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Sci Rep. 2017 Sep 11;7(1):11072. doi: 10.1038/s41598-017-11325-7.

Effect of prenatal DINCH plasticizer exposure on rat offspring testicular function and metabolism.

Campioli E1,2, Lee S1,3, Lau M1,4, Marques L1,4, Papadopoulos V5,6,7,8,9.

Author information

1
Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.
2
Department of Medicine, McGill University, Montréal, Québec, Canada.
3
Department of Biochemistry, McGill University, Montréal, Québec, Canada.
4
Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
5
Research Institute of the McGill University Health Centre, Montréal, Québec, Canada. vpapadop@usc.edu.
6
Department of Medicine, McGill University, Montréal, Québec, Canada. vpapadop@usc.edu.
7
Department of Biochemistry, McGill University, Montréal, Québec, Canada. vpapadop@usc.edu.
8
Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada. vpapadop@usc.edu.
9
Department of Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, California, USA. vpapadop@usc.edu.

Abstract

In 2002, the plasticizer 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH) was introduced in the European market as a substitute for endocrine-disrupting phthalates. We found that in utero exposure of rats to DINCH from gestational day 14 until parturition affected reproductive organ physiology and reduced circulating testosterone levels at post-natal day 60, indicating a long-term effect on Leydig cells of the testis. Metabolically, animals exhibited randomly increased serum glucose concentrations not associated with impaired glucose utilization. Analysis of liver markers in the serum showed a hepatic effect; e.g. reduced bilirubin levels and albumin/globulin ratio. At post-natal day 200, random appearance of testicular atrophy was noted in exposed offspring, and limited changes in other reproductive parameters were observed. In conclusion, DINCH exposure appears to directly affect Leydig cell function, likely causing premature aging of the testes and impaired liver metabolic capacity. These effects might be attenuated with physiologic aging.

PMID:
28894178
PMCID:
PMC5593853
DOI:
10.1038/s41598-017-11325-7
[Indexed for MEDLINE]
Free PMC Article

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