Analysis of the Response of Chlamydomonas reinhardtii to Cobalt Ions Reveals the Protective Role of Thiols, Ascorbate, and Prenyllipid Antioxidants, and the Negative Impact of Cobalt Toxicity on Photoprotective Mechanisms

Cobalt (Co) is an essential micronutrient for many organisms, but, at higher concentrations, it becomes harmful, primarily due to competitive interactions with other metal ions. Enzyme inhibition and disruption of nutrient homeostasis may lead to oxidative stress in Co-exposed cells. Compared to other heavy metals, such as Cd, Cu, Cr, Pb, or Ni, this element has been less studied in algae with respect to its toxicity and tolerance. Taking into account Co-induced oxidative stress and antioxidant response, the studies on algae usually did not cover a wider range of antioxidants and ROS-detoxifying enzymes monitored in one model. The aim of this study was to assess the impact of CoCl₂ on the model green microalga <i>Chlamydomonas reinhardtii</i> from a broader perspective. We monitored algal growth, photosynthetic pigment content, the maximum quantum yield of photosystem II (F_v/F_m), the efficiency of nonphotochemical quenching of chlorophyll fluorescence (NPQ), and oxidative stress markers (superoxide production, lipid peroxidation). The measured antioxidants included soluble thiols, ascorbate (Asc), proline (Pro), α-tocopherol (α-Toc), and plastoquinol (PQH₂-9). The superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) activities were also determined. Exposure to CoCl₂ resulted in increased levels of thiols, Asc, α-Toc, PQH₂-9, and CAT activity. At lower concentrations of CoCl₂, no increase in oxidative stress markers was observed, suggesting efficient antioxidant protection. On the contrary, exposure to higher concentrations of CoCl₂ caused the inhibition of growth and chlorophyll (Chl) synthesis, as well as the reduction in the Chl <i>a</i>/Chl <i>b</i> ratio, the F_v/F_m parameter, the efficiency of NPQ induction, and the levels of lipophilic antioxidants, along with an increase in lipid hydroperoxides. An interesting and novel result is the inhibitory effect of Co toxicity on state transitions in exposed algae.