Related Experiment Video
Updated: May 30, 2026

13:20
Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
[Effects of electric pulses on liver cancer cells: apoptosis induction and decrease of mitochondrial transmembrane
Jie Cheng1, Liling Tang, Deyou Xiao
1Key Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, China.
Summary
Electric pulses can induce cancer cell apoptosis, with longer exposure times increasing the effect. Tumor cells are more sensitive to electric pulses than normal cells, suggesting a potential therapeutic mechanism.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Cancer Research
Context:
- Investigating novel cancer treatment modalities.
- Understanding cellular responses to physical stimuli.
- Exploring apoptosis induction mechanisms in cancer cells.
Purpose:
- To determine the efficacy of electric pulses in inducing apoptosis in HepG2 and L02 cancer cells.
- To analyze the dose-dependent relationship between electric pulse duration and cancer cell apoptosis.
- To investigate the role of mitochondrial transmembrane potential in electric pulse-induced apoptosis.
Summary:
- HepG2 and L02 cells were exposed to electric pulses (1 kV/cm, 100 µs, 1 Hz) for varying durations (8s, 15s, 30s, 60s).
- Apoptosis was induced at stimulation times of 15s and longer, with increased apoptosis percentage correlating with longer exposure.
- Tumor cells exhibited higher sensitivity to electric pulses compared to normal cells, and mitochondrial pathway involvement was suggested by changes in mitochondrial transmembrane potential.
Impact:
- Establishes electric pulses as a potential method for inducing cancer cell apoptosis.
- Highlights the differential sensitivity of tumor versus normal cells to electric pulses.
- Provides insights into the biophysical mechanisms underlying electric pulse-induced cell death, particularly the mitochondrial pathway.
Related Concept Videos
Cellular Injury IV: Necrosis
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

