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Abstract Arsenic (As) and mercury (Hg) were examined in the Yellowstone Lake food chain, focusing on two lake locations separated by approximately 20 km and differing in lake floor hydrothermal vent activity. Sampling spanned from femtoplankton to the main fish species, Yellowstone cutthroat trout and the apex predator lake trout. Mercury bioaccumulated in muscle and liver of both trout species, biomagnifying with age, whereas As decreased in older fish, which indicates differential exposure routes for these metal(loid)s. Mercury and As concentrations were higher in all food chain filter fractions (0.1-, 0.8-, and 3.0-μm filters) at the vent-associated Inflated Plain site, illustrating the impact of localized hydrothermal inputs. Femtoplankton and picoplankton size biomass (0.1- and 0.8-μm filters) accounted for 30%–70% of total Hg or As at both locations. By contrast, only approximately 4% of As and <1% of Hg were found in the 0.1-μm filtrate, indicating that comparatively little As or Hg actually exists as an ionic form or intercalated with humic compounds, a frequent assumption in freshwaters and marine waters. Ribosomal RNA (18S) gene sequencing of DNA derived from the 0.1-, 0.8-, and 3.0-μm filters showed significant eukaryote biomass in these fractions, providing a novel view of the femtoplankton and picoplankton size biomass, which assists in explaining why these fractions may contain such significant Hg and As. These results infer that femtoplankton and picoplankton metal(loid) loads represent aquatic food chain entry points that need to be accounted for and that are important for better understanding Hg and As biochemistry in aquatic systems. Environ Toxicol Chem 2023;42:225–241. © 2022 SETAC 

Summary Arsenic is a toxin, ranking first on the Agency for Toxic Substances and Disease Registry and the Environmental Protection Agency Priority List of Hazardous Substances. Chronic exposure increases the risk of a broad range of human illnesses, most notably cancer; however, there is significant variability in arsenic‐induced disease among exposed individuals. Human genetics is a known component, but it alone cannot account for the large inter‐individual variability in the presentation of arsenicosis symptoms. Each part of the gastrointestinal tract (GIT) may be considered as a unique environment with characteristic pH, oxygen concentration, and microbiome. Given the well‐established arsenic redox transformation activities of microorganisms, it is reasonable to imagine how the GIT microbiome composition variability among individuals could play a significant role in determining the fate, mobility and toxicity of arsenic, whether inhaled or ingested. This is a relatively new field of research that would benefit from early dialogue aimed at summarizing what is known and identifying reasonable research targets and concepts. Herein, we strive to initiate this dialogue by reviewing known aspects of microbe–arsenic interactions and placing it in the context of potential for influencing host exposure and health risks. We finish by considering future experimental approaches that might be of value. 

Summary In environments where arsenic and microbes coexist, microbes are the principal drivers of arsenic speciation, which directly affects bioavailability, toxicity and bioaccumulation. Speciation reactions influence arsenic behaviour in environmental systems, directly affecting human and agricultural exposures. Arsenite oxidation decreases arsenic toxicity and mobility in the environment, and therefore understanding its regulation and overall influence on cellular metabolism is of significant interest. The arsenite oxidase (AioBA) is regulated by a three‐component signal transduction system AioXSR, which is in turn regulated by the phosphate stress response, with PhoR acting as the master regulator. Using RNA‐sequencing, we characterized the global effects of arsenite on gene expression inAgrobacterium tumefaciens5A. To further elucidate regulatory controls, mutant strains for histidine kinases PhoR and AioS were employed, and illustrate that in addition to arsenic metabolism, a host of other functional responses are regulated in parallel. Impacted functions include arsenic and phosphate metabolism, carbohydrate metabolism, solute transport systems and iron metabolism, in addition to others. These findings contribute significantly to the current understanding of the metabolic impact and genetic circuitry involved during arsenite exposure in bacteria. This informs how arsenic contamination will impact microbial activities involving several biogeochemical cycles in nature.