Engel D W, Fowler B A
Environ Health Perspect. 1979 Feb;28:81-8. doi: 10.1289/ehp.792881.
The toxicity of dissolved cadmium to a variety of marine animals has been found to be related to salinity, with decreased toxicity observed at higher salinities. Recent data from our laboratory have demonstrated that the toxicity of cadmium to estuarine shrimp and larval fish is a function of free cadmium ion concentration, which in turn is controlled by the chloride concentration of the water. As the chloride concentration (i.e., salinity of the water) increases, the concentration of free cadmium ion decreases relative to total dissolved metal, due to its complexation with chloride ions. These observations have been given further support by measurements involving the uptake of (115m)Cd by shrimp which showed that accumulation of (115m)Cd and chloride concentration also are inversely related. Experiments also have been conducted on the physiological effects of cadmium on the respiration of excised oyster gill tissue. Although tissues from oysters exposed for 14 days to 0.1 ppm total dissolved cadmium accumulated significant quantities of metal, no measurable effects on respiration rates were detected. Higher doses (0.3 and 0.6 ppm) caused both mortalities of oysters and accelerated respiration of excised oyster gill. Exposure to 0.1 ppm cadmium also caused the induction of and/or increased binding of cadmium to a specific low molecular weight protein in oysters. This protein appeared to have a detoxification function at low cadmium exposure levels, but in animals exposed to 0.6 ppm cadmium the induction mechanism apparently became saturated, allowing the excess cadmium to bind critical sites with resultant damage.
已发现溶解态镉对多种海洋动物的毒性与盐度有关,在较高盐度下毒性会降低。我们实验室的最新数据表明,镉对河口虾和幼鱼的毒性是游离镉离子浓度的函数,而游离镉离子浓度又受水体氯化物浓度的控制。随着氯化物浓度(即水体盐度)的增加,由于游离镉离子与氯离子络合,相对于总溶解金属而言,其浓度会降低。涉及虾对(115m)镉吸收的测量结果进一步支持了这些观察结果,结果表明(115m)镉的积累与氯化物浓度也呈负相关。还对镉对离体牡蛎鳃组织呼吸的生理影响进行了实验。尽管暴露于0.1 ppm总溶解镉14天的牡蛎组织积累了大量金属,但未检测到对呼吸速率有可测量的影响。较高剂量(0.3和0.6 ppm)导致牡蛎死亡并加速离体牡蛎鳃的呼吸。暴露于0.1 ppm镉还会诱导和/或增加镉与牡蛎中一种特定低分子量蛋白质的结合。这种蛋白质在低镉暴露水平下似乎具有解毒功能,但在暴露于0.6 ppm镉的动物中,诱导机制显然变得饱和,使过量的镉能够结合关键位点,从而造成损害。