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

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
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...
Renal Failure: Dose Adjustments01:11

Renal Failure: Dose Adjustments

In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Hepatic Drug Excretion: Influencing Factors01:16

Hepatic Drug Excretion: Influencing Factors

The biliary system of the liver, crucial for bile secretion and drug excretion, comprises intrahepatic bile ducts that merge to form the common hepatic duct. This duct, carrying hepatic bile, combines with the cystic duct, draining the gallbladder and forming the common bile duct, which empties into the duodenum. Bile, produced by hepatic cells lining the bile canaliculi, is composed primarily of water, bile salts, pigments, electrolytes, and lesser amounts of cholesterol and fatty acids. Bile...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...

You might also read

Related Articles

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

Sort by
Same author

Improving colorectal polyp size classification with virtual scale endoscopy: implications for resection strategy and surveillance.

Gastrointestinal endoscopy·2026
Same author

Missing barrier in coeliac disease: why the gut vascular barrier matters.

Gut·2026
Same author

Optimizing bowel preparation regimens for colon capsule endoscopy: an umbrella review (overview of systematic reviews).

Therapeutic advances in gastrointestinal endoscopy·2026
Same author

Enhancing the Evidence: Critical Insights and Future Directions for Texture and Color Enhancement Imaging in Colorectal Neoplasia Detection.

JGH open : an open access journal of gastroenterology and hepatology·2026
Same author

Patient-Level Predictors of Procedural Success in Colon Capsule Endoscopy: A Systematic Review and Meta-Analysis.

Journal of gastroenterology and hepatology·2026
Same author

Non-visualized Ultrasonography Should Remain Indeterminate in Patency Capsule Localization.

DEN open·2026

Related Experiment Video

Updated: Jul 14, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

Nitrofurantoin-induced lung- and hepatotoxicity.

Anastasios Koulaouzidis1, Shivaram Bhat, John Moschos

  • 1Department of Gastroenterology, Warrington Hospital, Warrington. akoulaouzidis@hotmail.com

Annals of Hepatology
|May 24, 2007
PubMed
Summary

Nitrofurantoin, used for urinary tract infections, can cause rare lung pneumonitis and liver toxicity. Stopping the drug resolved the patient's symptoms and liver function abnormalities.

More Related Videos

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
09:27

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat

Published on: June 17, 2016

Related Experiment Videos

Last Updated: Jul 14, 2026

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity
09:32

Drug-Induced Senescence in Liver Cells Promotes M2 Macrophage Polarization: Implications for Tyrosine Kinase Inhibitor-Associated Hepatotoxicity

Published on: October 17, 2025

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
09:27

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat

Published on: June 17, 2016

Area of Science:

  • Gastroenterology
  • Pulmonology
  • Clinical Pharmacology

Background:

  • Nitrofurantoin is a common antibiotic for urinary tract infections.
  • Long-term prophylaxis with nitrofurantoin can be associated with adverse effects.
  • Abnormal liver function tests warrant thorough investigation into potential drug-induced causes.

Observation:

  • A patient on long-term nitrofurantoin prophylaxis presented with abnormal liver function tests.
  • Computed tomography (CT) revealed lung pneumonitis and liver parenchymal changes.
  • The patient had been taking nitrofurantoin for 16 months.

Findings:

  • The patient was diagnosed with concurrent nitrofurantoin-induced pneumonitis and hepatotoxicity.
  • Withdrawal of nitrofurantoin led to significant clinical and biochemical improvement.
  • This dual organ toxicity from nitrofurantoin is an uncommon adverse event.

Implications:

  • Highlights the importance of considering nitrofurantoin as a cause of both pneumonitis and hepatotoxicity.
  • Emphasizes the need for vigilant monitoring of liver function and pulmonary symptoms in patients on long-term nitrofurantoin therapy.
  • Suggests that early recognition and drug cessation can reverse these rare adverse reactions.