Cisplatin effects on evolution of reactive oxygen species from single human bladder cancer cells investigated by scanning electrochemical microscopy

Reactive oxygen species (ROS) have gained great interests as they are closely related to cellular homeostasis and functions. New insights into physiology of cancer cells are anticipated from the analysis of their ROS evolution at single cell level. We discovered a periodical ROS evolution of human bladder cancer (T24) cells by time-lapse scanning electrochemical microscopy (SECM). We define one ROS generation cycle consists of one active stage when the cell is releasing ROS and one resting stage when the cell is not releasing ROS. Quantitative study of the extracellular ROS profile of a T24 cell in different stages was accomplished by comparison of experimental and simulated probe approach curves. In the active stage, the distribution of ROS around an untreated T24 cell was found to be steady with a long cycle of alternation. When apoptosis is triggered by cisplatin, the periodicity of the ROS generation cycle is significantly accelerated. Enhanced ROS productivity was observed with cisplatin-treated T24 cells in the active stage. With ROS released from the cells as the redox mediator, SECM provides an excellent label-free method to monitor the physiological activities of single cancer cells.

Time-lapse scanning electrochemical microscopy was applied to investigate cisplatin effects on the evolution of extracellular reactive oxygen species in the vicinity of single live human bladder cancer cells.Figure optionsDownload as PowerPoint slideHighlights
► We discovered a periodical ROS evolution of T24 cells by time-lapse SECM.
► We proposed ROS generation cycles consisting of an active stage and a resting stage.
► Depth scan images provided topography and ROS profiles simultaneously.
► ROS profiles were quantified by comparing experimental and simulated PACs.
► Cisplatin-induced apoptosis lead to greatly accelerated and enhanced ROS generation.