共存Zn(Ⅱ)抑制Pannonibacter phragmitetus BB还原Cr(Ⅵ)的分子机理

MOLECULAR MECHANISM OF Cr(Ⅵ) REDUCTION INHIBITION BY PANNONIBACTER PHRAGMITETUS BB WITH CO-EXISTING Zn(Ⅱ)

通过电子传递体系活性、酶活性以及实时定量PCR技术,揭示共存Zn(Ⅱ)延迟Pannonibacter phragmitetus BB(BB)生长,抑制Cr(Ⅵ)还原的分子机理。结果表明:共存Zn(Ⅱ)抑制BB菌还原Cr(Ⅵ)主要表现为胞内和胞外抑制,共存Zn(Ⅱ)通过降低电子传递体系活性和细胞色素c氧化酶活性,抑制其胞外Cr(Ⅵ)还原;共存Zn(Ⅱ)通过降低铬转运效率的方式,抑制其胞内Cr(Ⅵ)还原。SOD、CAT、POD、GST 4种抗氧化酶活性的研究表明:共存Zn(Ⅱ)引起的胞内氧化压力较小,对BB菌造成的毒性较低,从侧面印证了共存Zn(Ⅱ)对BB菌生长的延迟作用。

The mechanisms of microbial growth delay and Cr(Ⅵ) reduction inhibition by co-existing Zn(Ⅱ) were revealed through the electron transport system activity, enzyme activity, and real-time quantitative PCR technology. The Cr(Ⅵ) reduction by strain BB was intracellularly and extracellularly inhibited by co-existing Zn(Ⅱ). The decrease of microbial electron transport system activity and cytochrome c oxidase activity caused by co-existing Zn(Ⅱ) were responsible for the extracellular inhibition. While intracellular Cr(Ⅵ) reduction was inhibited by reducing the efficiency of chromium transport. The activities of SOD, CAT, POD, and GST indicated that the co-existing Zn(Ⅱ) was lower toxic to strain BB, which could explained the growth delay of strain BB caused by co-existing Zn(Ⅱ).