Henry Raymond P, Gehnrich Stephen, Weihrauch Dirk, Towle David W
Department of Biological Sciences, Auburn University, 101 Life Science Building, Auburn, AL 36849, USA.
Comp Biochem Physiol A Mol Integr Physiol. 2003 Oct;136(2):243-58. doi: 10.1016/s1095-6433(03)00113-2.
The euryhaline green crab, Carcinus maenas, is a relatively strong osmotic and ionic regulator, being able to maintain its hemolymph osmolality as much as 300 mOsm higher than that in the medium when the crab is acclimated to low salinity. It makes the transition from osmoconformity to osmoregulation at a critical salinity of 26 ppt, and new acclimated concentrations of hemolymph osmotic and ionic constituents are reached within 12 h after transfer to low salinity. One of the central features of this transition is an 8-fold induction of the enzyme carbonic anhydrase (CA) in the gills. This induction occurs primarily in the cytoplasmic pool of CA in the posterior, ion-transporting gills, although the membrane-associated fraction of CA also shows some induction in response to low salinity. Inhibition of branchial CA activity with acetazolamide (Az) has no effect in crabs acclimated to 32 ppt but causes a depression in hemolymph osmotic and ionic concentrations in crabs acclimated to 10 ppt. The salinity-sensitive nature of the cytoplasmic CA pool and the sensitivity of hemolymph osmotic/ionic regulation to Az confirm the enzyme's role in ion transport and regulation in this species. CA induction is a result of gene activation, as evidenced by an increase in CA mRNA at 24 h after transfer to low salinity and an increase in protein-specific CA activity immediately following at 48 h post-transfer. CA gene expression appears to be under inhibitory control by an as-yet unidentified repressor substance found in the major endocrine complex of the crab, the eyestalk.
广盐性的绿蟹(Carcinus maenas)是一种相对较强的渗透和离子调节者,当蟹适应低盐度环境时,其血淋巴渗透压能够比周围介质高出多达300 mOsm。它在临界盐度26 ppt时从渗透顺应性转变为渗透调节,转移到低盐度环境后12小时内就能达到新的适应后的血淋巴渗透和离子成分浓度。这种转变的一个核心特征是鳃中碳酸酐酶(CA)的活性诱导增加了8倍。这种诱导主要发生在后部离子转运鳃中CA的细胞质池中,尽管CA的膜结合部分对低盐度也有一定的诱导反应。用乙酰唑胺(Az)抑制鳃CA活性对适应32 ppt的蟹没有影响,但会导致适应10 ppt的蟹的血淋巴渗透和离子浓度降低。细胞质CA池对盐度敏感的性质以及血淋巴渗透/离子调节对Az的敏感性证实了该酶在该物种离子转运和调节中的作用。CA诱导是基因激活的结果,转移到低盐度环境24小时后CA mRNA增加以及转移后48小时立即出现蛋白质特异性CA活性增加证明了这一点。CA基因表达似乎受到蟹主要内分泌复合体眼柄中一种尚未鉴定的抑制物质的抑制控制。