Abstract
Many anti-tumor drugs can induce tumor apoptosis by increasing intracellular ROS. In the present study, we build a model which did not directly cause DNA damage, but simulated damage products. The model of this injury was transferred into the cell so that the cell’s damage recognition mechanism mistakenly recognized that its own DNA was damaged, which in turn induced a response. Based on this model, the damaged plasmids (exogenous DNA damage) were transferred into the cells and the amount of reactive oxygen in the cells was improved, and DNA damage of the cells was increased. Therefore, exogenous DNA damage can affect the accumulation of damage in cells by affecting the level of reactive oxygen species, which provides a reference for DNA damage repair research.
Highlights
Exogenous injury refers to the treatment of oligonucleotides in vitro with drugs, resulting in various types of DNA damage
The plasmid was treated with different concentrations of drug and the Reactive oxygen species (ROS) produced by the cells were transfected (Fig. 2a, 2b, 2c)
Green represents the ROS produced by the cells, and red is the plamid color, indicating that the plasmid was successfully transferred into the cell, and the last column is the merge of ROS plasmid
Summary
Exogenous injury refers to the treatment of oligonucleotides in vitro with drugs, resulting in various types of DNA damage. The main target of DNA, which can cause DNA chain cross-linking, thereby inhibiting cell DNA replication, cisplatin is the first generation of platinum anti-cancer drugs [1,2]. Oxaliplatin is combined covalently with G and may form an inter-chain crosslink, blocking DNA replication and transcription [3,4,5]. Under ultraviolet (UVA) exposure, react with DNA to form a type of DNA injury - inter-strand crosslink (ICL) [6,7]. The DNA containing the damage is transferred to the human cells, whether the response in the cell will be induced. The response change of reactive oxygen was mainly explored
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