Beauvais S L, Jones S B, Parris J T, Brewer S K, Little E E
Columbia Environmental Research Center, USGS/BRD, Columbia, Missouri 65201, USA.
Ecotoxicol Environ Saf. 2001 May;49(1):84-90. doi: 10.1006/eesa.2000.2032.
Pesticides and heavy metals are common environmental contaminants that can cause neurotoxicity to aquatic organisms, impairing reproduction and survival. Neurotoxic effects of cadmium and carbaryl exposures were estimated in larval rainbow trout (RBT; Oncorhynchus mykiss) using changes in physiological endpoints and correlations with behavioral responses. Following exposures, RBT were videotaped to assess swimming speed. Brain tissue was used to measure cholinesterase (ChE) activity, muscarinic cholinergic receptor (MChR) number, and MChR affinity. ChE activity decreased with increasing concentrations of carbaryl but not of cadmium. MChR were not affected by exposure to either carbaryl or cadmium. Swimming speed correlated with ChE activity in carbaryl-exposed RBT, but no correlation occurred in cadmium-exposed fish. Thus, carbaryl exposure resulted in neurotoxicity reflected by changes in physiological and behavioral parameters measured, while cadmium exposure did not. Correlations between behavior and physiology provide a useful assessment of neurotoxicity.
农药和重金属是常见的环境污染物,可对水生生物造成神经毒性,损害其繁殖和生存能力。利用生理指标的变化以及与行为反应的相关性,评估了镉和西维因暴露对虹鳟幼鱼(RBT;Oncorhynchus mykiss)的神经毒性作用。暴露后,对虹鳟幼鱼进行录像以评估游泳速度。利用脑组织测量胆碱酯酶(ChE)活性、毒蕈碱型胆碱能受体(MChR)数量和MChR亲和力。ChE活性随西维因浓度升高而降低,但不受镉浓度影响。暴露于西维因或镉对MChR均无影响。在暴露于西维因的虹鳟幼鱼中,游泳速度与ChE活性相关,但在暴露于镉的鱼中未发现相关性。因此,西维因暴露导致了所测生理和行为参数变化所反映的神经毒性,而镉暴露则未导致这种情况。行为与生理之间的相关性为神经毒性提供了有用的评估。