Abstract
3,4-Dichloroaniline (3,4-DCA) is a transformation product of herbicides that is commonly used as a reference in developmental toxicity studies (OECD TG 236) (Bonnet et al. in Environ Toxicol 22:78–91, 2007). However, the mechanisms underlying 3,4-DCA-induced hepatotoxicity are not well known. We exposed zebrafish larvae at 72 hpf to 3,4-DCA for 3 days and observed lipid accumulation in liver treated with 10-μM 3,4-DCA using oil red O staining. Subsequently, we performed qRT-PCR analysis to determine the genes involved in the observed lipid accumulation. We found that genes related to lipogenesis (srebp1, pparγ, lipin1, and scd1) and ER stress (bip, atf4, ddit3, dnajc3, and edem1) were significantly upregulated. In addition, we found that ROS generation increased in the larvae treated with 10-μM 3,4-DCA. Moreover, glutathione-S-transferase activity in these larvae was increased by 3,4-DCA in a dose-dependent manner, and the expression of the inflammation marker il-1β increased. Our results indicated that exposure to 3,4-DCA induced fatty liver in zebrafish larvae and that this, in association with additional factors such as ER stress response, can promote liver damage. We accordingly suggest that 3,4-DCA could be used to induce fatty liver in zebrafish larvae.
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