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

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

4.2K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
4.2K
Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems01:19

Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems

682
Phase I biotransformation reactions are integral to drug metabolism, predominantly involving oxidative, reductive, and hydrolytic transformations. Chief among these are oxidative reactions, which enhance the hydrophilicity of xenobiotics and introduce polar functional groups to facilitate their elimination from the body.
Oxidation reactions are fundamental in aromatic carbon-containing systems. An example is the hydroxylation of phenobarbital, a process that transforms it into...
682
Phase I Reactions: Oxidation of Carbon-Heteroatom and Miscellaneous Systems01:15

Phase I Reactions: Oxidation of Carbon-Heteroatom and Miscellaneous Systems

382
Oxidative reactions are pivotal in metabolizing numerous compounds, including pharmaceutical drugs. These reactions often occur in carbon-heteroatom systems, such as carbon-nitrogen, carbon-sulfur, and carbon-oxygen.
In carbon-nitrogen systems, aliphatic and aromatic amines can undergo oxidative reactions. Secondary and tertiary amines, like those found in tricyclic antidepressants, can undergo N-dealkylation, a process that involves the oxidation of the alkyl group. In addition, oxidative...
382
Phase I Oxidative Reactions: Overview01:19

Phase I Oxidative Reactions: Overview

703
Phase I biotransformation, or functionalization, is a crucial chemical process that converts drugs and other xenobiotics into more water-soluble forms, facilitating expulsion from the body. It involves oxidative, reductive, and hydrolytic reactions that add or unveil polar functional groups on lipophilic substrates. Key players in phase I reactions are the mixed-function oxidases. Situated in liver cell microsomes, these enzymes predominantly carry out drug metabolism. They require molecular...
703
Types of Toxins01:36

Types of Toxins

3.1K
Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
3.1K
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

1.8K
When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
1.8K

You might also read

Related Articles

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

Sort by
Same author

Development of Albumin Nanocarriers for Enhanced Curcumin Delivery and In Vitro Anticancer Activity in Colon Cancer Cells.

Pharmaceuticals (Basel, Switzerland)·2026
Same author

Comparative Efficacy of Four Different Types of Medicaments for Pulpotomy of Primary Molars: A Clinical and Radiographic Study.

International journal of clinical pediatric dentistry·2026
Same author

Macrophage in the crosshairs: chemical inhalation and lung immune defense.

American journal of physiology. Lung cellular and molecular physiology·2026
Same author

Kaempferol-loaded solid lipid nanoparticles attenuate cartilage degradation and inflammation by modulating the expression of pro and inflammatory cytokines, MMP-13 and oxidative stress markers in adjuvant induced arthritic rats.

Inflammopharmacology·2026
Same author

Rosemary leaves extract mediated green synthesis of silver functionalized BiFeO<sub>3</sub> nanoparticles with improved visible light photocatalytic performance.

Discover nano·2026
Same author

CRISPR/Cas9-mediated editing of the <i>GhJAZ2</i> gene improves fiber length and lint percentage in <i>Gossypium hirsutum</i> L.

GM crops & food·2026

Related Experiment Video

Updated: Jan 13, 2026

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.4K

Inhaled Halogen-Induced Oxidative Renal Damage and Dysfunction: A Lung Heart Kidney Axis.

Juan Xavier Masjoan Juncos1, Ahmed Zaky1, Wesam Nasser1

  • 1Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.

Comprehensive Physiology
|January 7, 2026
PubMed
Summary

Acute halogen gas exposure severely damages lungs and heart, leading to significant kidney injury. This study reveals halogen exposure causes acute kidney injury (AKI) and potential progression to chronic kidney disease (CKD) due to oxidative stress.

Keywords:
halogeninhaledinjuryorgan damageoxidative stressrenalrodent

More Related Videos

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.5K
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

257

Related Experiment Videos

Last Updated: Jan 13, 2026

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

11.4K
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.5K
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

257

Area of Science:

  • Toxicology
  • Nephrology
  • Cardiovascular Medicine

Background:

  • Acute exposure to halogen gases like bromine and chlorine causes severe pulmonary and cardiac injury.
  • Secondary renal complications following halogen-induced organ damage are not well understood.

Purpose of the Study:

  • To evaluate secondary renal complications after acute exposure to bromine and chlorine.
  • To assess renal function, injury biomarkers, and structural changes in response to halogen gas exposure.

Main Methods:

  • Rats were exposed to bromine or chlorine.
  • Renal function, urine and kidney injury biomarkers (creatinine, BUN, KIM-1, NGAL), hemodynamic parameters (MAP, RVR), and kidney tissue structure were assessed.
  • Long-term effects including fibrosis and oxidative stress markers were evaluated after 4 weeks.

Main Results:

  • Halogen exposure significantly increased blood creatinine and BUN, indicating acute renal stress.
  • Elevated urinary protein, albumin, and RBP4, along with increased KIM-1, NGAL, and osteopontin, demonstrated substantial kidney damage and tubular injury.
  • Hemodynamic changes included increased MAP and RVR, decreased renal artery diameter and blood flow, and evidence of oxidative stress and fibrosis, suggesting progression from AKI to CKD.

Conclusions:

  • Acute halogen gas exposure induces significant renal dysfunction and injury, characterized by oxidative stress and potential progression to chronic kidney disease.
  • Victims of halogen exposure face increased risks of cardiovascular events and renal complications, including AKI.