Related Experiment Video

Updated: Jul 22, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

The effect of drugs and toxins on the process of apoptosis

R Cameron1, G Feuer

  • 1Department of Pathology, University of Toronto, Toronto General Hospital, Canada.

Drug Metabolism and Drug Interactions
|August 28, 2001
PubMed

Insights

This review explores how drugs modify apoptosis, a crucial cell death process. Understanding these drug-cell interactions could lead to new treatments for diseases involving apoptosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Apoptosis, or programmed cell death, is fundamental to numerous physiological and pathological processes.
  • This complex process involves distinct stages: initiation, signal transduction, effector mechanisms, nuclear fragmentation, and clearance via phagocytosis.
  • Dysregulation of apoptosis is implicated in various human diseases.

Purpose of the Study:

  • To review the modifying effects of specific drugs on apoptosis.
  • To elucidate the mechanisms by which pharmacological agents interact with apoptotic pathways.
  • To highlight the therapeutic potential of targeting drug-induced apoptosis modulation.

Main Methods:

  • Literature review of studies investigating drug effects on apoptosis.
  • Analysis of experimental data on drug-induced apoptosis in different cell types.
  • Examination of the concentration-dependent and drug-specific modulatory actions.

Main Results:

  • Specific drugs, such as glucocorticoids, can either induce or inhibit apoptosis.
  • The effect of a drug on apoptosis is dependent on the drug type, concentration, and cell context.
  • Evidence suggests diverse mechanisms of drug interaction with apoptotic pathways.

Conclusions:

  • Modulating apoptosis with pharmacological agents presents a promising therapeutic strategy.
  • Further understanding of drug-apoptosis interactions is essential for developing novel treatments.
  • Targeting apoptosis holds potential for managing diseases where this cell death pathway is critical.

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Detection and Isolation of Apoptotic Bodies to High Purity12:17

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Related Concept Videos

Apoptosis01:30

Apoptosis

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.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Cellular Injury V: Apoptosis and Autophagy01:22

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...