Effects and Mechanisms of Cadmium on the Degradation of Microcystin-LR by Sphingopyxis sp. YF1

Abstract

In this study, we investigated the effects of cadmium concentration on the degradation of microcystin-LR by Sphingopyxis sp. YF1, a highly efficient microcystins degrading bacterium. Our results demonstrate that 0. 25 mg/L cadmium decreased the degradation rate at 30 min, but had no significant effect on the biodegradation of MC-LR after 60 min; however, 4 mg/L cadmium significantly reduced the biodegradation rate of MC-LR throught the time points tested. The morphologies of cells in the presence of 0. 25 mg/L cadmium and in the absence of cadmium were similar. However, aggregation of cells was observed at a cadmium concentration of 4 mg/L. At the concentrations of 0. 25 mg/L (for 30 min and 60 min) and 4 mg/L (for 60 min and 90 min), there was an increase in cell membrane permeability, along with a significant rise in intracellular ATP content within 30 minutes. However, no significant changes were observed in MDA content or in the expression of degradation genes. When treated with 4 mg/L cadmium, cell membrane permeability increased, while intracellular ATP content rose within 30 minutes but declined at 60 minutes. Furthermore, MDA content increased significantly, indicating that 4 mg/L cadmium could induce oxidative damage to cells. Additionally, the expression of the gene encoding the ATP synthase B subunit was upregulated. Cadmium exerted a substantial influence on the degradation rate, cell morphology, energy metabolism and oxidative stress state of Sphingopyxis sp. YF1 during microcystin-LR degradation process providing valuable insights into how heavy metal pollution impacts microbial-mediated microcystinLR degradation. The present study demonstrated distinct effects of low and high concentrations of cadmium on the degradation of MC-LR by bacteria. Specifically, the high concentration of cadmium primarily impacts the biodegradation of MC-LR by inducing cellular damage through oxidative stress, rather than suppressing the expression of genes associated with MC-LR degradation.