Nostoc entophytum cell response to cadmium exposure: A possible role of chaperon proteins GroEl and HtpG in cadmium-induced stress.

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.