Effects of long-term treatment with low concentration butylparaben on prostate organoids

Endocrine-disrupting compounds (EDCs), such as butylparaben (BP), which are used as preservatives in food and cosmetics, have been shown to negatively affect male reproductive health. Organs under the control of hormones such as androgens and estrogens, such as the prostate, are vulnerable to EDC stimulation. It is well known that BP can cause hormonal imbalances in the prostate and lead to various prostate diseases. However, studies on the long-term exposure of low-dose BP, which is common in daily life, are lacking, and existing studies rely heavily on in vitro tests to assess the risk of EDCs. Therefore, in this study, we investigated the long-term exposure effects of low-dose BP using a prostate organoid model that more closely resembles the target organ. When prostate organoids were treated with BP for a long period, hormonal imbalance was confirmed through differences in the expression of hormone receptors. In addition, reactive oxygen species (ROS) production was confirmed by DCFDA staining, and the protective effect of prostate organoids against stimulation was confirmed by increased protein levels of antioxidant factors. Through transcriptome analysis, we confirmed the occurrence of reproductive toxicity caused by BP. The long-term treatment of prostate organoids with BP causes hormonal imbalance and increased ROS exhibits reproductive toxicity and exerts a protective mechanism against BP through the expression of antioxidant factors. Our results highlight the potential of prostrate organoids as an alternative to animal experimental model and the need for further research on the effects of low EDC concentrations on male reproductive function. [Display omitted] •Long-term treatment with BP 0.33 mg/L causes reproductive toxicity in Daphnia, and long-term treatment with BP 0.59 mg/L causes hormonal imbalance and reproductive toxicity in prostate organoids.•Long-term treatment with BP causes ROS generation in prostate organoids and activation of antioxidant factors as a defense mechanism.