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 Experiment Videos

Expression profiling of acetaminophen liver toxicity in mice using microarray technology.

T P Reilly1, M Bourdi, J N Brady

  • 1Molecular and Cellular Toxicology Section, National Institutes of Health, Bethesda, Maryland, USA. ReillyT@nhlbi.nih.gov

Biochemical and Biophysical Research Communications
|March 27, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Mitotic Count and the Field of View Area: Time to Standardize.

Veterinary pathology·2015
Same author

The glucagon-like peptide-1-based therapeutics exenatide and saxagliptin did not cause detrimental effects on the pancreas in mice, rats, dogs and monkeys.

Diabetes, obesity & metabolism·2014
Same author

Effects of physical efforts on injury in elite soccer.

International journal of sports medicine·2009
Same author

The tax protein from the primate T-cell lymphotropic virus type 3 is expressed in vivo and is functionally related to HTLV-1 Tax rather than HTLV-2 Tax.

Oncogene·2006
Same author

Human T-cell leukemia virus type 1 Tax attenuates gamma-irradiation-induced apoptosis through physical interaction with Chk2.

Oncogene·2005
Same author

A protective role for cyclooxygenase-2 in drug-induced liver injury in mice.

Chemical research in toxicology·2001
Same journal

Biosynthesis, characterization and biological potential of microbe-mediated silver nanoparticles using thermophilic actinomycetes, Streptomyces nigra.

Biochemical and biophysical research communications·2026
Same journal

COP9 signalosome 8 mediated autophagy drives proliferation, invasion, and metastasis in pancreatic ductal adenocarcinoma.

Biochemical and biophysical research communications·2026
Same journal

Tumor budding in colorectal cancer: partial EMT, microenvironmental remodeling, and metastatic competence.

Biochemical and biophysical research communications·2026
Same journal

Exploring the therapeutic versatility and multitarget pharmacological potential of acyl hydrazone-hydrazide scaffolds.

Biochemical and biophysical research communications·2026
Same journal

The plasma membrane H<sup>+</sup>-ATPase OSA2 negatively regulates salt tolerance in rice seedlings.

Biochemical and biophysical research communications·2026
Same journal

MiR-425-5p modulation of CREB1 affects inflammatory response and motor recovery after spinal cord injury.

Biochemical and biophysical research communications·2026
See all related articles

Acetaminophen (APAP) liver injury was studied by analyzing gene expression changes in mice. This research reveals key molecular pathways involved in drug-induced liver injury, aiding safer drug development.

Area of Science:

  • Hepatology
  • Toxicology
  • Molecular Biology

Background:

  • Drug-induced hepatotoxicity is a significant concern in drug development.
  • Understanding the mechanisms of drug-induced liver injury (DILI) is crucial.
  • Current knowledge of DILI mechanisms is insufficient.

Purpose of the Study:

  • To investigate gene expression modulation in mouse livers following acetaminophen (APAP) administration.
  • To identify genes and expressed sequence tags (ESTs) involved in APAP-induced liver injury.
  • To provide insights into the molecular basis of DILI for safer drug design.

Main Methods:

  • High-density oligonucleotide microarrays were used to analyze gene expression profiles.
  • Over 11,000 genes and ESTs were evaluated in mouse liver tissue.

Related Experiment Videos

  • Mice were treated with a hepatotoxic dose of acetaminophen (APAP).

    • Main Results:

    • Significant alterations in gene expression were observed in APAP-treated mouse livers.
    • Increased expression of genes related to growth arrest, cell cycle regulation, and stress responses was noted.
    • Specific genes and ESTs, including LRG-21, SOCS-2, and PAI-1, were identified as potentially important in APAP toxicity.

    Conclusions:

    • Acetaminophen (APAP) significantly alters liver gene expression, impacting various physiological processes.
    • The study identified novel genes and ESTs potentially involved in the propagation or prevention of drug-induced liver injury.
    • These findings offer new directions for mechanistic studies to improve drug safety and design.