The freshwater fish Galaxias maculatus (inanga) is a widespread Southern hemisphere species, but despite its habitation of lowland near-coastal waters with a high potential for cadmium contamination, nothing is known regarding its sensitivity to this toxic trace metal. Acute (96 h) exposures were therefore performed to determine sublethal responses of inanga to waterborne cadmium at a regulatory trigger value (nominally 0.2 μg L⁻¹; measured 1 μg L⁻¹), an environmental level (measured at 2.5 μg L⁻¹), and an effect level (measured at 10 μg L⁻¹). Whole body (tissue remaining following excision of kidney and liver) cadmium burden remained constant up until an exposure concentration of 10 μg L⁻¹, at which point cadmium concentration increased significantly. A transient effect of cadmium on metabolic rate was observed, with an impaired oxygen consumption noted at 2.5, but not 1 or 10, μg L⁻¹. Cadmium did not impair influx rates of either sodium or calcium, and no effects of cadmium on oxidative stress parameters (catalase activity, lipid peroxidation) were noted in the kidney. However, at cadmium concentrations of 2.5 and 10 μg L⁻¹, lipid peroxidation in the liver increased, concomitant with a decline in hepatic catalase activity. These data indicate that there are significant differences in the mechanisms of cadmium toxicity in inanga, relative to better-studied Northern hemisphere species, especially with respect to ionoregulatory impacts. However, effects were induced at cadmium concentrations unlikely to be encountered in any but the most highly contaminated waterways, and thus our data suggest that current trigger values for cadmium concentrations in Australian and New Zealand waters are likely to be protective of inanga.

淡水鱼类Galaxias maculatus（inanga）是南半球的一种广泛分布的物种，但是尽管其栖息于低陆近岸水域中，但镉污染的可能性很高，但对其对这种有毒微量金属的敏感性尚无定论。因此急性（96小时）暴露进行在调节触发值，以确定inanga到水性镉的亚致死响应（名义上0.2微克大号^-1 ;测量1微克大号^-1），环境电平（在2.5微克大号测量^-1）和效果水平（以10μgL ^-1测得）。整个人体（切除肾脏和肝脏后残留的组织）的镉负荷一直保持恒定，直到暴露浓度为10μgL ^-1，此时镉浓度显着增加。观察到镉对代谢率的瞬时作用，氧消耗受损为2.5μgL ^-1，而不是1或10μgL ^-1。镉不会损害钠或钙的流入速率，并且在肾脏中未发现镉对氧化应激参数（过氧化氢酶活性，脂质过氧化反应）的影响。但是，在2.5和10μgL ^-1的镉浓度下，肝脏中脂质过氧化作用增加，同时肝过氧化氢酶活性下降。这些数据表明，相对于经过研究的北半球物种，尤其是在离子调节作用方面，相对于经过研究的北半球物种而言，铟铝中镉毒性的机理存在显着差异。但是，在污染最严重的水道中，几乎不可能遇到镉浓度而引起的影响，因此，我们的数据表明，澳大利亚和新西兰水域中当前镉浓度的触发值很可能是对Inanga的保护。