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铜离子(Cu(2+))抑制铜绿微囊藻的光系统II活性,但提高其光系统I的量子产率。

Cu(2+) inhibits photosystem II activities but enhances photosystem I quantum yield of Microcystis aeruginosa.

作者信息

Deng Chunnuan, Pan Xiangliang, Wang Shuzhi, Zhang Daoyong

机构信息

Key Lab of Plateau Lake Ecology and Global Change, College of Tourism and Geographic Science, Yunnan Normal University, Kunming, 650500, China.

出版信息

Biol Trace Elem Res. 2014 Aug;160(2):268-75. doi: 10.1007/s12011-014-0039-z. Epub 2014 Jun 13.

Abstract

Responses of photosystem I and II activities of Microcystis aeruginosa to various concentrations of Cu(2+) were simultaneously examined using a Dual-PAM-100 fluorometer. Cell growth and contents of chlorophyll a were significantly inhibited by Cu(2+). Photosystem II activity [Y(II)] and electron transport [rETRmax(II)] were significantly altered by Cu(2+). The quantum yield of photosystem II [Y(II)] decreased by 29 % at 100 μg L(-1) Cu(2+) compared to control. On the contrary, photosystem I was stable under Cu(2+) stress and showed an obvious increase of quantum yield [Y(I)] and electron transport [rETRmax(I)] due to activation of cyclic electron flow (CEF). Yield of cyclic electron flow [Y(CEF)] was enhanced by 17 % at 100 μg L(-1) Cu(2+) compared to control. The contribution of linear electron flow to photosystem I [Y(II)/Y(I)] decreased with increasing Cu(2+) concentration. Yield of cyclic electron flow [Y(CEF)] was negatively correlated with the maximal photosystem II photochemical efficiency (F v/F m). In summary, photosystem II was the major target sites of toxicity of Cu(2+), while photosystem I activity was enhanced under Cu(2+) stress.

摘要

使用双调制叶绿素荧光仪(Dual-PAM-100)同时检测了铜绿微囊藻光系统I和II活性对不同浓度Cu(2+)的响应。Cu(2+)显著抑制了细胞生长和叶绿素a含量。光系统II活性[Y(II)]和电子传递[rETRmax(II)]受到Cu(2+)的显著影响。与对照组相比,在100 μg L(-1) Cu(2+)浓度下,光系统II的量子产率[Y(II)]下降了29%。相反,在Cu(2+)胁迫下光系统I较为稳定,并且由于循环电子流(CEF)的激活,其量子产率[Y(I)]和电子传递[rETRmax(I)]显著增加。与对照组相比,在100 μg L(-1) Cu(2+)浓度下,循环电子流的产率[Y(CEF)]提高了17%。线性电子流对光系统I的贡献[Y(II)/Y(I)]随着Cu(2+)浓度的增加而降低。循环电子流的产率[Y(CEF)]与光系统II的最大光化学效率(F v/F m)呈负相关。总之,光系统II是Cu(2+)毒性作用的主要靶点,而在Cu(2+)胁迫下光系统I的活性增强。

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