Isothiazolinones, such as 1,2-benzisothiazol-3(2H)-one (BIT), are widely used as biocides for bacterial growth control in many domestic and industrial processes. Despite their advantages as biocides, they are highly toxic and pose a potential risk to the environment. This study investigated the inhibition process and detoxification mechanism involved in microalgal survival and growth recovery after BIT poisoning. BIT could seriously inhibit the growth of Scenedesmus sp. LX1, Chlorella sp. HQ, and Chlamydomonas reinhardtii with half maximal effective concentrations at 72 h (72h-EC₅₀) of 1.70, 0.41, and 1.16 mg/L, respectively. The primary inhibition mechanism was the BIT-induced damage to microalgal photosynthetic systems. However, the inhibited strains could recover when their growth was not completely inhibited. The influence of this inhibiting effect on subsequent algal regrowth was negligible or weak. BIT consumption was the primary reason for their recovery. Notably, algae did not die even if their growth was completely inhibited. If the BIT concentration did not exceed a certain high level, then the inhibited algae could recover their growth relatively well. Microalgal generation of reduced glutathione (GSH) and the oxygen radical scavenging enzymes, superoxide dismutase (SOD) and catalase (CAT), played a key role in detoxification against BIT poisoning.

异噻唑啉酮类化合物，例如1,2-苯并噻唑啉-3（2H）-one（BIT），在许多家庭和工业过程中被广泛用作控制细菌生长的杀生物剂。尽管它们具有杀生物剂的优势，但它们仍然具有剧毒并且对环境构成潜在风险。本研究探讨了BIT中毒后微藻存活和生长恢复所涉及的抑制过程和解毒机理。BIT可能严重抑制Scenedesmus sp。的生长。LX1，小球藻属。总部和莱茵衣藻在72 h（72h-EC ₅₀）分别为1.70、0.41和1.16 mg / L。主要的抑制机制是BIT诱导的对微藻光合系统的损害。但是，当未完全抑制其生长时，受抑制的菌株可以恢复。这种抑制作用对随后的藻类再生的影响微不足道或微弱。BIT消耗是其恢复的主要原因。值得注意的是，即使藻类的生长被完全抑制，藻类也不会死亡。如果BIT浓度不超过某个高水平，则受抑制的藻类可以相对良好地恢复其生长。还原型谷胱甘肽（GSH）和氧自由基清除酶，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的微藻生成在针对BIT中毒的排毒中起着关键作用。