Avobenzone suppresses proliferative activity of human trophoblast cells and induces apoptosis mediated by mitochondrial disruption

Changwon Yang, Whasun Lim, Fuller W. Bazer, Gwonhwa Song

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Avobenzone is widely used in various personal care products, is present in swimming pools, and is toxic to aquatic organisms. However, it is unclear how avobenzone affects human trophoblast cells. Results of the present study demonstrated that avobenzone inhibited the proliferation of HTR8/SVneo cells, the immortalized human trophoblast cell line, and inhibited the expression of PCNA. In addition, avobenzone increased the activity of AKT and ERK1/2 in HTR8/SVneo cells. When LY294002 (AKT inhibitor) and U0126 (ERK1/2 inhibitor) were treated with avobenzone, the anti-proliferative effect of avobenzone was alleviated. Moreover, avobenzone promoted Ca2+ overload into the mitochondria and induced depolarization of the mitochondrial membrane. Expression of IFI27, which is located in the mitochondria, was elevated by avobenzone via inhibition of expression through siRNA transfection against IFI27, but did not alter cell properties. This study suggests that avobenzone induces mitochondrial dysfunction-mediated apoptosis leading to abnormal placentation during early pregnancy.

Original languageEnglish
Pages (from-to)50-57
Number of pages8
JournalReproductive Toxicology
Volume81
DOIs
Publication statusPublished - 2018 Oct 1

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Keywords

  • Apoptosis
  • Avobenzone
  • Mitochondria
  • Proliferation
  • Trophoblast

ASJC Scopus subject areas

  • Toxicology

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