Toxicity and Mechanism of Di-(2-ethylhexyl) Phthalate on Testis
10.16476/j.pibb.2023.0114
- VernacularTitle:邻苯二甲酸二（2-乙基己基）酯对睾丸的毒性作用及机制
- Author:
An-Ni FENG
1
;
Ren-Ren SUN
1
;
Yu-Bo XIAO
2
;
Zhao-Ming ZENG
3
;
Zhong-Cheng MO
1
;
Yuan-Jie XIE
1
Author Information
1. Department of Histology and Embryology, Institute of Basic Medical Sciences, Guilin Medical University, Guilin 541199, China
2. School of Public Health and Laboratory Medicine, Hunan University of Medicine, Huaihua 418000, China
3. Joint Laboratory of Chronic Disease Prevention and Research in Guilin Medical University & Hunan Mingshun Pharmaceutical Co., Ltd, Shaodong 422800, China
- Publication Type:Journal Article
- Keywords:
di (2-ethylhexyl) phthalate;
testis;
reproductive toxicity;
oxidative stress;
ferroptosis
- From:
Progress in Biochemistry and Biophysics
2024;51(3):555-563
- CountryChina
- Language:Chinese
-
Abstract:
Di-(2-ethylhexyl) phthalate (DEHP) is currently one of the most widely used plasticizers, widely found in all kinds of items, such as children’s toys and food packaging materials, but also added to wallpaper, cable protective agents and other building decoration materials. DEHP is toxic and absorbed by the human body through respiratory tract, digestive tract and skin contact, which can cause damage to multiple systems, especially the male reproductive system, and testis is an important target organ. Oxidative stress injury is the core mechanism of spermatogenesis disorder caused by DEHP. DEHP exposure can cause oxidative stress or reactive oxygen species (ROS) increase in germ cells, and on this basis, promote cell apoptosis or cause excessive autophagy. The toxicity of DEHP to Leydig cells is mainly to interfere with the synthesis of steroid hormones. For Sertoli cells, ferroptosis and destruction of the blood-testis barrier are common injury mechanisms. In addition, gene methylation caused by DEHP not only affects the spermatogenic process, but also has epigenetic effects on offspring. In this paper, we reviewed the pathological damage, germ cell toxicity and epigenetic effects of DEHP on testis, and focused on the damage and molecular mechanism on testicular spermatogenic cells, Leydig cells and Sertoli cells. Future research is required to elucidate the body’s clearance mechanism and treatment plan after exposure to DEHP and whether DEHP will damage the function of myoid cells. It is hoped that this can provide new ideas for prevention and treatment of male reproductive disorders resulting from long-term exposure to plastic products.
