β-Ionone causes endocrine disruption, hyperpigmentation and hypoactivity in zebrafish early life stages

In nature, the odorous substance beta-ionone has been widely detected in aquatic ecosystems. However, little is known about its ecotoxicological effects on freshwater vertebrates. In this study, we aimed to assess the acute toxicity of beta-ionone in zebrafish (Danio rerio) embryos from 2 to 120 h post fertilization (hpf) and investigate embryo development, locomotor behavior and pigmentation under different concentrations. The results showed that exposure to beta-ionone had an acute toxicity to early life stages of zebrafish and induced a decrease in hatching rate and an increase in the mortality and malformation rate. The median lethal concentration (LC50) of beta-ionone at 96 h was observed as 1321 mu g/L. In addition, beta-ionone not only affected the body length of zebrafish larvae but also regulated the transcription of genes and the levels of hormones involved in the growth hormone/insulin-like growth factor (GH/IGF) and the hypothalamic-pituitary-thyroid (HPT) axes. Moreover, exposure to beta-ionone induced significant decreases in locomotor activity and catecholamine neurotransmitters levels. Furthermore, beta-ionone stimulated pigmentation via regulation of tyrosinase activity and melanin-related gene expression. Overall, this research could provide new insights into the potential risk of odorants to aquatic organisms.

Automated summary

In this study, the acute toxicity of beta-ionone on zebrafish embryos was assessed, and its effects on embryo development, locomotor behavior, and pigmentation were investigated. Exposure to beta-ionone resulted in decreased hatching rate, increased mortality and malformation rate in zebrafish embryos. It also affected the body length, gene transcription, hormone levels, locomotor activity, neurotransmitter levels, and pigmentation in zebrafish larvae. Overall, this research provides new insights into the potential risk of odorants on aquatic organisms.