n-Alkyl glucopyranosides completely inhibit ultrasound-induced cytolysis.
n-Alkyl glucopyranosides completely inhibit ultrasound-induced cytolysis.
复制标题
正烷基吡喃葡萄糖苷完全抑制超声诱导的细胞溶解。
DOI:
10.1016/j.freeradbiomed.2005.07.020
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发表时间:
2005
影响因子:
7.4
通讯作者:
Mitchell,JamesB
中科院分区:
文献类型:
--
作者:
Sostaric,JoeZ;Miyoshi,Norio;Riesz,Peter;DeGraff,WilliamG;Mitchell,JamesB
The mechanism(s) responsible for sudden cytolysis observed when cells are exposed to ultrasound could be mechanical and/or free radical in nature. Free radical reactions are initiated in the core and in the interfacial regions of collapsing acoustic cavitation bubbles. Because cyclic sugars are known to inhibit free radical chain reactions, we investigated the effects of n-alkyl-β-d-glucopyranosides of varying hydrophobicity on ultrasound (1.057 MHz)-induced cytolysis of HL-60 cells in vitro. n-Alkyl glucopyranosides with hexyl- (5 mM), heptyl- (3 mM), or octyl- (2 mM) n-alkyl chains protected 100% of the cell population from ultrasound-induced cytolysis under a range of conditions that resulted in 35 to 100% cytolysis in the absence of glucopyranosides. The protected cell populations also possessed long-term reproductive viability. However, the hydrophilic methyl-β-d-glucopyranoside could not protect cells, even up to a concentration of 30 mM. Furthermore, none of the glucopyranosides could prevent cytolysis of cells from a mechanically induced shear stress. Spin trapping and electron spin resonance experiments confirmed the presence of inertial cavitation in cell suspensions both in the presence and in the absence of the surfactants. It is concluded that surface-active glucopyranosides efficiently quench cytotoxic radicals and/or their precursors at the gas/solution interface of collapsing cavitation bubbles.