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新型卟啉衍生物 DCPH-P-Na(I)通过声动力学诱导细胞损伤和膜脂质过氧化。

Sonodynamically induced cell damage and membrane lipid peroxidation by novel porphyrin derivative, DCPH-P-Na(I).

机构信息

Yokohama College of Pharmacy, 601, Matano-cho, Totsuka-ku, Yokohama, Kanagawa 245-0066, Japan.

出版信息

Anticancer Res. 2010 Jun;30(6):2241-6.

Abstract

BACKGROUND

Ultrasonically induced cell damage and active oxygen generation with a novel porphyrin derivative DCPH-P-Na(I), were compared in the same in vitro insonation setup.

MATERIALS AND METHODS

Sarcoma 180 cells suspended in air-saturated PBS were exposed to ultrasound at 2 MHz for up to 60 s in the presence and absence of DCPH-P-Na(I). Cell viability was determined with the trypan blue exclusion test. Lipid peroxidation in cell membranes was estimated by measuring the amount of reactive substance produced immediately following the addition of thiobarbituric acid.

RESULTS

Significant enhancement of the rates of both ultrasonically induced cell damage and lipid peroxidation was observed in the presence of 2-8 muM DCPH-P-Na(I). Both rates correlated very well.

CONCLUSION

The enhancement of both rates with DCPH-P-Na(I) was suppressed by 10 mM histidine. These results suggest that ultrasonically generated active oxygen plays a primary role in the ultrasonically induced cell damage in the presence of DCPH-P-Na(I).

摘要

背景

在相同的体外超声设置中,比较了新型卟啉衍生物 DCPH-P-Na(I)诱导的超声细胞损伤和活性氧生成。

材料和方法

悬浮在空气饱和 PBS 中的肉瘤 180 细胞在 2MHz 超声下暴露长达 60 秒,存在和不存在 DCPH-P-Na(I)的情况下。用台盼蓝排除试验测定细胞活力。通过测量加入硫代巴比妥酸后立即产生的反应物质的量来估计细胞膜中的脂质过氧化。

结果

在 2-8 μM DCPH-P-Na(I)存在下,超声诱导的细胞损伤和脂质过氧化的速率均显著增强。两种速率相关性非常好。

结论

DCPH-P-Na(I)增强两种速率的作用被 10mM 组氨酸抑制。这些结果表明,在 DCPH-P-Na(I)存在下,超声产生的活性氧在超声诱导的细胞损伤中起主要作用。

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