KAUST Collaborative Research Program, Division of Life Science, Hong Kong University of Science and Technology, Hong Kong SAR, China.
PLoS One. 2011;6(8):e23803. doi: 10.1371/journal.pone.0023803. Epub 2011 Aug 29.
Butenolide [5-octylfuran-2(5H)-one] is a recently discovered and very promising anti-marine-fouling compound. In this study, the acute toxicity of butenolide was assessed in several non-target organisms, including micro algae, crustaceans, and fish. Results were compared with previously reported results on the effective concentrations used on fouling (target) organisms. According to OECD's guideline, the predicted no effect concentration (PNEC) was 0.168 µg l(-1), which was among one of the highest in representative new biocides. Mechanistically, the phenotype of butenolide-treated Danio rerio (zebrafish) embryos was similar to the phenotype of the pro-caspase-3 over-expression mutant with pericardial edema, small eyes, small brains, and increased numbers of apoptotic cells in the bodies of zebrafish embryos. Butenolide also induced apoptosis in HeLa cells, with the activation of c-Jun N-terminal kinases (JNK), Bcl-2 family proteins, and caspases and proteasomes/lysosomes involved in this process. This is the first detailed toxicity and toxicology study on this antifouling compound.
丁烯内酯[5-辛基呋喃-2(5H)-酮]是一种最近发现的、很有前途的抗海洋污损化合物。在这项研究中，评估了丁烯内酯对几种非靶标生物的急性毒性，包括微藻、甲壳类动物和鱼类。结果与先前报道的用于污损（靶）生物的有效浓度进行了比较。根据 OECD 的指南，预测无效应浓度（PNEC）为 0.168µg/L，在有代表性的新型生物杀灭剂中属于最高水平之一。从机制上讲，丁烯内酯处理的斑马鱼胚胎的表型与原 Caspase-3 过表达突变体的表型相似，具有心包水肿、小眼睛、小脑袋以及斑马鱼胚胎体内凋亡细胞数量增加。丁烯内酯还诱导 HeLa 细胞凋亡，涉及该过程的有 c-Jun N-末端激酶（JNK）、Bcl-2 家族蛋白以及半胱天冬酶和蛋白酶体/溶酶体的激活。这是对这种防污化合物的首次详细毒性和毒理学研究。
