L-carnitine protects DNA oxidative damage induced by phenylalanine and its keto acid derivatives in neural cells: a possible pathomechanism and adjuvant therapy for brain injury in phenylketonuria

Guanine (G) oxidation products, such as 8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-oxo-guanine (8-OXOG), have been widely studied as promising biomarkers for DNA oxidative damage.

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-Carotene exacerbates DNA oxidative damage and modifies p53-related pathways of cell proliferation and apoptosis in cultured cells exposed to tobacco smoke condensate

Carcinogenesis ◽

10.1093/carcin/bgh142 ◽

2004 ◽

Vol 25 (8) ◽

pp. 1315-1325 ◽

Cited By ~ 53

Author(s):

P. Palozza

Keyword(s):

Cell Proliferation ◽

Oxidative Damage ◽

Tobacco Smoke ◽

Cultured Cells ◽

Dna Oxidative Damage ◽

Proliferation And Apoptosis ◽

Tobacco Smoke Condensate

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Acrolein Aggravates Secondary Brain Injury After Intracerebral Hemorrhage Through Drp1-Mediated Mitochondrial Oxidative Damage in Mice

Neuroscience Bulletin ◽

10.1007/s12264-020-00505-7 ◽

2020 ◽

Vol 36 (10) ◽

pp. 1158-1170

Author(s):

Xun Wu ◽

Wenxing Cui ◽

Wei Guo ◽

Haixiao Liu ◽

Jianing Luo ◽

...

Keyword(s):

Brain Injury ◽

Oxidative Damage ◽

Mitochondrial Membrane ◽

Molecular Mechanisms ◽

Mitochondrial Fission ◽

Secondary Brain Injury ◽

Functional Deficits ◽

Highly Active ◽

Neural Apoptosis ◽

Mitochondrial Oxidative Damage

Abstract Clinical advances in the treatment of intracranial hemorrhage (ICH) are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury. Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases. Our results indicated a significant increase in the level of acrolein after ICH in mouse brain. In primary neurons, acrolein induced an increase in mitochondrial fragmentation, loss of mitochondrial membrane potential, generation of reactive oxidative species, and release of mitochondrial cytochrome c. Mechanistically, acrolein facilitated the translocation of dynamin-related protein1 (Drp1) from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission. Further studies found that treatment with hydralazine (an acrolein scavenger) significantly reversed Drp1 translocation and the morphological damage of mitochondria after ICH. In parallel, the neural apoptosis, brain edema, and neurological functional deficits induced by ICH were also remarkably alleviated. In conclusion, our results identify acrolein as an important contributor to the secondary brain injury following ICH. Meanwhile, we uncovered a novel mechanism by which Drp1-mediated mitochondrial oxidative damage is involved in acrolein-induced brain injury.

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The Relationship between Nkx2.1 and DNA Oxidative Damage Repair in Nickel Smelting Workers: Jinchang Cohort Study

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph16010120 ◽

2019 ◽

Vol 16 (1) ◽

pp. 120 ◽

Cited By ~ 2

Author(s):

Zhiyuan Cheng ◽

Ning Cheng ◽

Dian Shi ◽

Xiaoyu Ren ◽

Ting Gan ◽

...

Keyword(s):

Lung Cancer ◽

Dna Repair ◽

Oxidative Damage ◽

Underlying Mechanism ◽

Dna Oxidative Damage ◽

Damage Repair ◽

Smad2 Phosphorylation ◽

Nickel Exposure ◽

Nickel Smelting ◽

The Relationship

Background: Occupational nickel exposure can cause DNA oxidative damage and influence DNA repair. However, the underlying mechanism of nickel-induced high-risk of lung cancer has not been fully understood. Our study aims to evaluate whether the nickel-induced oxidative damage and DNA repair were correlated with the alterations in Smad2 phosphorylation status and Nkx2.1 expression levels, which has been considered as the lung cancer initiation gene. Methods: 140 nickel smelters and 140 age-matched administrative officers were randomly stratified by service length from Jinchang Cohort. Canonical regression, χ2 test, Spearman correlation etc. were used to evaluate the association among service length, MDA, 8-OHdG, hOGG1, PARP, pSmad2, and Nkx2.1. Results: The concentrations of MDA, PARP, pSmad2, and Nkx2.1 significantly increased. Nkx2.1 (rs = 0.312, p < 0.001) and Smad2 phosphorylation levels (rs = 0.232, p = 0.006) were positively correlated with the employment length in nickel smelters, which was not observed in the administrative officer group. Also, elevation of Nkx2.1 expression was positively correlated with service length, 8-OHdG, PARP, hOGG1 and pSmad2 levels in nickel smelters. Conclusions: Occupational nickel exposure could increase the expression of Nkx2.1 and pSmad2, which correlated with the nickel-induced oxidative damage and DNA repair change.

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