A comparative study on endocrine disrupting effects of leachates from virgin and aged plastics under simulated media in marine medaka larvae (Oryzias melastigma)

Marine plastic pollution has garnered substantial attention, but the potential endocrine disrupting effects of plastic leachates in marine organisms remain unclear. In this study, the larvae of marine medaka (Oryzias melastigma) were exposed to the leachates from virgin and aged plastics soaked in simulated seawater and fish digest for 3 days. The concentrations of vitellogenin (VTG), estradiol (E2), and 11-ketotestosterone (11-KT), as well as the transcripts of endocrine-related genes were measured in the larvae. The results revealed that endogenous E2 was more sensitive to plastic leachates than VTG and 11-KT, which was significantly affected by 26.7 % of all plastic leachates. Among all genes, estrogen receptor alpha was impacted mostly, being up-regulated by 53.3 % of leachates from aged plastics. The comparative results demonstrated that the leachates from plastics with different statuses caused a greater difference than those from plastics in different simulated media, and the leachates from aged plastics resulted in higher endocrine disrupting effects than those from virgin plastics. In addition, seven leached additives (plasticizers and flame retardants) could explain 25.6 % of the hormonal effects using redundancy analysis, indicating that other additives in the plastic leachates can also play important roles in regulating the endocrine system of O. melastigma larvae.

Automated summary

This study investigates the potential endocrine disrupting effects of plastic leachates on marine organisms, particularly on marine medaka larvae. The results show that endogenous estradiol is more sensitive to plastic leachates than other hormones, and estrogen receptor alpha is the most affected gene. Aged plastics have a greater endocrine disrupting effect compared to virgin plastics, and the additives in plastic leachates also play an important role in regulating the endocrine system.