Polymer coating of copper oxide nanoparticles increases nanoparticles uptake and toxicity in the green alga Chlamydomonas reinhardtii

Copper oxide nanoparticles (CuO NPs) are frequently used in a polymer-coated form, to be included in paints or fabrics for antimicrobial properties. Their application in antifouling paints may lead to the contamination of aquatic ecosystems. However, the toxicological risk of NPs in the environment is hard to evaluate due to a lack of knowledge on the mechanisms of NP interaction with biological systems. In this study, we investigated the effect of polymer coating on CuO NP toxicity in the green alga Chlamydomonas reinhardtii by comparing bare and polymer-coated CuO NPs prepared from the same CuO nanopowder. Both CuO NP suspensions were toxic to C. reinhardtii after 6 h treatment to concentrations of 0.005-0.04 g L⁻¹. Bare and polymer-coated CuO NPs induced a decrease of Photosystem II activity and the formation of reactive oxygen species. Polymer-coated CuO NP was found to be more toxic than the uncoated CuO NP. The higher toxicity of CS-CuO NP was mainly associated with the increased capacity of polymer-coated CuO NP to penetrate the cell compared to bare CuO NPs. These results indicates that the high toxicity of polymer-coated CuO NPs in algal cells results of intracellular interactions between NPs and the cellular system.     

Induction to oxidative stress by saxitoxin investigated through lipid peroxidation in Neuro 2A cells and Chlamydomonas reinhardtii alga

Saxitoxin (STX) is a cyanotoxin, which can cause neurotoxic effects and induce ecological changes in aquatic environments, a potential risk to public and environmental health. Many studies of cytotoxicity on animal cells and algae have been performed, although few compare the toxic effects between the two models. In this sense, we investigated the oxidative stress induced by STX (0.4-3.0 nM) in two different cellular models: Neuro-2A (N2A) cells and Chlamydomonas reinhardtii alga by quantification of malondialdehyde (MDA) levels as indicative of lipid peroxidation (LPO). Also was evaluated the antioxidant defense of these cells systems after exposure to STX by the addition of antioxidants in N2A cells culture, and by the measure of antioxidants enzymes activity in C. reinhardtii cells. The MDA levels of N2A cells increased from 15% to 113% for 0.4 and 3.0 nM of STX, respectively, as compared to control. Superoxide-dismutase and catalase did not appear to protect the cell from STX effect while, in cells treated with vitamin E, the rates of MDA production decreased significantly, except for higher concentrations of STX. No MDA productions were observed in algal cells however some effects on antioxidant enzymes activity were observed when algae were exposed to 3.0 nM STX. Our results indicate that the concentrations of STX that may induce oxidative stress through LPO are different in animal and phytoplankton communities. A combination of algal and animal bioassays should be conducted for reliable assessment of oxidative stress induced by STX.