ArticleScientific reports2015
Apoptosome activation, an important molecular instigator in 6-mercaptopurine induced Leydig cell death.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Chemotherapy-induced oxidative injury in pediatric acute lymphoblastic leukemia: The role of N-acetylcysteine (Review).Biomedical reports · 2026Review
- Single versus intermittent cycle exposure effect of 6-mercaptopurine in juvenile Sprague-Dawley rat: a germ cell-specific mechanistic study.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- In Vitro and In Vivo Models for Drug Transport Across the Blood-Testis Barrier.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Drug Transporters at the Human Blood-Testis Barrier.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Cell Migration Related to MDR-Another Impediment to Effective Chemotherapy?Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Leydig cells are crucial to the production of testosterone in males. It is unknown if the cancer chemotherapeutic drug, 6-mercaptopurine (6 MP), produces Leydig cell failure among adult survivors of childhood acute lymphoblastic leukemia. Moreover, it is not known whether Leydig cell failure is due to either a loss of cells or an impairment in their function. Herein, we show, in a subset of childhood cancer survivors, that Leydig cell failure is related to the dose of 6 MP. This was extended, in a murine model, to demonstrate that 6 MP exposure induced caspase 3 activation, and the loss of Leydig cells was independent of Bak and Bax activation. The death of these non-proliferating cells was triggered by 6 MP metabolism, requiring formation of both cytosolic reactive oxygen species and thiopurine nucleotide triphosphates. The thiopurine nucleotide triphosphates (with physiological amounts of dATP) uniquely activated the apoptosome. An ABC transporter (Abcc4/Mrp4) reduced the amount of thiopurines, thereby providing protection for Leydig cells. The studies reported here demonstrate that the apoptosome is uniquely activated by thiopurine nucleotides and suggest that 6 MP induced Leydig cell death is likely a cause of Leydig cell failure in some survivors of childhood cancer.
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