8-Hydroxy-2′-deoxyguanosine (8-OHdG) as a biomarker of oxidative DNA damage induced by occupational exposure to nanomaterials: a systematic review

Shekaftik, Soqrat Omari; Nasirzadeh, Nafiseh

doi:10.1080/17435390.2021.1936254

Cited by 60 publications

(33 citation statements)

References 58 publications

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“…In addition, to determine whether sesamol prevents the SCOP-induced oxidative stress, an immunohistochemical test for 8-OHdG was performed on mice hippocampus slices. 8-OHdG is an indicator of oxidative DNA damage, which could be induced by ROS . According to Figure E,F, the expression of 8-OHdG in CA3 and cortex regions in the SCOP group was significantly increased in comparison with the CON group, and sesamol could downregulate the expression of 8-OHdG in SCOP-treated mice brains ( p < 0.05).…”

Section: Resultsmentioning

confidence: 99%

“…8-OHdG is an indicator of oxidative DNA damage, which could be induced by ROS. 30 According to Figure 7E,F, the expression of 8-OHdG in CA3 and cortex regions in the SCOP group was significantly increased in comparison with the CON group, and sesamol could downregulate the expression of 8-OHdG in SCOP-treated mice brains (p < 0.05). These results exhibited that sesamol pretreatment could inhibit oxidative stress.…”

Section: Effects Of Sesamol On Neuronal Damage In Scop-treated Micementioning

confidence: 86%

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Sesamol Attenuates Scopolamine-Induced Cholinergic Disorders, Neuroinflammation, and Cognitive Deficits in Mice

Yun

Wang

Zhang

et al. 2022

J. Agric. Food Chem.

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Alzheimer’s disease (AD) is a neurodegenerative disease, characterized by memory loss and cognitive deficits accompanied by neuronal damage and cholinergic disorders. Sesamol, a lignan component in sesame oil, has been proven to have neuroprotective effects. This research aimed to investigate the preventive effects of sesamol on scopolamine (SCOP)-induced cholinergic disorders in C57BL/6 mice. The mice were pretreated with sesamol (100 mg/kg/d, p.o.) for 30 days. Behavioral tests indicated that sesamol supplement prevented SCOP-induced cognitive deficits. Sesamol enhanced the expression of neurotrophic factors and postsynaptic density (PSD) in SCOP-treated mice, reversing neuronal damage and synaptic dysfunction. Importantly, sesamol could balance the cholinergic system by suppressing the AChE activity and increasing the ChAT activity and M1 mAChR expression. Sesamol treatment also inhibited the expression of inflammatory factors and overactivation of microglia in SCOP-treated mice. Meanwhile, sesamol improved the antioxidant enzyme activity and suppressed oxidative stress in SCOP-treated mice and ameliorated the oxidized cellular status and mitochondrial dysfunction in SCOP-treated SH-SY5Y cells. In conclusion, these results indicated that sesamol attenuated SCOP-induced cognitive dysfunction via balancing the cholinergic system and reducing neuroinflammation and oxidative stress.

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Section: Resultsmentioning

confidence: 99%

Section: Effects Of Sesamol On Neuronal Damage In Scop-treated Micementioning

confidence: 86%

Sesamol Attenuates Scopolamine-Induced Cholinergic Disorders, Neuroinflammation, and Cognitive Deficits in Mice

Yun

Wang

Zhang

et al. 2022

J. Agric. Food Chem.

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“…The DNA-damage status of oral cancer cells was assessed by the 8-OHdG level [ 21 ]. After the SK2 treatment of oral cancer cells, the 8-OHdG levels were assessed ( Figure 9 ).…”

Section: Resultsmentioning

confidence: 99%

Antiproliferation- and Apoptosis-Inducible Effects of a Novel Nitrated [6,6,6]Tricycle Derivative (SK2) on Oral Cancer Cells

et al. 2022

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The benzo-fused dioxabicyclo[3.3.1]nonane core is the central framework in several natural products. Using this core, we had developed a novel nitrated [6,6,6]tricycle-derived compound containing an n-butyloxy group, namely, SK2. The anticancer potential of SK2 was not assessed. This study aimed to determine the antiproliferative function and investigated possible mechanisms of SK2 acting on oral cancer cells. SK2 preferentially killed oral cancer cells but caused no harmful effect on non-malignant oral cells. After the SK2 exposure of oral cancer cells, cells in the sub-G1 phase accumulated. This apoptosis-like outcome of SK2 treatment was validated to be apoptosis via observing an increasing annexin V population. Mechanistically, apoptosis signalers such as pancaspase, caspases 8, caspase 9, and caspase 3 were activated by SK2 in oral cancer cells. SK2 induced oxidative-stress-associated changes. Furthermore, SK2 caused DNA damage (γH2AX and 8-hydroxy-2′-deoxyguanosine). In conclusion, a novel nitrated [6,6,6]tricycle-derived compound, SK2, exhibits a preferential antiproliferative effect on oral cancer cells, accompanied by apoptosis, oxidative stress, and DNA damage.

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“…Образование • OH зачастую сопровождается активацией NO-синтаз, стимулирующих образование оксида азота ( • NO), который может взаимодействовать с анион-радикалом с образованием достаточно мощного окислителя пероксинитрита (ONOO -), относящегося к реактивным формам азота и также участвующего в повреждении ДНК [14]. Для оценки свободнорадикального повреждения ДНК наиболее часто используется такой маркер, как 8-OHdG [15].…”

Section: Discussionunclassified

Oxidative stress in the endothelial cell culture exposed to mitomycin C

Sinitsky

Цепокина

Шишкова

et al. 2022

SJCEM

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Background. Atherosclerosis is one of the leading cardiovascular pathologies. Evidence suggests that DNA damage caused by endothelial cell exposure to mitomycin C (MMC) leads to endothelial dysfunction and is the risk factor for this disease. MMC is an alkylating mutagen involved in the development of oxidative stress, which is also a risk factor for atherosclerosis. Aim. To access the levels of oxidative stress markers in the primary human endothelial cell culture exposed to alkylating mutagen MMC.Material and Methods. Commercially available primary cultures of endothelial cells obtained from human coronary artery (HCAEC) and human internal thoracic artery (HITAEC) were used in the study. The cells were cultivated in the presence of 500 ng/mL MMC (experimental group) and without mutagenic load (control group). The levels of reactive oxygen species, reactive nitrogen species, and 8-OH-deoxyguanosine (8-OHdG) in cell growth media were assessed by enzyme-linked immunosorbent assay. The relative telomere length and expression of TERT and POT1 genes were accessed in endothelial cells by quantitative polymerase chain reaction. Statistical analysis of data was performed using GraphPad Prism 9 software.Results. There were no diff erences in the concentrations of reactive oxygen species, reactive nitrogen species (NO2 -, NO3 -, NO2 -/NO3 -), and 8-OHdG in HCAEC and HITAEC cultures exposed to MMC compared to the corresponding parameters in the non-exposed controls. At the same time, HCAEC and HITAEC exposed to MMC were characterized by a decrease in the relative telomere length compared to control (10.97 vs. 27.03 in HCAEC, p = 0.002 and 9.12 vs. 25.64 in HITAEC, p = 0.001). Moreover, we discovered 1.75-fold increase in the expression of POT1 gene in the experimental HCAEC compared to control (p = 0.019). No expression of TERT gene was observed in study groups.Conclusions. Alkylating mutagen MMC did not induce any pronounced oxidative stress in the primary human endothelial cells in vitro. The development of endothelial dysfunction caused by MMC exposure was triggered mainly by DNA alkylation resulting in the genotoxic stress in the endothelial cells.

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8-Hydroxy-2′-deoxyguanosine (8-OHdG) as a biomarker of oxidative DNA damage induced by occupational exposure to nanomaterials: a systematic review

Cited by 60 publications

References 58 publications

Sesamol Attenuates Scopolamine-Induced Cholinergic Disorders, Neuroinflammation, and Cognitive Deficits in Mice

Sesamol Attenuates Scopolamine-Induced Cholinergic Disorders, Neuroinflammation, and Cognitive Deficits in Mice

Antiproliferation- and Apoptosis-Inducible Effects of a Novel Nitrated [6,6,6]Tricycle Derivative (SK2) on Oral Cancer Cells

Oxidative stress in the endothelial cell culture exposed to mitomycin C

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