School of Biological Sciences, University of Canterbury, Private Bag 4800, Christchurch 8140, New Zealand.
Aquat Toxicol. 2013 Sep 15;140-141:303-13. doi: 10.1016/j.aquatox.2013.06.015. Epub 2013 Jun 29.
The biochemical responses of the green-lipped mussel, Perna canaliculus, to waterborne cadmium (Cd) were investigated in order to delineate toxic mechanisms, and the impacts of exposure dose and duration, of this important toxicant in a potential sentinel species. Mussels were exposed for either 96 h (acute: 0, 2000, 4000 μgL(-1) Cd) or for 28 d (subchronic: 0, 200, 2000 μgL(-1) Cd), and the digestive gland, gill and haemolymph were examined for impacts. Biochemical responses measured included those associated with metal detoxification (metallothionein-like protein; MTLP), oxidative stress (catalase, lipid peroxidation), cellular homeostasis (alkaline phosphatase, Na(+), K(+)-ATPase; NKA), and energy utilisation (glycogen, haemolymph protein). Following acute exposure, digestive gland glycogen and gill NKA activity were significantly altered by Cd exposure relative to levels in mussels exposed to Cd-free seawater. Subchronic Cd exposure resulted in a significant increase in MTLP levels in both the gill and the digestive gland. This increase was correlated strongly with the levels of Cd accumulation measured in these tissues (R=0.957 for gill, 0.964 for digestive gland). Catalase activity followed a similar pattern, although the correlation with tissue Cd accumulation was not as strong (R=0.907 for gill, 0.708 for digestive gland) as that for MTLP. Lipid peroxidation increased in the digestive gland at Days 7 and 14 at both subchronic Cd levels tested, but this effect had largely dissipated by Days 21 and 28 (with the exception of the 2,000 μgL(-1) group at Day 28). Alkaline phosphatase activity decreased significantly with Cd exposure in both tissues. This effect was observed at both tested concentrations in the gill, but only at the highest concentration for digestive gland. A decrease in digestive gland glycogen levels was observed in Cd-exposed mussels (Days 14 and 21 at 2,000 μgL(-1)), while haemolymph protein levels increased as a result of subchronic Cd exposure. These findings indicated that biochemical responses in Cd-exposed mussels were tissue-specific, dose- and time-dependent, with duration of exposure being the predominant effect. This study shows that biochemical changes in Cd-exposed green-lipped mussels can be linked to tissue metal accumulation and are consistent with previously reported physiological effects. It also suggests that green-lipped mussels are amenable to a multiple biomarker approach and may be of use as a bioindicator species for monitoring coastal metal pollution.
为了阐明这种重要毒物的毒性机制，并探讨暴露剂量和时间对绿唇贻贝（Perna canaliculus）的影响，我们研究了其对水基镉（Cd）的生化反应。贻贝分别暴露 96 小时（急性：0、2000、4000 μgL(-1) Cd）或 28 天（亚慢性：0、200、2000 μgL(-1) Cd），并检测了消化腺、鳃和血淋巴的影响。测定的生化反应包括与金属解毒（金属硫蛋白样蛋白；MTLP）、氧化应激（过氧化氢酶、脂质过氧化）、细胞内稳态（碱性磷酸酶、Na(+), K(+)-ATP 酶；NKA）和能量利用（糖原、血淋巴蛋白）相关的反应。在急性暴露后，与暴露于无 Cd 海水的贻贝相比，Cd 暴露显著改变了消化腺糖原和鳃 NKA 活性。亚慢性 Cd 暴露导致贻贝鳃和消化腺 MTLP 水平显著升高。这种增加与这些组织中测量的 Cd 积累水平密切相关（与鳃相关的 R=0.957，与消化腺相关的 R=0.964）。过氧化氢酶活性也呈现出类似的模式，尽管与组织 Cd 积累的相关性不如 MTLP 强（与鳃相关的 R=0.907，与消化腺相关的 R=0.708）。在亚慢性 Cd 测试的两个浓度下，消化腺中的脂质过氧化在第 7 天和第 14 天均增加，但到第 21 天和第 28 天（28 天的 2000 μgL(-1)组除外），这种影响已经基本消散。在两个组织中，碱性磷酸酶活性均随 Cd 暴露而显著降低。在鳃中，这种影响在两个测试浓度下都观察到，但在消化腺中仅在最高浓度下观察到。在 Cd 暴露的贻贝中，观察到消化腺糖原水平降低（第 14 天和第 21 天在 2000 μgL(-1)），而血淋巴蛋白水平因亚慢性 Cd 暴露而升高。这些发现表明，Cd 暴露贻贝的生化反应具有组织特异性、剂量依赖性和时间依赖性，暴露时间是主要影响因素。本研究表明，Cd 暴露贻贝的生化变化与组织金属积累有关，与先前报道的生理效应一致。这也表明，绿唇贻贝适合采用多生物标志物方法，可用作监测沿海金属污染的生物指示剂种。
