ArticleJournal of clinical biochemistry and nutrition2010
Protection by Exogenously Added Coenzyme Q(9) against Free Radical-Induced Injuries in Human Liver Cells.
Article in Journal of clinical biochemistry and nutrition, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Molecular mechanisms underlying the promotion of wound repair by coenzyme Q10: PI3K/Akt signal activation via alterations to cell membrane domains.Journal of clinical biochemistry and nutrition · 2022Article
- Study on Hepatotoxicity of Rhubarb Based on Metabolomics and Network Pharmacology.Drug design, development and therapy · 2021Article
- Protective effects of methanolic extract form fruits of Lycium ruthenicum Murr on 2,2'-azobis (2-amidinopropane) dihydrochloride-induced oxidative stress in LLC-PK1 cells.Pharmacognosy magazine · 2014Article
- Antcin C from Antrodia cinnamomea Protects Liver Cells Against Free Radical-Induced Oxidative Stress and Apoptosis In Vitro and In Vivo through Nrf2-Dependent Mechanism.Evidence-based complementary and alternative medicine : eCAM · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Reduced coenzyme Q(10) (CoQ(10)H(2)) is known as a potent antioxidant in biological systems. However, it is not yet known whether CoQ(9)H(2) could act as an antioxidant in human cells. The aim of this study is to assess whether exogenously added CoQ(9) can protect human liver cells against injuries induced by a water-soluble radical initiator, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and a lipid-soluble radical initiator, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). CoQ(9)-enriched cells were obtained by treatment of HepG2 cells with 10 microM CoQ(9) liposomes for 24 h. CoQ(9)-enriched cells were exposed to 10 mM AAPH and 500 microM AMVN over 4 h and 24 h, respectively. The loss of viability after treatment with AAPH or AMVN was much less in CoQ(9)-enriched cells than in naive HepG2 cells. The decrease in glutathione and the increase in thiobarbituric acid-reactive substance after treatment with AAPH or AMVN were also suppressed in CoQ(9)-enriched cells. The incubation of CoQ(9)-enriched cells with AAPH or AMVN led to a decrease in cellular CoQ(9)H(2) and reciprocal increase in cellular CoQ(9) resulting from its antioxidant function. Taken together, it was demonstrated for the first time that exogenously added CoQ(9) could prevent oxidative stress-mediated damage to human cells by virtue of its antioxidant activity.
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