New mechanistic insights into soil ecological risk assessment of arsenite (III) and arsenate (V)：Cellular and molecular toxicity responses in Eisenia fetida.

Inorganic arsenic (iAs) is a persistent bioaccumulation carcinogen that is most abundant in soils in the form of arsenite-As (III) and arsenate-As (V). However, there is currently very little explicit evidence about cytotoxicity of As on soil organisms. Moreover, toxicological data for iAs and proteotoxicity is shortage. The purpose of the present work is to elucidate the cytotoxicity mechanism of As (III) and As (V) to earthworms, a soil ecological sentinel species, and the molecular mechanisms by which As (III)/As (V) directly bind to antioxidative enzyme Cu/Zn-superoxide dismutase (Cu/Zn-SOD). Results indicate that iAs triggered cell membrane injury and genotoxicity. As (V) (56.15 %) induced lower cell viability than As (III) (61.88 %). Higher ROS and lipid peroxidation level in As (V) support greater cytotoxicity. Differences in cellular uptake due to valence induced diverse levels of oxidative stress and cytotoxicity. At the molecular level, As (III) (129.33 %) induced higher Cu/Zn-SOD activity than As (V) (110.75 %). Changes in backbone, secondary structure, amino acid microenvironment and particle size of Cu/Zn-SOD further revealed the mechanisms of differential molecular toxicity of As (III) and As (V). Binding reactions with Cu/Zn-SOD explain differences in molecular toxicity. Collective research showed that iAs-induced oxidative stress and binding reactions determine the difference of SOD activity between As (III) and As (V) at the cellular level. This work offers new insights into the health risk assessment of As.