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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 lipid peroxidation in control cells and CoQ9-enriched cells following treatment with AAPH (A) or AMVN (B). Control and CoQ9-enriched cells were incubated as described in the legend to Fig. 2. Cellular TBARS content was measured as described in Materials and Methods. Data points represent the means ± SE (n = 3). *p<0.05, **p<0.01 vs control cells at the same incubation time.
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Figure 3: Changes in lipid peroxidation in control cells and CoQ9-enriched cells following treatment with AAPH (A) or AMVN (B). Control and CoQ9-enriched cells were incubated as described in the legend to Fig. 2. Cellular TBARS content was measured as described in Materials and Methods. Data points represent the means ± SE (n = 3). *p<0.05, **p<0.01 vs control cells at the same incubation time.

Mentions: We examined the effect of CoQ9 enrichment on lipid peroxidation in control cells after AAPH (10 mM) exposure (Fig. 3A). Thiobarbituric acid-reactive substance (TBARS) level in control cells increased in a time-dependent manner up to 2 h after AAPH, and thereafter reached the plateau. The TBARS level was 2.5-fold of normal level at 4 h after AAPH. In contrast, CoQ9-enriched cells kept normal TBARS levels during the incubation time period. TBARS level in control cells increased to 2.8-fold of normal level at 6 h after AMVN (500 µM) exposure, and thereafter reached the plateau (Fig. 3B). However, CoQ9-enriched cells kept almost normal TBARS levels during the incubation time period.


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 lipid peroxidation in control cells and CoQ9-enriched cells following treatment with AAPH (A) or AMVN (B). Control and CoQ9-enriched cells were incubated as described in the legend to Fig. 2. Cellular TBARS content was measured as described in Materials and Methods. Data points represent the means ± SE (n = 3). *p<0.05, **p<0.01 vs control cells at the same incubation time.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Changes in lipid peroxidation in control cells and CoQ9-enriched cells following treatment with AAPH (A) or AMVN (B). Control and CoQ9-enriched cells were incubated as described in the legend to Fig. 2. Cellular TBARS content was measured as described in Materials and Methods. Data points represent the means ± SE (n = 3). *p<0.05, **p<0.01 vs control cells at the same incubation time.
Mentions: We examined the effect of CoQ9 enrichment on lipid peroxidation in control cells after AAPH (10 mM) exposure (Fig. 3A). Thiobarbituric acid-reactive substance (TBARS) level in control cells increased in a time-dependent manner up to 2 h after AAPH, and thereafter reached the plateau. The TBARS level was 2.5-fold of normal level at 4 h after AAPH. In contrast, CoQ9-enriched cells kept normal TBARS levels during the incubation time period. TBARS level in control cells increased to 2.8-fold of normal level at 6 h after AMVN (500 µM) exposure, and thereafter reached the plateau (Fig. 3B). However, CoQ9-enriched cells kept almost normal TBARS levels during the incubation time period.

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