The present study is pursuing our previous research, focused on some aspects of Nostoc entophytum ISC32 cell response to the stress caused by exposure to cadmium at the cellular and molecular levels. Variations in the antioxidant system (catalase and ascorbate peroxidase activity) of N. entophytum ISC32 exposed to varying concentrations of Cd (2, and 5 mg/L) resulted in a significant increase in the activity of both catalase and peroxidase. Activity of these enzymes was, however, not significantly changed in the presence of Cd concentrations of 10 and 20 mg/L. Levels of lipid peroxidation, as measured by malondialdehyde (MDA) assay, were observed in response to exposure to Cd (20 mg/L). There was, however, a sharp drop in both antioxidant and lipid peroxidation activities of Cd treated cells after 5 days exposure, likely in consequence of cellular damage. The content of chlorophyll a and phycobiliproteins of living cells were altered under Cd-induced conditions. TEM images of cyanobacterial cells treated with Cd showed cell surface alteration and modification along with altered cellular microcompartments. Cyanobacterial cells treated with Cd at concentrations below the minimum inhibitory concentration (MIC) remained with no apparent structural changes. However, at a higher concentration of Cd (30 mg/L), a clear detachment effect was observed between the mucilage external layer and cell membrane which may be attributed to cell plasmolysis due to toxic effects of Cd. Subsequently, the thickness of the ring-shaped mucilage external layer increased likely as a result of the cell defense mechanisms against toxic concentrations of Cd. Characterization of cells treated with Cd (30 and 150 mg/L) by scanning electron microscopy (SEM) indicated cell shrinkage with varying degrees of distortion and surface wrinkling. Energy-dispersive X-ray spectrometry (EDS) analysis suggested that Cd was not present as nanoparticles within the cell, but in the form of salt or other molecular structures. The up-regulation of chaperons was confirmed for GroEL and HtpG using real-time PCR and northern blot analyses. Interestingly, the expression of GroEL was markedly increased at lower Cd concentration (5 mg/L). However, the ISC32 strain accrued higher levels of HtpG transcript in response to an elevated concentration of Cd (15 mg/L). This pattern seems to be related to the fast and early induction of GroEL, which may be necessary for induction of other factors and heat shock proteins such as HtpG in Cd-treated Nostoc cells. The result of this study paves the way for a more detailed exploration of Cd effects on the defense mechanisms of cyanobacteria. Our research also shed some light on how cyanobacterial cells have evolved to respond to the heavy metal toxicity at the cellular, molecular and ultrastructural levels.

本研究正在进行我们以前的研究，重点在于Nostoc内生菌ISC32细胞在细胞和分子水平上对因暴露于镉引起的应激反应的某些方面。内生烟草抗氧化系统的变化（过氧化氢酶和抗坏血酸过氧化物酶活性）暴露于不同浓度的Cd（2和5 mg / L）的ISC32导致过氧化氢酶和过氧化物酶的活性显着增加。但是，在Cd浓度为10和20 mg / L的情况下，这些酶的活性没有明显改变。通过丙二醛（MDA）分析测得的脂质过氧化水平是对Cd（20 mg / L）暴露的响应。但是，暴露5天后，经Cd处理的细胞的抗氧化剂和脂质过氧化活性均急剧下降，这可能是细胞损伤的结果。在镉诱导的条件下，活细胞的叶绿素a和藻胆蛋白的含量发生了变化。Cd处理的蓝细菌细胞的TEM图像显示了细胞表面的变化和修饰以及细胞微区室的变化。低于最小抑制浓度（MIC）的Cd处理的蓝细菌细胞没有明显的结构变化。然而，在较高浓度的Cd（30 mg / L）下，在粘液外层和细胞膜之间观察到明显的脱离效果，这可能归因于Cd的毒性作用引起的细胞质分解。随后，环形粘液外层的厚度可能由于抗Cd毒性浓度的细胞防御机制而增加。通过扫描电子显微镜（SEM）对用Cd（30和150 mg / L）处理的细胞进行表征，表明细胞在收缩的同时具有不同程度的变形和表面起皱。能量色散X射线能谱（EDS）分析表明，镉在细胞内不以纳米颗粒的形式存在，但以盐或其他分子结构的形式存在。使用实时PCR和Northern印迹分析证实了GroEL和HtpG分子伴侣的上调。有趣的是，在较低的Cd浓度（5 mg / L）下，GroEL的表达明显增加。但是，ISC32菌株响应高浓度的Cd（15 mg / L）产生更高水平的HtpG转录物。这种模式似乎与GroEL的快速早期诱导有关，这对于诱导其他因素和热休克蛋白（如Cd处理过的HtpG）可能是必需的 ISC32菌株响应高浓度的Cd（15 mg / L）产生更高水平的HtpG转录物。这种模式似乎与GroEL的快速早期诱导有关，这对于诱导其他因素和热休克蛋白（如Cd处理过的HtpG）可能是必需的 ISC32菌株响应高浓度的Cd（15 mg / L）产生更高水平的HtpG转录物。这种模式似乎与GroEL的快速早期诱导有关，这对于诱导其他因素和热休克蛋白（如Cd处理过的HtpG）可能是必需的鼻腔细胞。这项研究的结果为进一步研究Cd对蓝细菌防御机制的影响铺平了道路。我们的研究还揭示了蓝藻细胞如何演变成对细胞，分子和超微结构水平的重金属毒性作出反应。