Evidence map›Paper›PMID 39334937›Full record

ArticleBiomolecules2024

L-Cysteine Upregulates Testosterone Biosynthesis and Blood-Testis Barrier Genes in Cultured Human Leydig Cells and THP-1 Monocytes and Increases Testosterone Secretion in Human Leydig Cells.

Jeffrey Justin Margret, Sushil K Jain

Abstract read
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Age-Associated Metabolomic Changes in Human Spermatozoa.International journal of molecular sciences · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Jeffrey Justin MargretDepartment of Pediatrics, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA.ORCID 0000-0001-7905-1887
Sushil K JainDepartment of Pediatrics, Louisiana State University Health Sciences Center, Shreveport, LA 71103, USA.

Funding

Optimization of Glutathione Levels and Alzheimer Disease Risk in African AmericansR33AT010637 · NCCIH · LOUISIANA STATE UNIV HSC SHREVEPORT · PI JAIN, SUSHIL K · 2020 to 2022
$1.9M
NIH HHS 3R33AT010637-02S1NIH HHS 5R33AT010637-01A1
6 · The paper itself

Abstract

Leydig cells are the primary source of testosterone or androgen production in male mammals. The blood-testis barrier (BTB) maintains structural integrity and safeguards germ cells from harmful substances by blocking their entry into the seminiferous tubules. L-cysteine is essential to the production of glutathione, a powerful antioxidant crucial to protecting against oxidative stress-induced damage. Animal studies have demonstrated the protective effect of L-cysteine in preventing testicular damage caused by chemicals or radiation. This study examines whether L-cysteine enhances the expression of testosterone biosynthesis and the BTB genes in human Leydig cells and THP-1 monocytes. The Leydig cells and THP-1 monocytes were treated with L-cysteine for 24 h. RNA was extracted following treatment, and the gene expression was analyzed using quantitative RT-PCR. Testosterone levels in the cell supernatant were measured using an ELISA kit. L-cysteine treatment in Leydig cells significantly upregulated the expression of

Indexed as

Blood-Testis BarrierCysteineLeydig CellsMonocytesTestosteroneCells, CulturedHumansMaleTHP-1 CellsUp-RegulationCysteineTestosteroneblood–testis barrierClaudinCYP11A1L-cysteineLeydig cellsmale infertilitytestosteroneTHP-1 monocytes

Identifiers

PMID39334937
PMCPMC11430594

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.