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光催化TiO₂反应的杀菌活性:对其杀灭机制的理解

Bactericidal activity of photocatalytic TiO(2) reaction: toward an understanding of its killing mechanism.

作者信息

Maness P C, Smolinski S, Blake D M, Huang Z, Wolfrum E J, Jacoby W A

机构信息

The National Renewable Energy Laboratory, Golden, Colorado 80401-3393, USA.

出版信息

Appl Environ Microbiol. 1999 Sep;65(9):4094-8. doi: 10.1128/AEM.65.9.4094-4098.1999.

Abstract

When titanium dioxide (TiO(2)) is irradiated with near-UV light, this semiconductor exhibits strong bactericidal activity. In this paper, we present the first evidence that the lipid peroxidation reaction is the underlying mechanism of death of Escherichia coli K-12 cells that are irradiated in the presence of the TiO(2) photocatalyst. Using production of malondialdehyde (MDA) as an index to assess cell membrane damage by lipid peroxidation, we observed that there was an exponential increase in the production of MDA, whose concentration reached 1.1 to 2.4 nmol. mg (dry weight) of cells(-1) after 30 min of illumination, and that the kinetics of this process paralleled cell death. Under these conditions, concomitant losses of 77 to 93% of the cell respiratory activity were also detected, as measured by both oxygen uptake and reduction of 2,3,5-triphenyltetrazolium chloride from succinate as the electron donor. The occurrence of lipid peroxidation and the simultaneous losses of both membrane-dependent respiratory activity and cell viability depended strictly on the presence of both light and TiO(2). We concluded that TiO(2) photocatalysis promoted peroxidation of the polyunsaturated phospholipid component of the lipid membrane initially and induced major disorder in the E. coli cell membrane. Subsequently, essential functions that rely on intact cell membrane architecture, such as respiratory activity, were lost, and cell death was inevitable.

摘要

当用近紫外光照射二氧化钛(TiO₂)时,这种半导体表现出很强的杀菌活性。在本文中,我们首次证明脂质过氧化反应是在TiO₂光催化剂存在下被照射的大肠杆菌K - 12细胞死亡的潜在机制。以丙二醛(MDA)的产生作为评估脂质过氧化对细胞膜损伤的指标,我们观察到MDA的产生呈指数增加,光照30分钟后其浓度达到1.1至2.4 nmol·mg(干重)细胞⁻¹,并且这个过程的动力学与细胞死亡平行。在这些条件下,通过以琥珀酸盐作为电子供体的氧摄取和2,3,5 - 三苯基氯化四氮唑的还原测量,还检测到细胞呼吸活性同时损失了77%至93%。脂质过氧化的发生以及膜依赖性呼吸活性和细胞活力的同时丧失严格依赖于光和TiO₂的存在。我们得出结论,TiO₂光催化最初促进了脂质膜中多不饱和磷脂成分的过氧化,并在大肠杆菌细胞膜中引发了重大紊乱。随后,依赖完整细胞膜结构的基本功能,如呼吸活性,丧失,细胞死亡不可避免。

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