ArticleEnvironmental science and pollution research international2021
Di-(2-ethylhexyl) phthalate induces testicular endoplasmic reticulum stress and germ cell apoptosis in adolescent mice.
Article in Environmental science and pollution research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Mechanistic insights and ameliorative strategies: advances in DEHP-induced metabolic toxicity and intervention by natural bioactive compounds and probiotics.Lipids in health and disease · 2026Review
- Sulforaphane substantially impedes testicular ferroptosis in adult rats exposed to di-2-ethylhexyl phthalate through activation of NRF-2/SLC7A11/GPX-4 trajectory.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Investigation of protective effects of rutin\cyclodextrin inclusion complex against testicular damage caused by diisononyl phthalate in rats.Iranian journal of basic medical sciences · 2025Article
- Mixtures of phthalates disrupt expression of genes related to lipid metabolism and peroxisome proliferator-activated receptor signaling in mouse granulosa cells.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Role of Endoplasmic Reticulum Stress in The Male Reproductive System.Cell journal · 2023Review
- Effects of Lycium barbarum glycopeptide on renal and testicular injury induced by di(2-ethylhexyl) phthalate.Cell stress & chaperones · 2022Article
- Multiple transcriptomic profiling: potential novel metabolism-related genes predict prepubertal testis damage caused by DEHP exposure.Environmental science and pollution research international · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Di-(2-ethylhexyl) phthalate (DEHP) is a male reproductive toxicant. This research is aimed at investigating the effect of pubertal DEHP exposure on testicular endoplasmic reticulum (ER) stress and germ cell apoptosis. Five-week-old male mice were orally administered with DEHP (0, 0.5, 50, or 500 mg/kg/day) for 35 days. Testis weight and sperm count were reduced in mice exposed to 500 mg/kg/day DEHP. The number of seminiferous tubules in stages VII-VIII, mature seminiferous tubules, was reduced and the number of seminiferous tubules in stages IX-XII, immature seminiferous tubules, was elevated in mice treated with 500 mg/kg/day DEHP. Numerous apoptotic germ cells were observed in mouse seminiferous tubules exposed to 50 and 500 mg/kg/day DEHP. Moreover, cleaved caspase-3 was elevated in mouse testes exposed to 500 mg/kg/day DEHP. In addition, Bcl-2 was reduced and Bax/Bcl-2 was elevated in mouse testes exposed to 500 mg/kg/day DEHP. Additional experiment showed that GRP78, an ER molecular chaperone, was downregulated in mouse testes exposed to 500 mg/kg/day DEHP. Testicular p-IRE-1α, p-JNK, and CHOP, three markers of ER stress, were upregulated in mice exposed to 500 mg/kg/day DEHP. These results suggest that pubertal exposure to high doses of DEHP induces germ cell apoptosis partially through initiating ER stress in testes.
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Registered trials
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