ArticleBiology of reproduction2011
ATP synthesis, mitochondrial function, and steroid biosynthesis in rodent primary and tumor Leydig cells.
Article in Biology of reproduction, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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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.
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Who cites it
41 citing papers in PubMed, 92 citations in OpenAlex.
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- Hexaconazole-Induced Male Reproductive Toxicity Through ROS-Mediated Ferroptosis and Impaired Leydig Cell Steroidogenesis.International journal of molecular sciences · 2026Article
- Microsomal triglyceride transfer protein restricts steroid production in Leydig cells by regulating SREBP2.iScience · 2026Article
- An extracellular vesicle-mediated mitochondrial transfer network critical for testosterone synthesis.Nature cell biology · 2026Article
- The EV-mitochondrial outsourcing network as a therapeutic target for age-related testosterone deficiency: from network collapse to clinical intervention.Frontiers in endocrinology · 2026Review
- Mechanistic insights into targeting APLN/APJ for ameliorating testosterone deficiency and reproductive disorders in diabetic mice.Cell communication and signaling : CCS · 2025Article
- Environmental light deprivation disrupts Leydig cell maturation and male reproductive development in rats.Scientific reports · 2025Article
- Untargeted Plasma Metabolomics Extends the Biomarker Profile of Mitochondrial Neurogastrointestinal Encephalomyopathy.International journal of molecular sciences · 2025Article
- Circadian disruption impairs Leydig cell maturation and reproductive development in male rats.Reproductive biology and endocrinology : RB&E · 2025Article
- An update on the role of sex hormones in the function of the cardiorenal mitochondria.Biochemical Society transactions · 2024Review
- Age-related testosterone decline: mechanisms and intervention strategies.Reproductive biology and endocrinology : RB&E · 2024Review
- Reduced Levels of Neurosteroids in Cerebrospinal Fluid of Amyotrophic Lateral Sclerosis Patients.Biomolecules · 2024Article
- A narrative review on inflammaging and late-onset hypogonadism.Frontiers in endocrinology · 2024Review
- Use ofFrontiers in toxicology · 2024Article
- Maslinic Acid Supplementation during the In Vitro Culture Period Ameliorates Early Embryonic Development of Porcine Embryos by Regulating Oxidative Stress.Animals : an open access journal from MDPI · 2023Article
- Emerging Promise of Therapeutic Approaches Targeting Mitochondria in Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Mechanisms of Male Reproductive Toxicity of Polybrominated Diphenyl Ethers.International journal of molecular sciences · 2022Review
- The cost of the circadian desynchrony on the Leydig cell function.Scientific reports · 2022Article
- Metabolic Alteration Analysis of Steroid Hormones in Niemann-Pick Disease Type C Model Cell Using Liquid Chromatography/Tandem Mass Spectrometry.International journal of molecular sciences · 2022Article
- Effects of taurine and ginseng extracts on energy metabolism during exercise and their anti-fatigue properties in mice.Nutrition research and practice · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Previous studies in MA-10 tumor Leydig cells demonstrated that disruption of the mitochondrial electron-transport chain (ETC), membrane potential (ΔΨ(m)), or ATP synthesis independently inhibited steroidogenesis. In contrast, studies of primary Leydig cells indicated that the ETC, ΔΨ(m), and ATP synthesis cooperatively affected steroidogenesis. These results suggest significant differences between the two systems and call into question the extent to which results from tumor Leydig cells relate to primary cells. Thus, to further understand the similarities and differences between the two systems as well as the impact of ATP disruption on steroidogenesis, we performed comparative studies of MA-10 and primary Leydig cells under similar conditions of mitochondrial disruption. We show that mitochondrial ATP synthesis is critical for steroidogenesis in both primary and tumor Leydig cells. However, in striking contrast to primary cells, perturbation of ΔΨ(m) in MA-10 cells did not substantially decrease cellular ATP content, a perplexing finding because ΔΨ(m) powers the mitochondrial ATP synthase. Further studies revealed that a significant proportion of cellular ATP in MA-10 cells derives from glycolysis. In contrast, primary cells appear to be almost completely dependent on mitochondrial respiration for their energy provision. Inhibitor studies also suggested that the MA-10 ETC is impaired. This work underscores the importance of mitochondrial ATP for hormone-stimulated steroid production in both MA-10 and primary Leydig cells while indicating that caution must be exercised in extrapolating data from tumor cells to primary tissue.
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Registered trials
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 OpenQuestion graph.