ArticleToxicology research2023
Salidroside protect Chinese hamster V79 cells from genotoxicity and oxidative stress induced by CL-20.
Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Toxicological evaluation of bioengineered salidroside produced by a novel method.Toxicology reports · 2026Article
- Toxic Effects of the Most Common Components of Energetic Co-Crystals.Molecules (Basel, Switzerland) · 2025Review
- Article
- Biological Activity of Hexaazaisowurtzitane Derivatives.Molecules (Basel, Switzerland) · 2023Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hexanitrohexaazaisowurtzitane (CL-20) is a high-energy elemental explosive widely used in chemical and military fields. CL-20 harms environmental fate, biosafety, and occupational health. However, there is little known about the genotoxicity of CL-20, in particular its molecular mechanisms. Therefore, this study was framed to investigate the genotoxic mechanisms of CL-20 in V79 cells and evaluate whether the genotoxicity could be diminished by pretreating the cells with salidroside. The results showed that CL-20-induced genotoxicity in V79 cells primarily through oxidative damage to DNA and mitochondrial DNA (mtDNA) mutation. Salidroside could significantly reduce the inhibitory effect of CL-20 on the growth of V79 cells and reduce the levels of reactive oxygen species (ROS), 8-hydroxy-2 deoxyguanosine (8-OHdG), and malondialdehyde (MDA). Salidroside also restored CL-20-induced superoxide dismutase (SOD) and glutathione (GSH) in V79 cells. As a result, salidroside attenuated the DNA damage and mutations induced by CL-20. In conclusion, oxidative stress may be involved in CL-20-induced genotoxicity in V79 cells. Salidroside could protect V79 cells from oxidative damage induced by CL-20, mechanism of which may be related to scavenging intracellular ROS and increasing the expression of proteins that can promote the activity of intracellular antioxidant enzymes. The present study for the mechanisms and protection of CL-20-mediated genotoxicity will help further to understand the toxic effects of CL-20 and provide information on the therapeutic effect of salidroside in CL-20-induced genotoxicity.
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Registered trials
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