig.…”

Section: State Of Knowledgementioning

confidence: 99%

“…These oxidized guanine compounds are first detected by 8-oxoguanine DNA glycosylase that catalyzes the excision of the damaged base by cutting the glycosidic bond between the modified base and the sugar fraction, generating an abasic site (AP), which facilitates the subsequent addition of an unmodified base (Fig. 1A) [4,[23][24][25]. The OGG1 gene has 163 polymorphisms, being the SNP rs1052133 (exon 7 Ser326Cys; G>C) of clinical relevance, since the allele mutated with the amino acid cysteine produces a XRCC4.…”

Section: State Of Knowledgementioning

confidence: 99%

See 2 more Smart Citations

Genetic profile for the detection of susceptibility to poisoning by exposure to pesticides

Galvez¹,

Salazar-Flores²,

Sanchez³

et al. 2021

Ann Agric Environ Med.

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Section: State Of Knowledgementioning

confidence: 99%

Section: State Of Knowledgementioning

confidence: 99%

Section: State Of Knowledgementioning

confidence: 99%

See 1 more Smart Citation

Genetic profile for the detection of susceptibility to poisoning by exposure to pesticides

Galvez¹,

Salazar-Flores²,

Sanchez³

et al. 2021

Ann Agric Environ Med.

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show abstract

“…Moreover, mutations in the OGG1 gene, either resulting in a complete loss of OGG1 activity or reduced repair capacity, have been reported to be specific to AD patients [ 153 ]. Gene polymorphisms in OGG1 , but also XRCC1 , have been associated with increased DNA damage in AD patients [ 154 , 155 ]. Interestingly, expression of BER genes encoding APE1 , POLβ , OGG1 , and PARP1 was shown to be higher in brain tissue than in blood samples from AD patients, highlighting the importance of active BER in repairing antioxidant lesions in the brain.…”

Section: Oxidative Dna Base Lesions and Dna Glycosylases In Neurodegenerative Diseasesmentioning

confidence: 99%

Impact of Oxidative DNA Damage and the Role of DNA Glycosylases in Neurological Dysfunction

Sousa

Luna

et al. 2021

IJMS

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The human brain requires a high rate of oxygen consumption to perform intense metabolic activities, accounting for 20% of total body oxygen consumption. This high oxygen uptake results in the generation of free radicals, including reactive oxygen species (ROS), which, at physiological levels, are beneficial to the proper functioning of fundamental cellular processes. At supraphysiological levels, however, ROS and associated lesions cause detrimental effects in brain cells, commonly observed in several neurodegenerative disorders. In this review, we focus on the impact of oxidative DNA base lesions and the role of DNA glycosylase enzymes repairing these lesions on brain function and disease. Furthermore, we discuss the role of DNA base oxidation as an epigenetic mechanism involved in brain diseases, as well as potential roles of DNA glycosylases in different epigenetic contexts. We provide a detailed overview of the impact of DNA glycosylases on brain metabolism, cognition, inflammation, tissue loss and regeneration, and age-related neurodegenerative diseases based on evidence collected from animal and human models lacking these enzymes, as well as post-mortem studies on patients with neurological disorders.

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“…PM 2.5 adsorbs hazardous constituents such as transition metals and organic compounds, which generate reactive oxygen species (ROS) in organisms [ 7 , 8 ]. ROS produced by oxidative stress can over oxidize cellular biomolecules, and DNA is considered to be an important target for ROS [ 9 ]. ROS can result in increased levels of strand-breaking effects and DNA base oxidations [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

Niu

et al. 2020

IJERPH

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Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (<2.5 μm) (PM2.5) exposure. The toxic responses of PM2.5 are greatly influenced by the source of PM2.5. However, the effects of PM2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM2.5 from Beijing was sampled and applied in vitro to investigate its genotoxicity and the mechanisms behind it. Human bronchial epithelial cells 16HBE were used as a model for exposure. Low (67.5 μg/mL), medium (116.9 μg/mL), and high (202.5 μg/mL) doses of PM2.5 were used for cell exposure. After PM2.5 exposure, cell viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, and DNA repair gene expression were measured. The results showed that PM2.5 significantly induced cytotoxicity in 16HBE. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and cellular heme oxygenase (HO-1) were increased, and the level of glutathione (GSH) was decreased, which represented the occurrence of severe oxidative stress in 16HBE. The micronucleus rate was elevated, and DNA damage occurred as indicators of the comet assay, γ-H2AX and 8-OH-dG, were markedly enhanced by PM2.5, accompanied by the influence of 8-oxoguanine DNA glycosylase (OGG1), X-ray repair cross-complementing gene 1 (XRCC1), and poly (ADP-ribose) polymerase-1 (PARP1) expression. These results support the significant role of PM2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes.

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DNA repair gene OGG1 polymorphism and its relation with oxidative DNA damage in patients with Alzheimer’s disease

Cited by 19 publications

References 27 publications

Genetic profile for the detection of susceptibility to poisoning by exposure to pesticides

Genetic profile for the detection of susceptibility to poisoning by exposure to pesticides

Impact of Oxidative DNA Damage and the Role of DNA Glycosylases in Neurological Dysfunction

Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

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