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Copyright (c) 2025 Min Ju Park, Seung Ju Lee, Yong Joo Park, Eunsoo Yoo, Hye Kyung Kim, Min Hi Park
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Influence of di(2-ethylhexyl) phthalate on dysregulation of testosterone production via alteration of aromatase expression
Corresponding Author(s) : Hye Kyung Kim
Cellular and Molecular Biology,
Vol. 71 No. 4: Issue 4
Abstract
Di(2-ethylhexyl) phthalate (DEHP), an endocrine-disrupting chemicals (EDCs), is commonly used as a plasticizer to improve the flexibility and durability of plastics. On a daily basis, we are exposed to varying amounts of this compound. Several studies have demonstrated that exposure to DEHP and its metabolite, mono(2-ethylhexyl) phthalate (MEHP), leads to testosterone deficiency (TD) in both humans and animals. However, the precise mechanism that causes DEHP-induced TD is still not completely understood. This study aims to determine the effects of DEHP on testosterone levels and elucidate the underlying mechanisms. C57BL/6 mice and Leydig cells were exposed to various doses of DEHP (0, 0.5, and 5 mg/kg/day) for 9 weeks and MEHP (0, 0.05, 0.5, and 5 μM) for 24 hours, respectively. Both in vivo and in vitro results indicated significant reductions in testosterone levels due to DEHP and MEHP. Additionally, DEHP and MEHP increased the expression of aromatase, a gene that converts testosterone to estradiol and induced an increase in the expression of inflammatory cytokines such as IL-6, IL-1β, and TNF-α. Moreover, DEHP activated NF-κB, a key transcription factor regulating numerous genes associated with inflammation. These results suggest that sustained exposure to DEHP increases inflammatory factors, which may elevate aromatase activity and result in decreased testosterone levels in the body. Furthermore, this study provides a basis for discussing the potential correlation between persistent DEHP exposure and TD characterized by low testosterone levels in the body.
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