Gestational and pubertal exposure to low dose of di-(2-ethylhexyl) phthalate impairs sperm quality in adult mice
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
32619501
DOI
10.1016/j.reprotox.2020.06.014
PII: S0890-6238(20)30173-8
Knihovny.cz E-resources
- Keywords
- DEHP, Fertility, Gene expression, Spermatogenesis, Steroidogenesis,
- MeSH
- Anal Canal anatomy & histology drug effects MeSH
- Diethylhexyl Phthalate toxicity MeSH
- Endocrine Disruptors toxicity MeSH
- Maternal-Fetal Exchange MeSH
- Genitalia, Male anatomy & histology drug effects MeSH
- Mice, Inbred ICR MeSH
- Sexual Maturation drug effects MeSH
- Spermatozoa drug effects MeSH
- Pregnancy MeSH
- Testis anatomy & histology drug effects MeSH
- Gene Expression Regulation, Developmental drug effects MeSH
- Plasticizers toxicity MeSH
- Prenatal Exposure Delayed Effects chemically induced genetics MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Diethylhexyl Phthalate MeSH
- Endocrine Disruptors MeSH
- Plasticizers MeSH
Di-(2-ethylhexyl)-phthalate (DEHP) is a compound widely used as a plasticizer, which can leach from plastics into the environment and thus influence human health. The aim of this study was to analyze whether exposure to an environmentally relevant dose of DEHP during mice fetal development or puberty can cause long-lasting changes detectable month/s after the last exposure. We used a DEHP concentration relevant to a daily human intake of 2.4-3 μg/kg of body weight/day. CD1 outbred mice were treated either in utero or postnatally during puberty and analyzed in adulthood. Analyzing fertility parameters using morphometric, histologic, genomic and proteomic methods we showed that DEHP exposure leads to decreased sperm concentration and quality, in both experimental groups. Moreover, the changes in anogenital distance, seminal vesicle weight, and testicular gene expression suggest a disturbance of androgen signaling in exposed animals. In conclusion, we hereby present, that the prenatal and pubertal exposure to a low dose of DEHP negatively influenced reproductive endpoints in male mice, and some of the effects were persistent until adulthood.
References provided by Crossref.org
The Transgenerational Transmission of the Paternal Type 2 Diabetes-Induced Subfertility Phenotype
