Institute of Zoology, University of Innsbruck, Innsbruck, Austria.
Cell Tissue Res. 2010 Jul;341(1):159-71. doi: 10.1007/s00441-010-0980-x. Epub 2010 May 18.
In terrestrial pulmonate snails, cadmium (Cd) uptake leads to the induction of a Cd-specific metallothionein isoform (Cd-MT) that protects against adverse interactions of this toxic metal ion. Increasing concentrations of Cd cause increased individual mortality possibly linked to pathological alterations in the snail midgut gland. Histological, immuno-histochemical, and electron-microscopic methods in combination with tissue metal analyses and quantification of MT induction parameters were applied to the midgut gland of Cd-exposed Roman snails (Helix pomatia). Conspicuous concentration-dependent alterations occurred in this organ, including the metal-induced increase of Cd-MT concentration and manifestation of Cd-MT mRNA precipitations in all midgut gland cell types. The most evident alteration was an increase of cellular turnover reflected by enhanced cell proliferation. Intensified vesiculation of endoplasmic reticulum was noted in basophilic cells and an increasing formation of lipofuscin granules in excretory cells. At the highest Cd concentrations, mitochondrial membranes were disrupted in basophilic cells, and lipofuscin granules were released from excretory cells into the midgut gland tubular system. Some of these alterations (e.g., increased cell proliferation rate, vesiculation of endoplasmic reticulum) detected at low Cd concentrations were interpreted as adaptive response processes enhancing the tolerance of exposed individuals to metal stress. Cellular alterations at higher Cd concentrations (e.g., mitochondrial structural damage) clearly represented ongoing irreversible cellular disruption. Combined evaluation of cellular biomarkers and MT saturation levels indicated that the transition from stress resistance to depletion of resistance capacity occurred above a threshold of 0.8 micromol Cd/g dry weight in the midgut gland of H. pomatia. At these Cd concentrations, Cd-MT was saturated with Cd(2+) ions, whereas at the cellular level, structural alterations turned into pathological deterioration.
在陆生肺螺类蜗牛中，镉（Cd）的摄入会导致镉特异性金属硫蛋白（Cd-MT）的诱导，从而保护其免受这种有毒金属离子的不利影响。镉浓度的增加会导致个体死亡率的增加，这可能与蜗牛中肠腺的病理变化有关。本研究采用组织金属分析和 MT 诱导参数定量相结合的组织学、免疫组织化学和电子显微镜方法，研究了 Cd 暴露的罗曼蜗牛（Helix pomatia）中肠腺。该器官发生了明显的浓度依赖性变化，包括金属诱导的 Cd-MT 浓度增加和所有中肠腺细胞类型中 Cd-MT mRNA 沉淀的出现。最明显的变化是细胞更新增加，反映为细胞增殖增强。嗜碱性细胞内质网泡状化加剧，排泄细胞中脂褐素颗粒形成增加。在最高 Cd 浓度下，嗜碱性细胞中线粒体膜被破坏，脂褐素颗粒从排泄细胞释放到中肠腺管状系统中。在低 Cd 浓度下检测到的一些变化（如细胞增殖率增加、内质网泡状化）被解释为增强暴露个体对金属胁迫的耐受能力的适应性反应过程。在较高 Cd 浓度下（如线粒体结构损伤）发生的细胞变化明显代表了持续的不可逆转的细胞破坏。细胞生物标志物和 MT 饱和度水平的综合评估表明，从中肠腺抵抗应激到耗尽抵抗能力的转变发生在 0.8 微摩尔 Cd/g 干重以上的阈值之上。在这些 Cd 浓度下，Cd-MT 被 Cd(2+)离子饱和，而在细胞水平上，结构变化转变为病理恶化。
