Abstract
Cyanobacterial blooms have become more frequent and serious in recent years. Not only do massive blooms cause environmental pollution and nutrient eutrophication, but they also produce microcystins (MCs), a group of toxic cycloheptapeptides, which threaten aquatic ecosystem and human health. As such, clarifying the allelopathic interactions between cyanobacteria and other algae is critical to better understand the driving factors of blooms. To date, however, such studies remain largely insufficient. Here, we treated model alga Chlamydomonas reinhardtii with microcystin-LR (MC-LR) to determine its allelopathic effects. Results showed that MC-LR markedly suppressed C. reinhardtii cell viability. Comparative proteomic and physiological analyses revealed that MC-LR significantly up-regulated protein abundance of antioxidants ascorbate peroxidase (APX) and catalase (CAT) at the beginning stage of exposure. This was accompanied by an over-accumulation of hydrogen peroxide (H2O2), suggesting that MC-LR suppresses cell viability via oxidative damage. Furthermore, we found that MCs induced desulfhydrase (DES) activity for hydrogen sulfide (H2S) generation at the beginning stage. Additional H2S donors reactivated antioxidant enzyme activity, which reduced H2O2 accumulation and ultimately enhanced C. reinhardtii tolerance to MC-LR damage. This effect could be reserved by inhibiting H2S biosynthesis. Simultaneously, we found that H2S also suppressed MC-LR-induced cell autophagy, and thus attenuated the toxic effects of MC-LR. Our findings suggest that oxidative bursts may be the main reason for the allelopathic effects of MC-LR on C. reinhardtii viability and that H2S signaling may enhance C. reinhardtii tolerance to MC-LR through the activation of antioxidant enzyme activity and suppression of cell autophagy.
Highlights
Toxic cyanobacterial algal blooms have become more frequent and serious in freshwater environments in recent years due to the effects of climatic change and nutrient overload
We found that MC-LR markedly suppressed C. reinhardtii growth, as presented by lower cell density and Fv/Fm ratio and higher cell death, suggesting general toxic allelopathic effects of MC-LR on C. reinhardtii
To better understand the detailed mechanism by which MC-LR attacks C. reinhardtii, we performed proteomic iTRAQ analysis and found several proteins that were differentially regulated by MC-LR treatment, including several defense proteins and antioxidant enzymes, suggesting that these proteins are possibly related to the effects of MC-LR on C. reinhardtii growth
Summary
Toxic cyanobacterial algal blooms have become more frequent and serious in freshwater environments in recent years due to the effects of climatic change and nutrient overload. These blooms threaten ecosystem functioning and are directly harmful to aquatic algae, macrophytes, invertebrates, fish, and humans (Duan et al, 2009; Paerl and Paul, 2012; Jiang et al, 2014). MCs belong to a group of cycloheptapeptide inhibitors of intracellular protein phosphatases 1&2A (PP1/PP2A) These toxins have been found to have adverse effects on the liver, small intestine, colon, brain, kidney, lung, heart, and reproductive system, and exhibit potential cancer-promoting activity (MankiewiczBoczek et al, 2006; Chen et al, 2009; Xu et al, 2018). The related mechanism of MC toxicity remains poorly known
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