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Food Chem Toxicol. 2019 Jun;128:193-201. doi: 10.1016/j.fct.2019.04.013. Epub 2019 Apr 12.

Oral exposure of rats to dienestrol during gestation and lactation: Effects on the reproductive system of male offspring.

Author information

1
Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain.
2
Department of Pathology, University Hospital Joan XXIII, Tarragona, Catalonia, Spain.
3
Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain; Research Center in Behavioral Assessment (CRAMC), Department of Psychology, Universitat Rovira i Virgili, Tarragona, Catalonia, Spain.
4
Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Reus, Catalonia, Spain. Electronic address: joseluis.domingo@urv.cat.

Abstract

This study was aimed at determining whether dienestrol (DIES) affects reproduction in male offspring of rats following oral maternal exposure during gestation and lactation. Pregnant rats were treated from GD 6 to PND 21. Animals received 0 (control-vehicle), 0.75, 1.5, 3.12, 6.25, 12.5, 50, 75 μg/kg bw/d of DIES. A control group -without vehicle-was also included. High DIES concentrations caused abortions at 75 and 50 μg/kg bw/d, while at 12.5 μg/kg bw/d had still miscarriages. Ten male rats per group were kept alive until PND 90 to ensure sexual maturity. Body and organ weights, anogenital distance (AGD) at PNDs 21 and 90, biochemical and sperm parameters like motility, viability, morphology, spermatozoa and resistant spermatid counts, and histopathology for sexual organs and liver were determined. An increase in organ weight (liver and sexual organs) and a decrease in AGD due to vehicle were found. A reduction of sperm motility and viability, and an increase of abnormal sperm morphology were caused by DIES, which provoked a dose-dependent prostatitis. Maternal exposure to DIES induced toxicity on the reproductive system of the male offspring, which could affect the capacity of fertilization.

KEYWORDS:

Dienestrol; Endocrine disruptors; Maternal exposure; Reproductive toxicity; Sperm

PMID:
30986439
DOI:
10.1016/j.fct.2019.04.013
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