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Updated: Jun 14, 2026

Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Antimutagenic activity of mitochondria-targeted plastoquinone derivative
V A Chistyakov1, M A Sazykina, A A Alexandrova
1Research Institute of Biology, Southern Federal University, Rostov-on-Don, Russia. vladimirchi@yandex.ru
Abstract:
The ability of cationic plastoquinone derivative 10-(6'-plastoquinonyl) decyltriphenylphosphonium (SkQ1) to modify processes of spontaneous and induced mutagenesis was studied. It is shown that daily introduction of this compound into male Wistar rats in doses of 25 and 250 nmol/kg during two weeks decreases spontaneous level of chromosome aberrations in anaphase in the eye cornea from 0.39 +/- 0.09 to 0.13 +/- 0.08 and 0.14 +/- 0.05, respectively. The level of 8-hydroxy-2'-deoxyguanosine in blood serum of the investigated animals decreases from 32.12 +/- 1.55 to 25.90 +/- 2.26 and 25.76 +/- 1.50 ng/ml, respectively. These facts indicate that the decrease in spontaneous clastogenesis is caused by decreased level of DNA damage by endogenous reactive oxygen species. A higher dose of SkQ1 also decreases to control level chromosome aberrations caused by oxygen under pressure of 0.5 MPa for 60 min. It is also shown in experiments with bacterial biosensors that SkQ1 is able to efficiently protect cells against genotoxic effect of UV radiation at 300-400 nm.
Insights
The cationic plastoquinone derivative SkQ1 significantly reduces spontaneous and induced mutagenesis in rats by lowering DNA damage from reactive oxygen species. SkQ1 also protects against genotoxicity from UV radiation.
Area of Science:
- Mitochondrial biochemistry
- Genetics
- Toxicology
Background:
- Mitochondria are key sources of reactive oxygen species (ROS) implicated in mutagenesis.
- Plastoquinone derivatives are investigated for their potential antioxidant and antimutagenic properties.
Purpose of the Study:
- To evaluate the antimutagenic and radioprotective effects of the cationic plastoquinone derivative SkQ1.
- To assess SkQ1's impact on spontaneous and induced mutagenesis in vivo and in vitro.
Main Methods:
- Administration of SkQ1 to male Wistar rats to measure chromosome aberrations and 8-hydroxy-2'-deoxyguanosine levels.
- Exposure of rats to hyperoxia to induce chromosome aberrations.
- Testing SkQ1's protective effects against UV radiation using bacterial biosensors.
Main Results:
- Daily SkQ1 administration decreased spontaneous chromosome aberrations and 8-hydroxy-2'-deoxyguanosine levels in rats.
- A high dose of SkQ1 reduced hyperoxia-induced chromosome aberrations.
- SkQ1 demonstrated protective effects against UV-induced genotoxicity in bacterial biosensors.
Conclusions:
- SkQ1 effectively reduces DNA damage caused by endogenous ROS, thereby decreasing spontaneous mutagenesis.
- SkQ1 exhibits protective capabilities against induced mutagenic factors, including oxidative stress and UV radiation.
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