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Updated: Apr 20, 2026
Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Lipophilic antioxidants prevent lipopolysaccharide-induced mitochondrial dysfunction through mitochondrial biogenesis
Pedro Bullón1, Lourdes Román-Malo2, Fabiola Marín-Aguilar2
1Department of Periodontology, Dental School, University of Sevilla, Spain; Research Laboratory, Dental School, University of Sevilla, Sevilla, Spain.
Abstract:
Oxidative stress is implicated in several infectious diseases. In this regard, lipopolysaccharide (LPS), an endotoxic component, induces mitochondrial dysfunction and oxidative stress in several pathological events such as periodontal disease or sepsis. In our experiments, LPS-treated fibroblasts provoked increased oxidative stress, mitochondrial dysfunction, reduced oxygen consumption and mitochondrial biogenesis. After comparing coenzyme Q10 (CoQ10) and N-acetylcysteine (NAC), we observed a more significant protection of CoQ10 than of NAC, which was comparable with other lipophilic and hydrophilic antioxidants such as vitamin E or BHA respectively. CoQ10 improved mitochondrial biogenesis by activating PGC-1α and TFAM. This lipophilic antioxidant protection was observed in mice after LPS injection. These results show that mitochondria-targeted lipophilic antioxidants could be a possible specific therapeutic strategy in pharmacology in the treatment of infectious diseases and their complications.
Insights
Coenzyme Q10 (CoQ10) significantly protects against lipopolysaccharide (LPS)-induced oxidative stress and mitochondrial dysfunction, offering a potential therapeutic strategy for infectious diseases.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Oxidative stress and mitochondrial dysfunction are linked to infectious diseases like sepsis.
- Lipopolysaccharide (LPS) is a key endotoxin that triggers these pathological events.
Purpose of the Study:
- To investigate the protective effects of antioxidants against LPS-induced mitochondrial damage.
- To compare the efficacy of coenzyme Q10 (CoQ10) and N-acetylcysteine (NAC) in mitigating oxidative stress.
Main Methods:
- Fibroblast cultures and mouse models were treated with LPS.
- Assessed oxidative stress markers, mitochondrial function, oxygen consumption, and biogenesis.
- Evaluated the impact of CoQ10, NAC, vitamin E, and BHA.
Main Results:
- LPS induced significant oxidative stress, mitochondrial dysfunction, and reduced oxygen consumption.
- CoQ10 demonstrated superior protection compared to NAC, vitamin E, and BHA.
- CoQ10 enhanced mitochondrial biogenesis by activating PGC-1α and TFAM.
Conclusions:
- Mitochondria-targeted lipophilic antioxidants, like CoQ10, show promise for treating infectious diseases.
- CoQ10's ability to restore mitochondrial function presents a novel therapeutic avenue.
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