ArticleToxicological sciences : an official journal of the Society of Toxicology2016
Establishing the "Biological Relevance" of Dipentyl Phthalate Reductions in Fetal Rat Testosterone Production and Plasma and Testis Testosterone Levels.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 39 citations in OpenAlex.
- Associations of endocrine disrupting chemicals with anogenital distance across infancy.The Journal of clinical endocrinology and metabolism · 2026Observational
- Comparison of in utero phthalate exposure on fetal rat testis transcript and endocrine alterations with apical reproductive alterations in male rats.Toxicology and applied pharmacology · 2025Article
- Dose-response assessment of dipentyl phthalate effects on testosterone production and morphogenesis of late-gestation fetal rat testis.Environment international · 2025Article
- Effect of Endocrine Disruptors on Testicular Function.Advances in experimental medicine and biology · 2025Review
- Using targeted fetal rat testis genomic and endocrine alterations to predict the effects of a phthalate mixture on the male reproductive tract.Current research in toxicology · 2024Article
- Biologically relevant reductions in fetal testosterone and Insl3 induced by in utero exposure to high levels of di-isononyl phthalate (DINP) in male rats.Toxicology and applied pharmacology · 2023Article
- Genomic and Hormonal Biomarkers of Phthalate-Induced Male Rat Reproductive Developmental Toxicity Part II: A Targeted RT-qPCR Array Approach That Defines a Unique Adverse Outcome Pathway.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Development of a putative adverse outcome pathway network for male rat reproductive tract abnormalities with specific considerations for the androgen sensitive window of development.Current research in toxicology · 2021Article
- A novel study evaluation strategy in the systematic review of animal toxicology studies for human health assessments of environmental chemicals.Environment international · 2020Review
- Intrauterine exposure to diethylhexyl phthalate disrupts gap junctions in the fetal rat testis.Current research in toxicology · 2020Article
- A Conflicted Tale of Two Novel AR Antagonists In Vitro and In Vivo: Pyrifluquinazon Versus Bisphenol C.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Tissue-specific changes inEnvironmental epigenetics · 2019Article
- All-trans Retinoic Acid Disrupts Development in Ex Vivo Cultured Fetal Rat Testes. II: Modulation of Mono-(2-ethylhexyl) Phthalate Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Phthalate-Induced Fetal Leydig Cell Dysfunction Mediates Male Reproductive Tract Anomalies.Frontiers in pharmacology · 2019Review
- Insulin-Like Peptide 3 (INSL3) Serum Concentration During Human Male Fetal Life.Frontiers in endocrinology · 2019Article
- Mixed "Antiandrogenic" Chemicals at Low Individual Doses Produce Reproductive Tract Malformations in the Male Rat.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Validation of an automated counting procedure for phthalate-induced testicular multinucleated germ cells.Toxicology letters · 2018Article
- Amniotic Fluid INSL3 Measured During the Critical Time Window in Human Pregnancy Relates to Cryptorchidism, Hypospadias, and Phthalate Load: A Large Case-Control Study.Frontiers in physiology · 2018Article
- Perspective: A Neuro-Hormonal Systems Approach to Understanding the Complexity of Cryptorchidism Susceptibility.Frontiers in endocrinology · 2018Article
- Relaxin-like peptides in male reproduction - a human perspective.British journal of pharmacology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Phthalate esters (PEs) constitute a large class of compounds that are used for many consumer product applications. Many of the C2-C7 di-ortho PEs reduce fetal testicular hormone and gene expression levels in rats resulting in adverse effects seen later in life but it appears that relatively large reductions in fetal testosterone (T) levels and testis gene expression may be required to adversely affect reproductive development (Hannas, B. R., Lambright, C. S., Furr, J., Evans, N., Foster, P. M., Gray, E. L., and Wilson, V. S. (2012). Genomic biomarkers of phthalate-induced male reproductive developmental toxicity: a targeted RT-PCR array approach for defining relative potency. Toxicol. Sci. 125, 544-557). The objectives of this study were (1) to model the relationships between changes in fetal male rat plasma testosterone (PT), T levels in the testis (TT), T production (PROD), and testis gene expression with the reproductive malformation rates, and (2) to quantify the "biologically relevant reductions" (BRRs) in fetal T necessary to induce adverse effects in the offspring. In the fetal experiment, Harlan Sprague-Dawley rats were dosed with dipentyl phthalate (DPeP) at 0, 11, 33, 100, and 300 mg/kg/day from gestational days (GD) 14-18 and fetal testicular T, PT levels, and T Prod and gene expression were assessed on GD 18. In the postnatal experiment, rats were dosed with DPeP from GD 8-18 and reproductive development was monitored through adulthood. The dose-response curves for TT levels (ED(50) = 53 mg/kg) and T PROD (ED(50) = 45 mg/kg) were similar, whereas PT was reduced at ED50 = 19 mg/kg. When the reductions in TPROD and Insl3 mRNA were compared with the postnatal effects of in utero DPeP, dose-related reproductive alterations were noted when T PROD and Insl3 mRNA were reduced by >45% and 42%, respectively. The determination of BRR levels may enable risk assessors to utilize fetal endocrine data to help establish points of departure for quantitative risk assessments.
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