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洗必泰诱导细胞毒性的潜在机制。

Mechanisms underlying chlorhexidine-induced cytotoxicity.

作者信息

Hidalgo E, Dominguez C

机构信息

Biochemistry & Molecular Biology Centre, Pharmacy Service, Vall d'Hebron Hospitals, Barcelona, Spain.

出版信息

Toxicol In Vitro. 2001 Aug-Oct;15(4-5):271-6. doi: 10.1016/s0887-2333(01)00020-0.

DOI:10.1016/s0887-2333(01)00020-0
PMID:11566548
Abstract

Chlorhexidine (CLX) is the most widely used antiseptic for wound and skin disinfection. Despite its potent bactericidal action, skin irritation is observed when it is used topically. This study aimed to evaluate the mechanisms underlying CLX-induced toxicity on human dermal fibroblasts with special emphasis on factors that may mediate or counteract its undesirable effects. Cells were exposed to CLX concentrations of 0.00005-0.025% for 3, 6, 8 or 24 h in the absence or presence of different concentrations of foetal calf serum (FCS) (2, 5 and 10%). Depletion of cell ATP occurred, in a time- and concentration-dependent manner, in all experimental conditions at [CLX] >0.001%. At 24 h of CLX exposure time, the decrease in intracellular ATP was produced from a 10-times lower CLX concentration (0.0001%). Concentrations > or =0.02% produced total loss of ATP. However, cell survival was maintained after CLX treatment for 3 and 8 h and CLX concentrations > or =0.005% were required to produce total cell death. CLX exerted an inhibitory concentration-dependent effect on DNA synthesis from concentrations as low as 0.0001%. Only FCS at 10% appeared to have a cytoprotective action against CLX-induced cytotoxicity.

摘要

氯己定(CLX)是伤口和皮肤消毒中使用最广泛的防腐剂。尽管其具有强大的杀菌作用,但局部使用时会观察到皮肤刺激。本研究旨在评估CLX对人真皮成纤维细胞产生毒性的潜在机制,特别关注可能介导或抵消其不良影响的因素。在不存在或存在不同浓度(2%、5%和10%)胎牛血清(FCS)的情况下,将细胞暴露于0.00005 - 0.025%的CLX浓度下3、6、8或24小时。在所有实验条件下,当[CLX] >0.001%时,细胞ATP以时间和浓度依赖性方式发生消耗。在CLX暴露24小时时,细胞内ATP的降低是由低10倍的CLX浓度(0.0001%)产生的。浓度≥0.02%导致ATP完全丧失。然而,CLX处理3小时和8小时后细胞存活得以维持,且需要CLX浓度≥0.005%才能导致细胞完全死亡。CLX从低至0.0001%的浓度起就对DNA合成产生浓度依赖性抑制作用。只有10%的FCS似乎对CLX诱导的细胞毒性具有细胞保护作用。

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