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Involvement of reactive oxygen species in sonodynamically induced apoptosis using a novel porphyrin derivative.

Yumita N, Iwase Y, Nishi K, Komatsu H, Takeda K, Onodera K, Fukai T, Ikeda T, Umemura S, Okudaira K, Momose Y - Theranostics (2012)

Bottom Line: Sonodynamically induced apoptosis, caspase-3 activation, and nitroxide generation were significantly suppressed by histidine.The significant reduction in sonodynamically induced apoptosis, nitroxide generation, and caspase-3 activation by histidine suggests active species such as singlet oxygen are important in the sonodynamic induction of apoptosis.These experimental results support the possibility of sonodynamic treatment for cancer using the induction of apoptosis.

View Article: PubMed Central - PubMed

Affiliation: 1. School of Pharmacy, Yokohama College of Pharmacy, 601, Matano-cho, Totsuka-ku, Yokohama, Kanagawa 245-0066, Japan;

ABSTRACT
In this study, we investigated the induction of apoptosis by ultrasound in the presence of the novel porphyrin derivative DCPH-P-Na(I). HL-60 cells were exposed to ultrasound for up to 3 min in the presence and absence of DCPH-P-Na(I), and the induction of apoptosis was examined by analyzing cell morphology, DNA fragmentation, and caspase-3 activity. Reactive oxygen species were measured by means of ESR and spin trapping technique. Cells treated with 8 μM DCPH-P-Na(I) and ultrasound clearly showed membrane blebbing and cell shrinkage, whereas significant morphologic changes were not observed in cells exposed to either ultrasound or DCPH-P-Na(I) alone. Also, DNA ladder formation and caspase-3 activation were observed in cells treated with both ultrasound and DCPH-P-Na(I) but not in cells treated with ultrasound or DCPH-P-Na(I) alone. In addition, the combination of DCPH-P-Na(I) and the same acoustical arrangement of ultrasound substantially enhanced nitroxide generation by the cells. Sonodynamically induced apoptosis, caspase-3 activation, and nitroxide generation were significantly suppressed by histidine. These results indicate that the combination of ultrasound and DCPH-P-Na(I) induced apoptosis in HL-60 cells. The significant reduction in sonodynamically induced apoptosis, nitroxide generation, and caspase-3 activation by histidine suggests active species such as singlet oxygen are important in the sonodynamic induction of apoptosis. These experimental results support the possibility of sonodynamic treatment for cancer using the induction of apoptosis.

No MeSH data available.


Related in: MedlinePlus

Effect of active oxygen scavengers on A) ultrasonically induced apoptosis, B) caspase-3 activation and C) ultrasonic nitroxide generation in the presence (●) and absence (○) of 8 μM DCPH-P-Na(I). Values represent the means ± S.D. of four independent experiments. The asterisk symbol indicates significant difference from no scavenger treatment at P < 0.05.
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Figure 5: Effect of active oxygen scavengers on A) ultrasonically induced apoptosis, B) caspase-3 activation and C) ultrasonic nitroxide generation in the presence (●) and absence (○) of 8 μM DCPH-P-Na(I). Values represent the means ± S.D. of four independent experiments. The asterisk symbol indicates significant difference from no scavenger treatment at P < 0.05.

Mentions: To determine whether reactive oxygen species including singlet oxygen and hydroxyl radicals participate in the induction of apoptosis by ultrasound, we examined the effect of reactive oxygen scavengers (10 mM histidine, 100 μg/ml SOD, and 100 mM mannitol) on the fraction of cells showing morphological changes associated with apoptosis as well as on the caspase-3 activity and the production of nitroxide (Figures 5A-C). Histidine significantly reduced the apoptosis induction, caspase-3 activation, and nitroxide generation caused by exposure to ultrasound in the presence of DCPH-P-Na(I). In contrast, SOD and mannitol did not affect these measurements.


Involvement of reactive oxygen species in sonodynamically induced apoptosis using a novel porphyrin derivative.

Yumita N, Iwase Y, Nishi K, Komatsu H, Takeda K, Onodera K, Fukai T, Ikeda T, Umemura S, Okudaira K, Momose Y - Theranostics (2012)

Effect of active oxygen scavengers on A) ultrasonically induced apoptosis, B) caspase-3 activation and C) ultrasonic nitroxide generation in the presence (●) and absence (○) of 8 μM DCPH-P-Na(I). Values represent the means ± S.D. of four independent experiments. The asterisk symbol indicates significant difference from no scavenger treatment at P < 0.05.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3475214&req=5

Figure 5: Effect of active oxygen scavengers on A) ultrasonically induced apoptosis, B) caspase-3 activation and C) ultrasonic nitroxide generation in the presence (●) and absence (○) of 8 μM DCPH-P-Na(I). Values represent the means ± S.D. of four independent experiments. The asterisk symbol indicates significant difference from no scavenger treatment at P < 0.05.
Mentions: To determine whether reactive oxygen species including singlet oxygen and hydroxyl radicals participate in the induction of apoptosis by ultrasound, we examined the effect of reactive oxygen scavengers (10 mM histidine, 100 μg/ml SOD, and 100 mM mannitol) on the fraction of cells showing morphological changes associated with apoptosis as well as on the caspase-3 activity and the production of nitroxide (Figures 5A-C). Histidine significantly reduced the apoptosis induction, caspase-3 activation, and nitroxide generation caused by exposure to ultrasound in the presence of DCPH-P-Na(I). In contrast, SOD and mannitol did not affect these measurements.

Bottom Line: Sonodynamically induced apoptosis, caspase-3 activation, and nitroxide generation were significantly suppressed by histidine.The significant reduction in sonodynamically induced apoptosis, nitroxide generation, and caspase-3 activation by histidine suggests active species such as singlet oxygen are important in the sonodynamic induction of apoptosis.These experimental results support the possibility of sonodynamic treatment for cancer using the induction of apoptosis.

View Article: PubMed Central - PubMed

Affiliation: 1. School of Pharmacy, Yokohama College of Pharmacy, 601, Matano-cho, Totsuka-ku, Yokohama, Kanagawa 245-0066, Japan;

ABSTRACT
In this study, we investigated the induction of apoptosis by ultrasound in the presence of the novel porphyrin derivative DCPH-P-Na(I). HL-60 cells were exposed to ultrasound for up to 3 min in the presence and absence of DCPH-P-Na(I), and the induction of apoptosis was examined by analyzing cell morphology, DNA fragmentation, and caspase-3 activity. Reactive oxygen species were measured by means of ESR and spin trapping technique. Cells treated with 8 μM DCPH-P-Na(I) and ultrasound clearly showed membrane blebbing and cell shrinkage, whereas significant morphologic changes were not observed in cells exposed to either ultrasound or DCPH-P-Na(I) alone. Also, DNA ladder formation and caspase-3 activation were observed in cells treated with both ultrasound and DCPH-P-Na(I) but not in cells treated with ultrasound or DCPH-P-Na(I) alone. In addition, the combination of DCPH-P-Na(I) and the same acoustical arrangement of ultrasound substantially enhanced nitroxide generation by the cells. Sonodynamically induced apoptosis, caspase-3 activation, and nitroxide generation were significantly suppressed by histidine. These results indicate that the combination of ultrasound and DCPH-P-Na(I) induced apoptosis in HL-60 cells. The significant reduction in sonodynamically induced apoptosis, nitroxide generation, and caspase-3 activation by histidine suggests active species such as singlet oxygen are important in the sonodynamic induction of apoptosis. These experimental results support the possibility of sonodynamic treatment for cancer using the induction of apoptosis.

No MeSH data available.


Related in: MedlinePlus