Karnatak University's Research Laboratory, Environmental and Molecular Toxicology Division, Department of Zoology, Karnatak Science College, Dharwad, Karnataka, India.
Drug Chem Toxicol. 2010 Apr;33(2):160-5. doi: 10.3109/01480540903196816.
A short-term definitive test by the static renewal bioassay method was conducted to determine the acute toxicity (LC(50)) of commercial-grade organophosphate insecticide, malathion (50% EC) on the freshwater fish, Labeo rohita. Carp fingerlings were exposed to different concentrations of malathion for 96 hours. The acute toxicity (LC(50)) of malathion was found to be 4.5 microg/L. One tenth (1/10, 0.45 microg/L) of the acute toxicity value was selected as the sublethal concentration for subacute studies. The fish were exposed to sublethal concentration for 1, 5, 10, and 15 days and allowed to recover in toxicant-free medium for 15 days. Behavioral responses and morphological deformities were studied in the experimental tenures. Fish in toxic media exhibited irregular, random, circular swimming movements, hyperexcitability, loss of equilibrium, and sinking to the bottom. Caudal bending was the prime morphological malformation. The behavioral and morphological deformities were due to inhibition of acetylcholinesterase (AChE) activity. Inhibition of AChE activity results in excess accumulation of acetylcholine in cholinergic synapses, leading to hyperstimulation and cessation of neuronal transmission (i.e., paralysis). The carp were found under stress, but mortality was insignificant at the sublethal concentration tested. Impaired behavioral responses and morphological deformities were observed during recovery. This may be a consequence due to inhibition of brain and muscular AChE by malaoxon, via the biotransformation of sequestered malathion.
采用静态更新生物测定法进行了短期限定性测试，以确定商业级有机磷杀虫剂马拉硫磷（50% EC）对淡水鱼罗非鱼的急性毒性（LC50）。将鲤鱼鱼苗暴露于不同浓度的马拉硫磷中 96 小时。发现马拉硫磷的急性毒性（LC50）为 4.5μg/L。选择急性毒性值的十分之一（1/10，0.45μg/L）作为亚急性研究的亚致死浓度。鱼在亚致死浓度下暴露 1、5、10 和 15 天，并在无毒物的介质中恢复 15 天。在实验期间研究了行为反应和形态畸形。在有毒介质中的鱼表现出不规则，随机，圆形的游泳运动，过度兴奋，失去平衡和沉到底部。尾弯曲是主要的形态畸形。行为和形态畸形是由于乙酰胆碱酯酶（AChE）活性的抑制。AChE 活性的抑制导致胆碱能突触中乙酰胆碱的过度积累，导致过度刺激和神经元传递的停止（即麻痹）。发现鲤鱼处于压力之下，但在测试的亚致死浓度下死亡率并不显著。在恢复期间观察到受损的行为反应和形态畸形。这可能是由于马拉氧磷通过隔离马拉硫磷的生物转化抑制脑和肌肉 AChE 所致。
