Author Correction: Forearc carbon sink reduces long-term volatile recycling into the mantle.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

Author Correction: Forearc carbon sink reduces long-term volatile recycling into the mantle.

Change history: In this Article, the original affiliation 2 was not applicable and has been removed. In addition, in the Acknowledgements there was a statement missing and an error in a name. These errors have been corrected online.

Forearc carbon sink reduces long-term volatile recycling into the mantle.

Carbon and other volatiles in the form of gases, fluids or mineral phases are transported from Earth's surface into the mantle at convergent margins, where the oceanic crust subducts beneath the continental crust. The efficiency of this transfer has profound implications for the nature and scale of geochemical heterogeneities in Earth's deep mantle and shallow crustal reservoirs, as well as Earth's oxidation state. However, the proportions of volatiles released from the forearc and backarc are not well constrained compared to fluxes from the volcanic arc front. Here we use helium and carbon isotope data from deeply sourced springs along two cross-arc transects to show that about 91 per cent of carbon released from the slab and mantle beneath the Costa Rican forearc is sequestered within the crust by calcite deposition. Around an additional three per cent is incorporated into the biomass through microbial chemolithoautotrophy, whereby microbes assimilate inorganic carbon into biomass. We estimate that between 1.2 × 108 and 1.3 × 1010 moles of carbon dioxide per year are released from the slab beneath the forearc, and thus up to about 19 per cent less carbon is being transferred into Earth's deep mantle than previously estimated.

Copper toxicosis in New Zealand White rabbits (Oryctolagus cuniculus).

Six 12- to 14-month-old New Zealand White rabbits were diagnosed with copper toxicosis. These rabbits were part of a group of 110 purchased and shipped overnight for research purposes. On arrival, the group experienced an abrupt diet change. Eight died over 3 weeks and 6 were submitted for postmortem examination. Microscopic findings included severe centrilobular to midzonal hepatocellular necrosis with rhodanine stain-positive copper granules in the remaining hepatocytes. Mild periportal fibrosis and biliary hyperplasia, hemoglobinuric nephrosis, and splenic erythrophagocytosis were also observed. Hepatic copper concentrations were elevated, ranging from 319 to 997 ppm. Clinical disease was not previously observed in younger rabbits gradually transitioned from the supplier's copper-supplemented diet. Copper toxicosis likely occurred in these rabbits from a combination of (1) increased duration of copper supplementation leading to increased hepatocellular stores and (2) stress leading to anorexia and release of hepatocellular copper stores similar to chronic copper toxicosis as described in sheep.