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

Phase II Reactions: Acetylation Reactions01:24

Phase II Reactions: Acetylation Reactions

328
Acetylation, a phase II biotransformation reaction, introduces an acetyl group to drugs or their metabolites. Acetyltransferase enzymes facilitate this reaction, which resembles α-amino acid conjugation due to the addition of a functional group to the drug molecule.
The substrates for acetylation are typically drugs or their metabolites with an amino, sulfonamide, or hydrazine functional group. Acetylation can occur at several points in the drug molecule, including primary, secondary, and...
328
Hepatic Drug Excretion: Influencing Factors01:16

Hepatic Drug Excretion: Influencing Factors

197
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...
197
Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation01:22

Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation

330
Glutathione, a tripeptide made up of glutamate, cysteine, and glycine, is a critical player in the detoxification of drugs and xenobiotics via a process known as glutathione conjugation or mercapturic acid formation. This phase II biotransformation reaction involves the covalent binding of glutathione to a drug or its metabolite, enhancing the compound's water solubility and enabling its excretion.
Several distinctive characteristics distinguish glutathione conjugation from other phase II...
330
Factors Affecting Drug Biotransformation: Biological01:19

Factors Affecting Drug Biotransformation: Biological

213
Biological factors significantly impact drug metabolism, influencing drug clearance, efficacy, and potential toxicity.
Species differences: Variations in enzyme systems across species can cause disparities in drug metabolism. For instance, humans may metabolize certain drugs faster than rodents, altering therapeutic effects.
Strain differences: Genetic variations within a species can result in differing enzyme activity, impacting drug response and toxicity. For example, some mouse strains may...
213
Comparing Copy Number Variations and SNPs02:26

Comparing Copy Number Variations and SNPs

17.9K
Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
Copy number variations or CNVs are the structural variations that cover more than 1kb of DNA sequence. The single nucleotide polymorphism (SNP), on the other hand, is a single nucleotide change or a point mutation that is found in more than 1%...
17.9K
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

226
Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
226

You might also read

Related Articles

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

Sort by
Same author

Prevalence and predictors of sexual and physical violence during psychedelic use in a US population-based study.

World psychiatry : official journal of the World Psychiatric Association (WPA)·2026
Same author

Fusing Specialized Surveys of Rare Populations to Larger Surveys for Generalized Inference: Cross-Sectional Survey Study.

Journal of medical Internet research·2026
Same author

Psychedelic Terminology Preference in the 2024 National Survey Investigating Hallucinogenic Trends (NSIHT).

Journal of psychoactive drugs·2026
Same author

Psilocybin Trends in States That Decriminalized Use.

JAMA·2026
Same author

Post-operative oxygen delivery and delirium after cardiac surgery with cardiopulmonary bypass: A multisite retrospective cohort study of 1,690 patients.

Perfusion·2026
Same author

Complexity of Pharmacologic Pain Control-The Allegory of the Pharmacogenetic Cave.

JAMA network open·2026

Related Experiment Video

Updated: Aug 28, 2025

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration
05:37

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration

Published on: May 31, 2018

12.3K

Genetic variants associated with ALT elevation from therapeutic acetaminophen.

Andrew A Monte1,2,3,4, Ian Arriaga Mackenzie5, Jack Pattee5

  • 1Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, CO, USA.

Clinical Toxicology (Philadelphia, Pa.)
|September 14, 2022
PubMed
Summary

Genetic variants in SULT1E1 may influence alanine aminotransferase (ALT) elevation during acetaminophen therapy. Further research is needed to explore SULT1E1

Keywords:
Acetaminophendrug induced liver injurygenetichepatotoxicitypharmacogeneticstherapeutic dose

More Related Videos

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

10.2K
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

830

Related Experiment Videos

Last Updated: Aug 28, 2025

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration
05:37

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration

Published on: May 31, 2018

12.3K
Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

10.2K
Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer
06:21

Author Spotlight: Genetic Profiling for Fluorouracil Response in Gastric Cancer

Published on: May 10, 2024

830

Area of Science:

  • Pharmacogenomics
  • Hepatology
  • Genetic Epidemiology

Background:

  • Genetic variants are linked to acetaminophen-induced liver injury (DILI) after overdose.
  • No prior studies examined genetic variation related to alanine aminotransferase (ALT) elevation during therapeutic acetaminophen dosing.

Purpose of the Study:

  • To investigate the association between genetic variation and ALT elevation in individuals taking therapeutic doses of acetaminophen.
  • To identify specific genes influencing acetaminophen metabolism and immune-mediated DILI.

Main Methods:

  • Genetic analysis of 192 subjects receiving therapeutic acetaminophen doses (up to 4 grams/day for 16 days).
  • Examined 20 candidate genes using Illumina Multi-Ethnic Global Array, with imputation via TOPMed.
  • Candidate gene region analysis employed the adaptive sum of powered scores (aSPU) test.

Main Results:

  • Age over 50 was the only clinical factor associated with maximum ALT increase.
  • Genetic variants within the SULT1E1 gene (Sulfotransferase Family 1E Member 1) were associated with maximum ALT.
  • The association with SULT1E1 was attributed to the cumulative effects of multiple variants, not a single one.

Conclusions:

  • Acetaminophen-induced ALT elevation at therapeutic doses is not strongly associated with variants in most studied genes.
  • The role of SULT1E1 gene polymorphisms in acetaminophen-induced ALT elevation warrants further investigation.