期刊
JOURNAL OF HAZARDOUS MATERIALS
卷 417, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.jhazmat.2021.126044
关键词
DEHP; Memory decline; Insulin; IGF-1 signaling; CRH-1; CREB
资金
- Ministry of Science and Technology of Taiwan [105-2320-B-002-024-MY3, 108-2320-B-002-014-MY3]
Chronic early-life exposure to DEHP worsens age-related decline in LTAM in C. elegans, with the effect being associated with CRH-1 and IIS signaling pathways.
The ubiquitous contamination of di(2-ethylhexyl)phthalate (DEHP) in the environment, biota, and food poses potential ecological and human health risks. DEHP exposure can adversely affect learning and memory, yet the underlying mechanisms remain unclear. In this study, Caenorhabditis elegans was used to investigate the effect of early-life DEHP exposure on age-related long-term associative memory (LTAM) decline, as well as the associations with the cAMP-responsive element-binding protein (CREB) transcription factor and insulin/IGF-1 signaling (IIS). We showed that early-life exposure to DEHP reduced LTAM in wild-type worms at day-0 adulthood. Chronic exposure to DEHP from the L1 stage to day-5 adulthood worsened the age-dependent decline of LTAM. Moreover, the effect of DEHP on age-related LTAM requires CRH-1, a homolog of CREB. Mutations in daf-2, the sole receptor of C. elegans IIS, ameliorated the inhibition of LTAM by DEHP, and the effect depended on daf-16. In addition, daf-2 mutation restored the CRH-1 level in DEHP-exposed worms, and the effect required daf-16. Our study suggests that early-life chronic exposure to DEHP worsens age-related LTAM decline and the effect is associated with CRH-1 and IIS in C. elegans. The evolutionary conservation of IIS and CREB implies possible adverse effects by DEHP across species.
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