Carbonic anhydrase activity in Mytilus galloprovincialis digestive gland: Sensitivity to heavy metal exposure

Carbonic anhydrase activity in Mytilus galloprovincialis digestive gland: Sensitivity to heavy metal exposure
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DOI:
10.1016/j.cbpc.2010.04.011
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发表时间:
2010-09-01
影响因子:
3.9
通讯作者:
Schettino, Trifone
Schettino, Trifone
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Caricato, Roberto;Lionetto, Maria Giulia;Schettino, Trifone

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已知重金属在体外会抑制多种生物体中的碳酸酐酶 (CA) 活性;然而,人们对它们对这种金属酶的活性和表达的体内影响知之甚少。本工作的目的是研究贻贝消化腺中 CA 对镉的体外和体内敏感性。首次在贻贝消化腺中证实了CA活性和蛋白表达(表观分子质量约28 kDa)。 CA 活性对体外镉暴露表现出较弱的敏感性,而在体内暴露两周后,CA 活性显着增加(约 40%)。与此同时,Western blotting 证明,CA 蛋白表达显着增强。实验室实验结果得到了现场实验的证实。与暴露于对照位点的动物相比,暴露于受影响位点30天的贻贝显示CA活性和蛋白质表达显着增加,同时金属硫蛋白组织浓度增加。总之,在本工作中,首次证明动物体内暴露于微量元素镉可以增强 CA 活性和蛋白质表达。 (C) 2010 Elsevier Inc. 保留所有权利。
Heavy metals are known to in vitro inhibit carbonic anhydrase (CA) activity in a variety of organisms; however, little is known about their in vivo effects on the activity and the expression of this metalloenzyme. The aim of this work was to investigate the in vitro and in vivo sensitivity to cadmium of CA in the digestive gland of Mytilus galloprovincialis. CA activity and protein expression (apparent molecular mass of about 28 kDa) were demonstrated in mussel digestive gland for the first time. CA activity showed week sensitivity to in vitro cadmium exposure, while it was significantly increased (about 40%) following two weeks in vivo exposure. In parallel, CA protein expression appeared significantly enhanced as demonstrated by Western blotting. Laboratory experimental results were confirmed by a field experiment. Mussels exposed for 30 days to an impacted site showed a significant increase of the CA activity and protein expression with respect to animals exposed to the control site in parallel to the increase of the metallothionein tissutal concentration. In conclusion in the present work for the first time CA activity and protein expression have been demonstrated to be enhanced by the exposure to the trace element cadmium in animals. (C) 2010 Elsevier Inc. All rights reserved.