DNA Damage and Repair

Martin, Lee J.

doi:10.1097/nen.0b013e31816ff780

Cited by 175 publications

(84 citation statements)

References 95 publications

(148 reference statements)

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“…8-OHdG is a product of highly mutagenic DNA oxidative damage; moreover, it is widely expressed in the nucleus, mitochondria, and metabolites in eukaryotic cells, and prokaryotic cells. Therefore, it can be used as a marker for the detection of DNA damage (Martin, 2008). In this study, we observed an increase in 8-OHdG expression in hepatocytes treated with increasing levels of UA for greater periods, indicating that UA enhances DNA damage in hepatocytes.…”

Section: Discussionsupporting

confidence: 49%

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

et al. 2016

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ABSTRACT. Here, we investigated the effect of uric acid (UA) on hepatocyte mitochondria. Hepatocytes cultured in vitro were treated with varying concentrations of UA. The change in apoptotic activity was detected by flow cytometry. The DNA damage index 8-hydroxy-deoxyguanosine (8-OHdG) and mitochondrial function indices succinate dehydrogenase (SDH), cytochrome C oxidase (CCO), and adenosine triphosphate (ATP) were detected by enzyme assays. Reactive oxygen species (ROS) accumulation was confirmed by a dichloro-dihydrofluorescein diacetate assay. We observed an increase in apoptotic activity, ROS accumulation, and 8-OHdG activity in hepatocytes treated with UA for extended periods, indicating DNA damage; specifically, we observed a significant increase in these activities 48, 72, and 96 h after UA addition, compared to those observed at 24 h (P < 0.05). Cells treated with 30 mg/dL UA for 96 h showed a peak in apoptotic activity. We also observed a significant decrease in ATP, SDH, and CCO activities with the increase in uric acid concentration over time. Cells treated with 30 mg/dL UA for 96 h showed the highest ATP levels, while SDH and CCO activities at 48, 72, and 96 h post-UA treatment were significantly lower than those at 24 h (P < 0.01). Moreover, cells treated with 30 mg/dL UA showed a 0.02 ± 0.02 and 0.15 ± 0.01 mmol/ mg/min decrease in SDH and CCO levels after 72 h. Therefore, we concluded that high concentrations of UA may induce oxidative stress in hepatocyte mitochondria, increasing ROS production and ultimately resulting in mitochondrial damage.

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Section: Discussionsupporting

confidence: 49%

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

et al. 2016

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“…When the rate of DNA damage by ethanol exceeds the capacity of the cell to repair it, the accumulation of errors may result in early senescence, apoptosis, or cancer. ROS has been pointed out as one of the main causes of single-strand DNA damage (Martin 2008). In this study, there was a positive moderate to strong correlation between ROS levels and single-strand DNA damage in the striatum, cerebellum, hypothalamus, and pre-frontal cortex.…”

Section: Discussionmentioning

confidence: 73%

Brain DNA damage and behavioral changes after repeated intermittent acute ethanol withdrawal by young rats

et al. 2015

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“…Neurotoxins have been shown to cause an increase in systemic DNA damage. Physiological and oxidative stresses relate to the pathogenic development of neurodegenerative and psychiatric diseases (Forlenza & Miller 2006, Martin 2008, Rybka et al 2013). Progressive neuronal DNA damage in aging brains are closely linked with the onset of neurodegenerative disorders (Lindahl 1993).…”

Section: Introductionmentioning

confidence: 99%

Effects of Antidepressants on DSP4/CPT-Induced DNA Damage Response in Neuroblastoma SH-SY5Y Cells

et al. 2015

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DNA damage is a form of cell stress and injury. Increased systemic DNA damage is related to the pathogenic development of neurodegenerative diseases. Depression occurs in a relatively high percentage of patients suffering from degenerative diseases, for whom antidepressants are often used to relieve depressive symptoms. However, few studies have attempted to elucidate why different groups of antidepressants have similar effects on relieving symptoms of depression. Previously, we demonstrated that neurotoxins N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4)- and camptothecin (CPT)-induced the DNA damage response in SH-SY5Y cells, and DSP4 caused cell cycle arrest which was predominately in the S-phase. The present study shows that CPT treatment also resulted in similar cell cycle arrest. Some classic antidepressants could reduce the DNA damage response induced by DSP4 or CPT in SH-SY5Y cells. Cell viability examination demonstrated that both DSP4 and CPT caused cell death, which was prevented by spontaneous administration of some tested antidepressants. Flow cytometric analysis demonstrated that a majority of the tested antidepressants protect cells from being arrested in S-phase. These results suggest that blocking the DNA damage response may be an important pharmacologic characteristic of antidepressants. Exploring the underlying mechanisms may allow for advances in the effort to improve therapeutic strategies for depression appearing in degenerative and psychiatric diseases.

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DNA Damage and Repair

Cited by 175 publications

References 95 publications

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

Brain DNA damage and behavioral changes after repeated intermittent acute ethanol withdrawal by young rats

Effects of Antidepressants on DSP4/CPT-Induced DNA Damage Response in Neuroblastoma SH-SY5Y Cells

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