Developmental cardiotoxicity of 4,5-dichloro-2-n-octyl-4-isothiazolin-3-one (DCOIT) in marine medaka (Oryzias melastigma)

Mengyuan Liu, Jing Li, Jiali Li, Bingsheng Zhou, Paul K.S. Lam, Chenyan Hu, Lianguo Chen

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

The application of 4,5-dichloro-2-n-octyl-4-isothiazolin-3-one (DCOIT) as an antifouling biocide causes high toxicity to non-target marine organisms. To examine the developmental cardiotoxicity and mechanisms of DCOIT, we concurrently performed sub-chronic exposure and life-cycle exposure experiments using marine medaka embryos. After sub-chronic exposure to DCOIT at 1, 3, 10, and 33 μg/L, cardiac defects were caused by upregulation of cardiac gene transcriptions, decreasing heart size, and accelerating heartbeat. Hyperthyroidism in medaka larvae was identified as the cause of developmental cardiotoxicity of DCOIT sub-chronic exposure. In addition, parental life-cycle exposure to 1, 3, and 10 μg/L DCOIT led to transgenerational impairment of cardiogenesis in offspring medaka. A crossbreeding strategy discriminated a concentration-dependent mechanism of transgenerational cardiotoxicity. At 1 μg/L, the DCOIT-exposed female parent transferred a significantly higher amount of triiodothyronine (T3) hormone to offspring, corresponding to an accelerated heart rate. However, DCOIT at higher exposure concentrations modified the methylome imprinting in larval offspring, which was associated with cardiac dysfunction. Overall, the findings provide novel insights into the developmental cardiotoxicity of DCOIT. The high risks of DCOIT—even at environmentally realistic concentrations—raise concerns about its applicability as an antifoulant in a marine environment.

Original languageEnglish
Article number133176
JournalJournal of Hazardous Materials
Volume465
DOIs
Publication statusPublished - 5 Mar 2024

Keywords

  • Antifouling
  • DCOIT
  • Developmental cardiotoxicity
  • Methylome
  • Thyroid

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