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

Spermatogenesis01:41

Spermatogenesis

Spermatogenesis is the process by which haploid sperm cells are produced in the male testes. It starts with stem cells located close to the outer rim of seminiferous tubules. These spermatogonial stem cells divide asymmetrically to give rise to additional stem cells (meaning that these structures “self-renew”), as well as sperm progenitors, called spermatocytes. Importantly, this method of asymmetric mitotic division maintains a population of spermatogonial stem cells in the male reproductive...
Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Toxicity Testing in Animals01:23

Toxicity Testing in Animals

Toxicity tests in animals are grounded on two main assumptions: first, the effects observed in laboratory animals can be extrapolated to humans, especially when adjusted for body surface area; second, high-dose exposure in animals is essential to identify potential human hazards from lower doses. This is based on the quantal dose-response concept, which faces the challenge of extrapolating results from relatively few test animals to much larger human populations. For example, a 0.01% incidence...

You might also read

Related Articles

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

Sort by
Same author

The causal relationship between immune cells and rheumatoid arthritis: A dual sample Mendelian randomization study.

Medicine·2025
Same author

Genetic causality and site-specific relationship between sarcopenia and osteoarthritis: a bidirectional Mendelian randomization study.

Frontiers in genetics·2024
Same author

Metformin Attenuates Silica-Induced Pulmonary Fibrosis by Activating Autophagy <i>via</i> the AMPK-mTOR Signaling Pathway.

Frontiers in pharmacology·2021
Same author

miR-7 Reduces High Glucose Induced-damage Via HoxB3 and PI3K/AKT/mTOR Signaling Pathways in Retinal Pigment Epithelial Cells.

Current molecular medicine·2019
Same author

Tree-based classification system incorporating the HVTT-PVTT score for personalized management of hepatocellular carcinoma patients with macroscopic vascular invasion.

Aging·2019
Same author

Radiosynthesis and in vivo evaluation of <sup>11</sup>C-labeled BMS-193885 and its desmethyl analog as PET tracers for neuropeptide Y1 receptors.

EJNMMI radiopharmacy and chemistry·2019

Related Experiment Video

Updated: Jun 21, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

[Carbendazim affects testicular development and spermatogenic function in rats].

Gong-chang Yu1, Lin Xie, Yan-zhong Liu

  • 1Department of Toxicology, Shandong Academy of Occupational Health and Diseases, Jinan, Shandong 250002, China.

Zhonghua Nan Ke Xue = National Journal of Andrology
|July 15, 2009
PubMed
Summary

Carbendazim exposure harms male rat testicular development and sperm production. This damage is linked to increased cell death (apoptosis) and altered protein expression (Bcl-2/Bax).

More Related Videos

Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
14:45

Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency

Published on: August 6, 2014

Related Experiment Videos

Last Updated: Jun 21, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
14:45

Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency

Published on: August 6, 2014

Area of Science:

  • Reproductive toxicology
  • Endocrinology
  • Cell biology

Context:

  • Carbendazim is a widely used fungicide with known reproductive toxicity.
  • Understanding its specific effects on male reproductive health is crucial for risk assessment.
  • Previous studies suggest potential adverse effects, but mechanisms require further elucidation.

Purpose:

  • To investigate the impact of carbendazim on testicular development and spermatogenesis in male rats.
  • To elucidate the underlying molecular mechanisms, including apoptosis and Bcl-2/Bax protein expression.

Summary:

  • Male Wistar rats were exposed to varying doses of carbendazim (20, 100, 200 mg/kg) for 80 days.
  • Carbendazim exposure led to testicular atrophy, reduced sperm count and motility, and altered histopathology.
  • Increased apoptosis and altered Bcl-2/Bax expression were observed in a dose-dependent manner.

Impact:

  • Carbendazim significantly impairs male reproductive function in rats.
  • The mechanism involves carbendazim-induced apoptosis mediated by the Bcl-2/Bax pathway.
  • Findings highlight the reproductive risks associated with carbendazim exposure.