Shandong Jinan Eco-environmental Monitoring Center, Jinan 250014, China; Environmental Sciences Division, Oak Ridge National Laboratory, Oak Ridge, Ten 37831, United States.
Environmental Sciences Division, Oak Ridge National Laboratory, Oak Ridge, Ten 37831, United States; Qilu University of Technology (Shandong Academy of Sciences), Shandong Analysis and Test Center, Jinan 250014, China.
J Hazard Mater. 2022 Jul 5;433:128835. doi: 10.1016/j.jhazmat.2022.128835. Epub 2022 Apr 1.
Mercury (Hg) is a pervasive environmental pollutant and poses serious health concerns as inorganic Hg(II) can be converted to the neurotoxin methylmercury (MeHg), which bioaccumulates and biomagnifies in food webs. Phytoplankton, representing the base of aquatic food webs, can take up Hg(II) and influence MeHg production, but currently little is known about how and to what extent phytoplankton may impact Hg(II) methylation by itself or by methylating bacteria it harbors. This study investigated whether some species of phytoplankton could produce MeHg and how the live or dead phytoplankton cells and excreted algal organic matter (AOM) impact Hg(II) methylation by several known methylators, including iron-reducing bacteria (FeRB), Geobacter anodireducens SD-1 and Geobacter sulfurreducens PCA, and the sulfate-reducing bacterium (SRB) Desulfovibrio desulfuricans ND132 (or Pseudodesulfovibrio mercurii). Our results indicate that, among the 4 phytoplankton species studied, none were capable of methylating Hg(II). However, the presence of phytoplankton cells (either live or dead) from Chlorella vulgaris (CV) generally inhibited Hg(II) methylation by FeRB but substantially enhanced methylation by SRB D. desulfuricans ND132. Enhanced methylation was attributed in part to CV-excreted AOM, which increased Hg(II) complexation and methylation by ND132 cells. In contrast, inhibition of methylation by FeRB was attributed to these bacteria incapable of competing with phytoplankton for Hg(II) binding and uptake. These observations suggest that phytoplankton could play different roles in affecting Hg(II) methylation by the two groups of anaerobic bacteria, FeRB and SRB, and thus shed additional light on how phytoplankton blooms may modulate MeHg production and bioaccumulation in the aquatic environment.
汞（Hg）是一种普遍存在的环境污染物，因其无机形式的 Hg(II) 可转化为神经毒素甲基汞（MeHg），而对健康构成严重威胁，后者在食物网中具有生物累积性和生物放大性。浮游植物是水生食物网的基础，能够摄取 Hg(II) 并影响 MeHg 的生成，但目前对于浮游植物本身或其所携带的甲基化细菌会以何种方式以及在何种程度上影响 Hg(II) 甲基化知之甚少。本研究调查了某些浮游植物物种是否能够生成 MeHg，以及活的或死的浮游植物细胞和分泌的藻类有机物质（AOM）会如何影响几种已知甲基供体（包括铁还原菌（FeRB）、Geobacter anodireducens SD-1 和 Geobacter sulfurreducens PCA 以及硫酸盐还原菌（SRB）Desulfovibrio desulfuricans ND132（或 Pseudodesulfovibrio mercurii））对 Hg(II) 的甲基化作用。结果表明，在所研究的 4 种浮游植物物种中，没有一种能够甲基化 Hg(II)。然而，Chlorella vulgaris (CV) 的浮游植物细胞（无论是活的还是死的）的存在通常会抑制 FeRB 对 Hg(II) 的甲基化，但会显著增强 SRB D. desulfuricans ND132 的甲基化作用。增强的甲基化作用部分归因于 CV 分泌的 AOM，它增加了 Hg(II)的络合和 ND132 细胞的甲基化作用。相反，FeRB 对甲基化的抑制归因于这些细菌无法与浮游植物竞争 Hg(II)的结合和摄取。这些观察结果表明，浮游植物可能在影响两种厌氧细菌（FeRB 和 SRB）对 Hg(II)甲基化方面发挥不同的作用，从而进一步阐明浮游植物爆发如何调节水生环境中 MeHg 的生成和生物累积。
