Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Cellular Injury IV: Necrosis

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

You might also read

Related Articles

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

Sort by

Same author

Cadmium Toxicity to the Animal Reproductive Systems: A Narrative Review.

Journal of applied toxicology : JAT·2026

Same author

Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.

Nature communications·2026

Same author

Material removal mechanism elucidated by a novel cross-scale model using a unified physical framework linking macroscopic stress distribution and microscopic motion states of abrasives for polishing.

Nanoscale·2026

Same author

Near-complete cryo-EM structure of the Klebsiella pneumoniae podophage RAN69 reveals tail fiber-spike interface and a divergent pre-ejectosome.

Structure (London, England : 1993)·2026

Same author

Saikosaponin A restores the IDO1-driven gut-testis kynurenine axis to alleviate oligozoospermia.

Phytomedicine : international journal of phytotherapy and phytopharmacology·2026

Same author

Development of a Closed One-Tube Colorimetric and Fluorescent LAMP Assay for the Rapid Detection of Feline Herpesvirus 1.

Animals : an open access journal from MDPI·2026

Search research articles

Related Experiment Video

Updated: Apr 18, 2026

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Published on: February 8, 2016

4-Methylcatechol-induced cell damage in TM4 Sertoli cells.

Chunjin Li¹, Wanhong Li¹, Shuxiong Chen¹

¹College of Animal Sciences, Jilin University, 5333 Xi'an Avenue, Changchun, Jilin Province, 130062, P.R. China.

Cell Biology International

|February 3, 2015

Summary

4-Methylcatechol (4-MC) induces apoptosis in mouse TM4 Sertoli cells. This cytotoxic effect is linked to increased Bax gene expression and caspase activation, impacting cell viability.

Keywords:

4-Methylcatechol TM4 Sertoli cells apoptosis cytotoxicity

More Related Videos

Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry

Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry

Published on: December 28, 2021

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Related Experiment Videos

Last Updated: Apr 18, 2026

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Isolation of Sertoli Cells and Peritubular Cells from Rat Testes

Published on: February 8, 2016

Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry

Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry

Published on: December 28, 2021

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Area of Science:

Toxicology
Cell Biology
Molecular Biology

Background:

Quercetin, a compound with potential neuroprotective and anti-tumor properties, is metabolized into 4-Methylcatechol (4-MC).
Understanding the biological effects of quercetin metabolites like 4-MC is crucial for drug development.

Purpose of the Study:

To investigate the cytotoxic effects of 4-Methylcatechol (4-MC) on mouse TM4 Sertoli cells.
To elucidate the molecular mechanisms underlying 4-MC-induced cytotoxicity in these cells.

Main Methods:

TM4 Sertoli cells were treated with varying concentrations and durations of 4-MC.
Cell viability assays, apoptosis detection, and caspase 3 activity measurements were performed.
Quantitative real-time PCR was used to analyze the expression of Bax and Bcl-2 genes.

Main Results:

4-MC significantly inhibited TM4 Sertoli cell viability in a time- and dose-dependent manner.
Increased numbers of apoptotic and dead cells, along with elevated caspase 3 activity, were observed post-4-MC treatment.
4-MC upregulated Bax gene expression and downregulated Bcl-2 gene expression in a concentration-dependent manner.

Conclusions:

4-Methylcatechol induces apoptosis in TM4 Sertoli cells.
The cytotoxic effects of 4-MC are associated with the upregulation of Bax, leading to caspase cascade activation.
These findings provide insights into the potential toxicity of 4-MC in reproductive cells.