Ros-mediated Apoptosis
Ros-mediated Apoptosis - Related Videos
03:50
ROS Detection with DCFH-DA Staining: Measuring Total ROS in Colorectal Cancer Cell Lines
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2023
This video describes the protocol for detecting total cellular reactive oxygen species (ROS) using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). This method helps visualize ROS localization in the adherent cells using a fluorescence microscope and further quantify ROS intensity with a fluorescence plate reader.
03:47
Determination of ROS Production by Neutrophils upon Interaction with Opsonized Biofilm
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2025
In this video, we demonstrate an in vitro chemiluminescence assay to detect the generation of reactive oxygen species by neutrophils upon exposure to an opsonized bacterial biofilm.
07:33
Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS
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Cited by 10 •
2011
An efficient method to gain insights into visualizing the paracrine-derived ROS induction of endothelial Ca2+ signaling is described. This method takes advantage of measuring paracrine derived ROS triggered Ca2+ mobilization in vascular endothelial cells in a co-culture model.
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Cited by 15 •
2011
In this protocol, we describe the direct cytoplasmic microinjection of cytochrome c protein into fibroblasts and primary sympathetic neurons. This technique allows for the introduction of cytochrome c protein into the cytoplasm of cells and mimics the release of cytochrome c from mitochondria, which occurs during apoptosis.
01:30
Apoptosis
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2023
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
FAQs
Once ROS production rises beyond a cell’s antioxidant capacity, oxidative stress can disrupt cellular homeostasis rather than remain a manageable signal. The resulting damage and redox signaling can impair mitochondria, shifting the cell toward mitochondrial outer-membrane permeabilization and downstream death signaling. This relationship helps explain why redox balance is central when evaluating cancer-cell survival.
Mitochondrial outer-membrane permeabilization is a key transition connecting oxidative disruption to the execution of apoptosis. After this membrane change, cytochrome c can be released, which contributes to caspase activation. Caspases then dismantle the cell through the apoptotic program. Tracking this sequence helps researchers determine whether mitochondrial injury has progressed toward programmed cell death.
Radiation and chemotherapy can be interpreted partly through their ability to initiate or amplify oxidative stress associated with apoptotic signaling. This framework connects treatment exposure with mitochondrial impairment, cytochrome c release, and caspase activation. It helps explain how these interventions can eliminate tumor cells while directing attention to oxidative-stress defenses that may limit effectiveness.
Antioxidant systems can protect cancer cells by keeping ROS within a range that does not produce sufficient mitochondrial or cellular disruption. Their activity therefore represents a potential resistance mechanism: a tumor cell with stronger antioxidant protection may be less vulnerable to ROS-amplifying treatments or compounds. Examining this protective capacity can help interpret differences in treatment response.
Redox-active compounds can be evaluated by asking whether they increase ROS-associated disruption and activate the downstream apoptotic sequence. Evidence of impaired mitochondria, cytochrome c release, and caspase activation would connect oxidative stress with cell death rather than treating ROS as an isolated measurement. This interpretation is relevant when comparing compounds designed to affect tumor-cell survival.
Selective increases in tumor oxidative stress aim to exploit differences in redox balance between cancer cells and their surrounding context. The strategy focuses on pushing tumor cells beyond their antioxidant capacity, potentially engaging mitochondrial damage and apoptotic signaling. Studying this approach can support treatment design while also revealing why some tumors resist redox-active compounds, radiation, or chemotherapy.