Does a short-term exposure to atrazine provoke cellular senescence in Chlamydomonas reinhardtii?

The aim of this study was to investigate the impacts and modes of action of a chemical and nutrient deprivation on the cellular senescence process of Chlamydomonas reinhardtii. Several molecular and cellular parameters related to senescence phenomena were monitored in C. reinhardtii cells exposed for 24h to a sublethal concentration (0.25μM) of the herbicide atrazine and in unexposed 96h cells in an early stationary phase of growth. All endpoints showed the same pattern of response between treatments, except for the intracellular level of calcium, where a significant increase was observed in 24h-exposed cultures compared to 24h-log controls. Results also indicated that cell viability remained above 98% for all conditions. Reactive oxygen species (ROS) levels and caspase activity increased in all experimental cultures with respect to 24h-log controls and alterations in the nuclear morphology and cells with auto-phagosomes were observed in all treatments. However, a decrease in lipid peroxidation was detected which could be related to the observed increment of autophagic vacuoles that recycle damaged material, such as altered lipids in microalgal membranes. Furthermore, responses at the molecular level were also investigated. Gene transcription analyses, carried out by RT-qPCR technique, indicated an increase in transcripts for genes encoding glutathione S-transferase (GST) and ascorbate peroxidase (APX I) and a decrease for those encoding catalase (CAT), glutathione peroxidase (GPX) and Mn-superoxide dismutase (SOD-1) in both experimental treatments. Overall molecular and cellular results suggest that a short-term exposure to a sublethal concentration of atrazine may induce senescence features in microalgal cells which are the base of aquatic food webs.