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Protection by Exogenously Added Coenzyme Q(9) against Free Radical-Induced Injuries in Human Liver Cells.

Kusumoto C, Kinugawa T, Morikawa H, Teraoka M, Nishida T, Murawaki Y, Yamada K, Matsura T - J Clin Biochem Nutr (2010)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.

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.

No MeSH data available.


Related in: MedlinePlus

Changes in contents of CoQn and CoQnH2 in HepG2 cells after exposure to CoQ9 liposomes. HepG2 cells were exposed to CoQ9 liposomes (10 µM) and harvested after 4, 8, 12, or 24 h. Intracellular CoQ9, CoQ9H2, CoQ10, and CoQ10H2 were measured by HPLC as described in Materials and Methods. Data points represent the means ± SE (n = 3). **p<0.01 vs CoQ9H2 at 24 h, ##p<0.01 vs CoQ9 at 24 h.
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Related In: Results  -  Collection


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Figure 1: Changes in contents of CoQn and CoQnH2 in HepG2 cells after exposure to CoQ9 liposomes. HepG2 cells were exposed to CoQ9 liposomes (10 µM) and harvested after 4, 8, 12, or 24 h. Intracellular CoQ9, CoQ9H2, CoQ10, and CoQ10H2 were measured by HPLC as described in Materials and Methods. Data points represent the means ± SE (n = 3). **p<0.01 vs CoQ9H2 at 24 h, ##p<0.01 vs CoQ9 at 24 h.

Mentions: To establish CoQ9-enriched HepG2 cells (referred to as CoQ9-enriched cells below), intracellular concentration of CoQ9, CoQ10, CoQ9H2 and CoQ10H2 was measured at 0, 4, 8, 12 or 24 h after treatment of naive HepG2 cells (referred to as control cells below) with 10 µM CoQ9 liposomes (Fig. 1). Cellular CoQ9 and CoQ9H2 levels increased in a time-dependent manner and the levels reached a maximum 24 h after addition of CoQ9 liposomes. In contrast, there were few changes in cellular contents of CoQ10 and CoQ10H2 except for the CoQ10 content at 12 h.


Protection by Exogenously Added Coenzyme Q(9) against Free Radical-Induced Injuries in Human Liver Cells.

Kusumoto C, Kinugawa T, Morikawa H, Teraoka M, Nishida T, Murawaki Y, Yamada K, Matsura T - J Clin Biochem Nutr (2010)

Changes in contents of CoQn and CoQnH2 in HepG2 cells after exposure to CoQ9 liposomes. HepG2 cells were exposed to CoQ9 liposomes (10 µM) and harvested after 4, 8, 12, or 24 h. Intracellular CoQ9, CoQ9H2, CoQ10, and CoQ10H2 were measured by HPLC as described in Materials and Methods. Data points represent the means ± SE (n = 3). **p<0.01 vs CoQ9H2 at 24 h, ##p<0.01 vs CoQ9 at 24 h.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2872230&req=5

Figure 1: Changes in contents of CoQn and CoQnH2 in HepG2 cells after exposure to CoQ9 liposomes. HepG2 cells were exposed to CoQ9 liposomes (10 µM) and harvested after 4, 8, 12, or 24 h. Intracellular CoQ9, CoQ9H2, CoQ10, and CoQ10H2 were measured by HPLC as described in Materials and Methods. Data points represent the means ± SE (n = 3). **p<0.01 vs CoQ9H2 at 24 h, ##p<0.01 vs CoQ9 at 24 h.
Mentions: To establish CoQ9-enriched HepG2 cells (referred to as CoQ9-enriched cells below), intracellular concentration of CoQ9, CoQ10, CoQ9H2 and CoQ10H2 was measured at 0, 4, 8, 12 or 24 h after treatment of naive HepG2 cells (referred to as control cells below) with 10 µM CoQ9 liposomes (Fig. 1). Cellular CoQ9 and CoQ9H2 levels increased in a time-dependent manner and the levels reached a maximum 24 h after addition of CoQ9 liposomes. In contrast, there were few changes in cellular contents of CoQ10 and CoQ10H2 except for the CoQ10 content at 12 h.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.

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.

No MeSH data available.


Related in: MedlinePlus