Oxidative stress‐related DNA damage and homologous recombination repairing induced by <i>N</i>,<i>N</i>‐dimethylformamide

Wang, Cui; Yang, Jinhuan; Lu, Dezhao; Fan, Yongsheng; Zhao, Meirong; Li, Zhuoyu

doi:10.1002/jat.3226

Cited by 27 publications

(16 citation statements)

References 53 publications

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“…4b, c), highlighting potential roles of internal m 7 G in CDS and 3′UTR in regulating stress response. Hence, we selected marker genes for DNA repair (GADD45A, 64 BTG2 65 and XRCC2 66 ) and reactive oxygen species (ROS)-related pathways (PCNA, 67 CBX4 68 and SOD2 69 ) and examined mRNA m 7 G modification profiles upon oxidative stress. These gene transcripts displayed a strong internal m 7 G enrichment in CDS and 3′UTR, (Fig.…”

Section: S Rrna M 7 G1639 Identification By a Modified Miclip-seqmentioning

confidence: 99%

Dynamic methylome of internal mRNA N7-methylguanosine and its regulatory role in translation

et al. 2019

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Over 150 types of RNA modifications are identified in RNA molecules. Transcriptome profiling is one of the key steps in decoding the epitranscriptomic panorama of these chemical modifications and their potential functions. N 7-methylguanosine (m 7 G) is one of the most abundant modifications present in tRNA, rRNA and mRNA 5′cap, and has critical roles in regulating RNA processing, metabolism and function. Besides its presence at the cap position in mRNAs, m 7 G is also identified in internal mRNA regions. However, its transcriptome-wide distribution and dynamic regulation within internal mRNA regions remain unknown. Here, we have established m 7 G individual-nucleotide-resolution cross-linking and immunoprecipitation with sequencing (m 7 G miCLIP-seq) to specifically detect internal mRNA m 7 G modification. Using this approach, we revealed that m 7 G is enriched at the 5′UTR region and AG-rich contexts, a feature that is well-conserved across different human/mouse cell lines and mouse tissues. Strikingly, the internal m 7 G modification is dynamically regulated under both H 2 O 2 and heat shock treatments, with remarkable accumulations in the CDS and 3′UTR regions, and functions in promoting mRNA translation efficiency. Consistently, a PCNA 3′UTR minigene reporter harboring the native m 7 G modification site displays both enriched m 7 G modification and increased mRNA translation upon H 2 O 2 treatment compared to the m 7 G site-mutated minigene reporter (G to A). Taken together, our findings unravel the dynamic profiles of internal mRNA m 7 G methylome and highlight m 7 G as a novel epitranscriptomic marker with regulatory roles in translation.

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Section: S Rrna M 7 G1639 Identification By a Modified Miclip-seqmentioning

confidence: 99%

Dynamic methylome of internal mRNA N7-methylguanosine and its regulatory role in translation

et al. 2019

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“…[8] Oxidation of DMF generated N-(hydroxymethyl)-N-methylformamide (HMMF) and the other derivatives, [9] which resulted in H 2 O 2 accumulation in hepatocytes [10] . On the contrary, our previous research and others have explored that reactive oxygen species (ROS) would be toxic to hepatocytes by injuring DNA, protein, and lipids [13][14][15] . The intermediate metabolite such as S-(N-methylcarbamoy1) glutathione (SMG) was regarded as the main agent of DMF toxicity [11,12] .…”

Section: Introductionmentioning

confidence: 99%

Study on the potential way of hepatic cytotoxicity of N,N‐dimethylformamide

Wang

2018

J Biochem & Molecular Tox

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The intermediate metabolites and redox status imbalance were supported as the two major points for N,N-dimethylformamide (DMF)-induced hepatotoxicity. However, the potential mechanism has not yet been concerned. By applying two inhibitors, this study tried to seek the major role in DMF-induced toxicity on HL7702 cell. We observed that DMF induced cell apoptosis through mitochondrial-dependent and p53 pathway. Inhibition reactive oxygen species by catalase remarkably attenuated the mitochondrial transmembrane potential (MMP), apoptotic proteins, and apoptosis. On the contrary, it reduced the biodegradation rate of DMF by coincubation with CYP2E1 antagonist (DDC) partially reduced late apoptosis. However, the change in MMP, the ratio of Bax to Bcl-xl, and cleaved-caspase 9 was not attenuated by DDC. The pathway in DDC coincubation groups was related to the p53 rather than the mitochondrial pathway. Restoring the redox balance during biodegradation is much more effective than attenuating the metabolite rate of DMF. This study may provide a suitable prevention method to occupational workers.

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“…Exposure to dimethylformamide in a human liver cell line exhibited reactive oxygen species production in a dose-dependent manner. This study also highlights that these reactive species inflicted oxidative DNA damage, and double strand DNA breaks, leading to cell death (Wang et al , 2016). Although benzene is a well-known hematoxicant, several mechanisms of action may also be applicable to other organ systems, such as the liver.…”

Section: Oxidative Stressmentioning

confidence: 68%

Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk

Lang

Beier

2018

Biological Chemistry

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Occupational and environmental exposures to industrial chemicals are known to cause hepatotoxicity and liver injury, in humans and in animal models. Historically, research has focused on severe acute liver injury (e.g. fulminant liver failure) or endstage diseases (e.g. cirrhosis and HCC). However, it has become recently recognized that toxicants can cause more subtle changes to the liver. For example, toxicant-associated steatohepatitis, characterized by hepatic steatosis, and inflammation, was recently recognized in an occupational cohort exposed to vinyl chloride. At high occupational levels, toxicants are sufficient to cause liver damage and disease even in healthy subjects with no comorbidities for liver injury. However, it is still largely unknown how exposure to toxicants initiate and possibly more importantly exacerbate liver disease, when combined with other factors, such as underlying non-alcoholic fatty liver disease caused by poor diet and/or obesity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease. The purpose of this review is to summarize established and proposed mechanisms of volatile organic compound-induced liver injury and to highlight key signaling events known or hypothesized to mediate these effects.

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Oxidative stress‐related DNA damage and homologous recombination repairing induced by N,N‐dimethylformamide

Cited by 27 publications

References 53 publications

Dynamic methylome of internal mRNA N7-methylguanosine and its regulatory role in translation

Dynamic methylome of internal mRNA N7-methylguanosine and its regulatory role in translation

Study on the potential way of hepatic cytotoxicity of N,N‐dimethylformamide

Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk

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