Cell Autonomous Toxicity
Cell Autonomous Toxicity - Related Videos
04:47
Autonomously Bioluminescent Mammalian Cells for Continuous and Real-time Monitoring of Cytotoxicity
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Cited by 7 •
2013
Mammalian cells expressing the bacterial bioluminescence gene cassette (lux) produce light autonomously. The resulting bioluminescent dynamics upon chemical exposure have been demonstrated to reflect the treatment effects on cellular growth and metabolism, making these cells an inexpensive, continuous, real-time toxicity screening tool that can easily be adapted for high-throughput automation.
11:40
Quantitative Autonomic Testing
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Cited by 179 •
2011
Standardized, comprehensive and fully quantitative testing of autonomic functions is described. The autonomic tests consist of evaluation of all three major autonomic domains including cardiovagal, adrenergic and sudomotor. The severity and distribution of dysautonomia is quantitated using Composite Autonomic Severity Scores.
09:49
Kupffer Cell Isolation for Nanoparticle Toxicity Testing
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Cited by 28 •
2015
Liver macrophages, named Kupffer cells, are responsible for the capture of circulating nanoparticles. We describe here a method, of high cell purity and yield, for Kupffer cell isolation. The modified LDH assay is used here to measure the toxicity induced by carbon nanotubes in Kupffer cells.
12:57
Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
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Cited by 189 •
2015
Prion-like propagation of protein aggregates has recently emerged as being implicated in many neurodegenerative diseases. The goal of this protocol is to describe, how to use the nematode C. elegans as a model system to monitor protein spreading and to investigate prion-like phenomena.
08:48
Stable and Efficient Genetic Modification of Cells in the Adult Mouse V-SVZ for the Analysis of Neural Stem Cell Autonomous and Non-autonomous Effects
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Cited by 2 •
2016
Here we describe a procedure based on the use of lentiviral particles for the long-term genetic modification of neural stem cells and/or their adjacent ependymal cells in the adult ventricular-subventricular neurogenic niche which allows the separate analysis of cell autonomous and non-autonomous, niche-dependent effects on neural stem cells.
FAQs
Cell-autonomous toxicity can become evident when a toxic agent disrupts mitochondrial function, protein homeostasis, or membrane integrity inside the affected cell. These failures compromise core cellular maintenance and can activate stress responses. Examining which process changes first helps investigators connect the agent’s intracellular action with subsequent injury or death.
To separate cell-intrinsic effects from non-cell-autonomous signaling, investigators ask whether injury tracks with direct intracellular action or with signals generated by neighboring cells. This distinction matters because tissue-level inflammation or intercellular communication can obscure the susceptibility of the affected cell. The comparison clarifies whether a response reflects cellular vulnerability or surrounding-cell influence.
The final cellular outcome is not the only informative result. A cell may activate stress responses, undergo apoptosis or necrosis, or lose function after exposure. Recording these outcomes separately can show whether toxicity produces a particular form of cell death, severe injury, or impaired activity, helping connect intracellular disruption to its biological consequence.
Cell-autonomous toxicity assays can focus on mitochondrial function, protein homeostasis, membrane integrity, stress responses, and cell fate. Measuring these features alongside injury, death, or loss of function provides a way to trace effects from intracellular disruption to outcome. This makes the assay useful for identifying the cellular process most closely associated with toxicity.
In genetic screening, these assays help identify genes or cellular pathways that alter responses to drugs or environmental toxins. Screening can connect differences in toxicity with machinery controlling mitochondrial function, protein homeostasis, membrane integrity, or stress responses. The resulting information supports discovery of factors that determine how susceptible individual cells are to harmful agents.
In disease modeling, the approach helps examine how intrinsic cellular susceptibility contributes to injury without treating neighboring-cell signals as the only explanation. In therapeutic safety testing, it can reveal direct cellular responses to a drug, while environmental-toxin studies can evaluate comparable intracellular damage. These applications connect mechanism-focused biology with practical assessment of harmful exposures.