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

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment01:08

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
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: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
Jaundice01:25

Jaundice

Jaundice, or icterus, is the yellow discoloration of the skin, sclerae, and mucous membranes. It happens when plasma bilirubin levels rise above 2.5-3 mg/dL, leading to bilirubin deposition in tissue.Bilirubin is a byproduct of hemoglobin degradation. In macrophages, hemoglobin breaks down into globin and heme. Globin is converted into amino acids, while heme is turned into biliverdin by heme oxygenase, which is then reduced to unconjugated bilirubin by biliverdin reductase.Unconjugated...

You might also read

Related Articles

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

Sort by
Same author

Changes in urinary retinol binding protein excretion and other indices of renal tubular damage in patients with non-insulin dependent diabetes.

Diabetes research and clinical practice·1992
Same author

Entrainment to external Ca2+ oscillation in ionophore-treated Physarum plasmodium.

Cell structure and function·1992
Same author

Modulation of C2 and C3 gene expression of human peripheral blood monocytes by interleukin 1 beta, interferon gamma, tumor necrosis factor alpha and lipopolysaccharide.

Experientia·1992
Same author

Do pigmented naevi in albinism provide evidence of tyrosinase positivity?

The British journal of dermatology·1992
Same author

Dexamethasone attenuates altered insulin secretion elicited by interleukin-1 beta in HIT cells.

European journal of pharmacology·1992
Same author

Effect of dichloroacetate on recovery of brain lactate, phosphorus energy metabolites, and glutamate during reperfusion after complete cerebral ischemia in rats.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·1992

Related Experiment Video

Updated: Jul 8, 2026

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

Liver dysfunction among workers handling 5-nitro-o-toluidine.

H Shimizu1, T Kumada, S Nakano

  • 1Department of Gastroenterology, Ogaki Municipal Hospital, Ogaki, Gifu, Japan.

Gut
|January 15, 2002
PubMed
Summary

Occupational exposure to 5-nitro-o-toluidine may cause liver damage. Workers experiencing more frequent handling of this chemical showed increased severity of liver dysfunction, which resolved after factory closure.

More Related Videos

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure
08:25

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Published on: June 5, 2020

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
11:06

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Published on: January 31, 2022

Related Experiment Videos

Last Updated: Jul 8, 2026

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

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure
08:25

Advanced 3D Liver Models for In vitro Genotoxicity Testing Following Long-Term Nanomaterial Exposure

Published on: June 5, 2020

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
11:06

Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro

Published on: January 31, 2022

Area of Science:

  • Toxicology
  • Occupational Health
  • Hepatology

Background:

  • 5-Nitro-o-toluidine is an aromatic nitro amino compound.
  • Limited toxicity data exists for 5-nitro-o-toluidine, unlike other known hepatotoxic aromatic compounds.
  • This study addresses the lack of information on its potential to harm the liver.

Purpose of the Study:

  • To investigate the potential hepatotoxicity of 5-nitro-o-toluidine.
  • To establish a link between occupational exposure to 5-nitro-o-toluidine and liver dysfunction.
  • To assess the correlation between exposure levels and the severity of liver damage.

Main Methods:

  • Studied 15 factory workers exposed to 5-nitro-o-toluidine.
  • Correlated workplace factors and clinical findings, including blood biochemistry.
  • Monitored workers for liver dysfunction symptoms and biochemical markers.

Main Results:

  • Seven out of 15 workers exhibited biochemical evidence of liver damage.
  • Higher frequency of handling 5-nitro-o-toluidine correlated with increased liver dysfunction severity.
  • Liver damage resolved in all subjects after cessation of exposure (factory closure).

Conclusions:

  • Occupational exposure to 5-nitro-o-toluidine is linked to acute liver dysfunction.
  • The severity of liver damage appears dose-dependent, related to the number of handling episodes.
  • Eliminating exposure effectively resolves the induced hepatotoxicity.