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

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

592
Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
592
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

890
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
890
The Periodic Table and Organismal Elements01:27

The Periodic Table and Organismal Elements

17.5K
Elements are the smallest units of matter that cannot be broken down further by chemical processes. There are 118 known elements, but not all of these are naturally occurring, and only a few of them are essential for life. Living matter is composed primarily of carbon, nitrogen, hydrogen, and oxygen, with smaller amounts of other elements like calcium, phosphorus, potassium, and sulfur. Other elements are also necessary for life but only in trace amounts.
Periodic Table Provides Information...
17.5K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

15
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
15
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

12.2K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
12.2K
Teratogenicity01:07

Teratogenicity

2.5K
The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
2.5K

You might also read

Related Articles

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

Sort by
Same author

Identification of the gene cluster for the dithiolopyrrolone antibiotic holomycin in Streptomyces clavuligerus.

Proceedings of the National Academy of Sciences of the United States of America·2010
Same author

Safety evaluation of tea (Camellia sinensis (L.) O. Kuntze) flower extract: assessment of mutagenicity, and acute and subchronic toxicity in rats.

Journal of ethnopharmacology·2010
Same author

Influences of soil properties and leaching on nickel toxicity to barley root elongation.

Ecotoxicology and environmental safety·2010
Same author

Effects of CO2 insufflation on cerebrum during endoscopic thyroidectomy in a porcine model.

Surgical endoscopy·2010
Same author

Plants' use of different nitrogen forms in response to crude oil contamination.

Environmental pollution (Barking, Essex : 1987)·2010
Same author

Overexpression of p35 in Min6 pancreatic beta cells induces a stressed neuron-like apoptosis.

Journal of the neurological sciences·2010

Related Experiment Video

Updated: Jul 28, 2025

Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production
06:46

Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production

Published on: June 2, 2023

1.8K

Dibutyl phthalate causes heart damage by disrupting Ca

Bo Li1, Siming Huo1, Jiayu Du1

  • 1Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.

The Science of the Total Environment
|June 3, 2023
PubMed
Summary

Dibutyl phthalate (DBP) causes heart damage by initiating endoplasmic reticulum (ER) stress. This stress disrupts calcium transfer, leading to mitochondrial damage, increased reactive oxygen species, and pyroptosis in heart cells.

Keywords:
Dibutyl phthalateEndoplasmic reticulum stressHeart damageMitochondrial Ca(2+) overloadPyroptosis

More Related Videos

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

6.1K
Assessment of the Effects of Endocrine Disrupting Compounds on the Development of Vertebrate Neural Network Function Using Multi-electrode Arrays
08:28

Assessment of the Effects of Endocrine Disrupting Compounds on the Development of Vertebrate Neural Network Function Using Multi-electrode Arrays

Published on: April 26, 2018

6.0K

Related Experiment Videos

Last Updated: Jul 28, 2025

Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production
06:46

Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production

Published on: June 2, 2023

1.8K
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

6.1K
Assessment of the Effects of Endocrine Disrupting Compounds on the Development of Vertebrate Neural Network Function Using Multi-electrode Arrays
08:28

Assessment of the Effects of Endocrine Disrupting Compounds on the Development of Vertebrate Neural Network Function Using Multi-electrode Arrays

Published on: April 26, 2018

6.0K

Area of Science:

  • Toxicology
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Dibutyl phthalate (DBP) is a common plasticizer with known cardiotoxic effects.
  • The precise molecular mechanisms underlying DBP-induced cardiotoxicity are not fully understood.
  • Previous studies indicate oxidative stress and inflammation contribute to DBP's harmful effects on the heart.

Purpose of the Study:

  • To elucidate the mechanism of heart damage induced by Dibutyl phthalate (DBP).
  • To investigate the role of endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and pyroptosis in DBP cardiotoxicity.
  • To determine the sequential events linking ER stress to pyroptosis in cardiomyocytes exposed to DBP.

Main Methods:

  • In vivo and in vitro experimental models were utilized.
  • Cardiomyocytes were exposed to DBP to assess cellular damage.
  • Key molecular pathways including ER stress, mitochondrial function, calcium transfer, reactive oxygen species (ROS) production, and pyroptosis were analyzed.

Main Results:

  • DBP exposure was found to induce endoplasmic reticulum (ER) stress, mitochondrial damage, and pyroptosis in cardiomyocytes.
  • ER stress was shown to increase mitochondrial-associated ER membranes (MAMs), leading to abnormal calcium (Ca2+) transfer and subsequent mitochondrial damage.
  • Mitochondrial damage resulted in increased mitochondrial ROS (mtROS) production, activating the NLRP3 inflammasome and promoting pyroptosis.

Conclusions:

  • Endoplasmic reticulum (ER) stress is the initiating event in DBP-induced cardiotoxicity.
  • DBP disrupts Ca2+ transfer from the ER to mitochondria, causing mitochondrial damage.
  • Increased mtROS subsequently activates the NLRP3 inflammasome and pyroptosis, culminating in heart damage.