ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Mono-2-ethylhexyl phthalate stimulates androgen production but suppresses mitochondrial function in mouse leydig cells with different steroidogenic potential.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 38 citations in OpenAlex.
- SLC7A11 as a therapeutic target to attenuate phthalates-driven testosterone level decline in mice.Journal of advanced research · 2025Article
- Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.Current environmental health reports · 2022Review
- Mechanisms of MEHP Inhibitory Action and Analysis of Potential Replacement Plasticizers on Leydig Cell Steroidogenesis.International journal of molecular sciences · 2021Article
- MEHP interferes with mitochondrial functions and homeostasis in skeletal muscle cells.Bioscience reports · 2020Article
- Redox regulation of hormone sensitive lipase: Potential role in the mechanism of MEHP-induced stimulation of basal steroid synthesis in MA-10 Leydig cells.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Water and soil pollution as determinant of water and food quality/contamination and its impact on male fertility.Reproductive biology and endocrinology : RB&E · 2019Review
- Nonmonotonic Effects of Chronic Low-Dose Di(2-ethylhexyl) Phthalate on Gonadal Weight and Reproductive.Development & reproduction · 2018Article
- Metabolomic Markers of Phthalate Exposure in Plasma and Urine of Pregnant Women.Frontiers in public health · 2018Article
- Cytotoxic effects of ZnO nanoparticles on mouse testicular cells.International journal of nanomedicineArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies have reported on testicular toxicity of phthalates in different experimental paradigms and showed that Leydig cells (LCs) were one of the main targets of phthalate actions. Adverse effects of phthalates on LCs steroidogenesis have been attributed to their metabolites, monophthalates. This study focuses on investigation whether LCs responsiveness to monophthalates action is associated with their potential to produce androgens. We found that of 3 monophthalates investigated [ie, mono-2-ethylhexyl phthalate (MEHP), mono-n-butyl phthalate, and mono-n-benzyl phthalate] only MEHP caused biological effects on the mouse LCs function. This monophthalate stimulated basal steroidogenesis associated with upregulation of StAR protein expression with no effect on hCG-stimulated androgen production by LCs from CBA/Lac and C57BL/6j mouse genotypes were observed. Further, MEHP attenuated ATP production and increased superoxide generation by both phenotypes of mouse LCs that indicated on mitochondrial dysfunction induced by the monophthalate. All together, our data indicate that MEHP-mediated stimulation of steroidogenesis and perturbation in mitochondrial function are not associated with the capacity of the LCs to synthesize androgens. We suggest that this effect of MEHP observed in LCs of rodent origin needs to be taken into consideration in analysis of earlier start of puberty in boys and may highlight a possible influence of phthalates on reproductive health in males.
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