Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
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...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Alpha1,4GlcNAc-capped mucin-type O-glycan inhibits cholesterol alpha-glucosyltransferase from Helicobacter pylori and suppresses H. pylori growth.

Glycobiology·2008
Same author

Molecularly imprinted poly (methacrylamide-co-methacrylic acid) composite membranes for recognition of curcumin.

Analytica chimica acta·2008
Same author

[Research progress of the olfactory neural system recognition model].

Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi·2008
Same author

Enzymic thin film coatings for bioactive materials.

Biotechnology progress·2008
Same author

Orexigenic hormone ghrelin attenuates local and remote organ injury after intestinal ischemia-reperfusion.

PloS one·2008
Same author

[Application of carboxylated polystyrene latex particles in the detection of aflatoxin B1].

Wei sheng yan jiu = Journal of hygiene research·2008

Related Experiment Video

Updated: Jun 12, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Induced endogenous autotoxicity in Camptotheca.

Shiyou Li1, Ping Wang, Wei Yuan

  • 1National Center for Pharmaceutical Crops, Arthur Temple College of Forestry and Agriculture, Stephen F Austin State University, Nacogdoches, TX 75962, USA. lis@sfasu.edu

Frontiers in Bioscience (Elite Edition)
|June 3, 2010
PubMed
Summary

Plants can experience autotoxicity from their own toxic compounds, like camptothecin. Pruning can trigger this, causing abnormal growth, but it resolves when the toxic compound levels decrease.

More Related Videos

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)
11:38

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)

Published on: May 10, 2016

Related Experiment Videos

Last Updated: Jun 12, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)
11:38

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents (HPHC)

Published on: May 10, 2016

Area of Science:

  • Plant physiology
  • Biochemistry
  • Developmental biology

Background:

  • Plants produce toxic secondary metabolites for defense.
  • Camptotheca plants tolerate high levels of endogenous camptothecin.
  • Pruning typically promotes lateral growth.

Purpose of the Study:

  • To investigate if plants can be harmed by their own toxic compounds (autotoxicity).
  • To determine the effect of pruning on endogenous camptothecin levels and plant morphology.
  • To explore the role of auxin in camptothecin-induced autotoxicity.

Main Methods:

  • Observing morphological changes in Camptotheca plants after decapitation pruning.
  • Measuring endogenous camptothecin levels in pruned and control plants.
  • Applying exogenous auxin to a high-camptothecin yielding mutant.

Main Results:

  • Decapitation pruning induced autotoxicity, leading to abnormal morphogenesis (serrated leaves, fasciated stems).
  • Abnormal growth correlated with elevated camptothecin levels post-pruning.
  • Autotoxicity symptoms resolved when camptothecin levels returned to normal.
  • Exogenous auxin application normalized a high-yield mutant's phenotype.

Conclusions:

  • Plants are not always immune to their endogenous toxic secondary metabolites.
  • Pruning can induce autotoxicity in Camptotheca, mediated by camptothecin.
  • Auxin may play a role in triggering this endogenous autotoxicity.