DCOIT (4,5-dichloro-2-n-octyl-4-isothiazolin-3-one) is the main active ingredient in an emerging water environment antifoulant, the toxicity and environmental impacts of which need to be further investigated. Thus, this study examined the toxicity of DCOIT on Nile tilapia (Oreochromis niloticus), including its effects on behavior, respiration and energy metabolism as well as the role of endoplasmic reticulum stress (ER stress) in mediating its toxicity and metabolic changes. The changes in fish behavior, respiration, neuronal signal transmission, energy metabolism, ER stress, and liver histology were examined via acute (4 days) and chronic (28 days) exposures to 0, 3, 15, 30 μg/L DCOIT in vivo. Additionally, ER stress levels were measured in 24-h periods of hepatocyte exposure to 0, 3, 15, 30 and 300 μg/L DCOIT in vitro. The hyper-locomotor activities decreased, but the respiration rate increased after a 4-day acute exposure period, indicating that DCOIT exposure altered fish energy metabolism. After acute exposure at a low DCOIT concentration, the activation of ER stress induced triglyceride accumulation in the liver. After chronic exposure for 28 days, the prolonged ER stress induced a series of pathological cellular changes. At the cellular level, exposure to a high DCOIT concentration induced ER stress in the hepatocytes. In addition, as a neurotoxin, DCOIT has the potential to disrupt the neurotransmission of the cholinergic system, resulting in motor behavior disruption. This study demonstrates that DCOIT plays a role in time- and concentration-dependent toxicity and that changes in lipid metabolism are directly related to endoplasmic reticulum function after exposure to an antifouling agent. This work advances the understanding of the toxic mechanism of DCOIT, which is necessary for its evaluation.

DCOIT（4,5-二氯-2-正辛基-4-异噻唑啉-3-酮）是新兴的水环境防污剂的主要活性成分，其毒性和环境影响尚待进一步研究。因此，本研究检查了DCOIT对尼罗罗非鱼（Oreochromis niloticus）的毒性，包括其对行为，呼吸和能量代谢的影响，以及内质网应激（ER应激）在介导其毒性和代谢变化中的作用。通过体内0、3、15、30μg/ L DCOIT的急性暴露（4天）和慢性暴露（28天）来检查鱼的行为，呼吸，神经元信号传导，能量代谢，内质网应激和肝脏组织学的变化。此外，在体外肝细胞暴露于0、3、15、30和300μg/ L DCOIT的24小时内测量了ER应激水平。在持续4天的急性暴露期后，运动能力下降，但呼吸速率增加，表明DCOIT暴露改变了鱼的能量代谢。在低DCOIT浓度下急性暴露后，内质网应激的激活引起肝脏中甘油三酸酯的积累。长期暴露28天后，ER应力延长导致一系列病理性细胞变化。在细胞水平上，暴露于高DCOIT浓度会诱导肝细胞的内质网应激。另外，作为神经毒素，DCOIT有可能破坏胆碱能系统的神经传递，从而导致运动行为破坏。这项研究表明，DCOIT在依赖于时间和浓度的毒性中起作用，并且脂质代谢的变化与抗污剂接触后与内质网功能直接相关。这项工作提高了对DCOIT毒性机理的理解，这对于对其进行评估是必不可少的。