Fe(III)-doped activated biochar sorbents trigger mitochondrial dysfunction with oxidative stress on Daphnia magna

This study investigates the ecotoxicological effects of the synthesized Fe(III)-doped activated biochar (FeAB) sorbents using Daphnia magna and elucidates the underline mechanism of potential oxidative stress that may be induced by the sorbent. The EC50 value was determined to be 68.8 mg L-1. The superoxide dismutase (SOD) activity of D. magna was generally inhibited and the glutathione (GSH) level was significantly reduced even at the lowest FeAB concentration used (i.e., 0.12 mg L-1). This means that the antioxidant system of D. magna can be significantly inhibited by exposure to even a small amount of FeAB. While the higher reactive oxygen species (ROS)/reactive nitrogen species (RNS) levels in the exposed samples than the control at low FeAB concentrations (i.e., <15.63 mg L-1) suggest the failure of the anti-oxidation mechanism of SOD and GSH, the lower average levels of ROS/RNS in the exposed samples than the control at relatively high concentrations (i.e., 31.25-1000 mg L-1) can be explained by the reduced ROS/RNS production due to cell damage. Furthermore, the mitochondrial complex III activities were significantly inhibited in a FeAB concentration-dependent manner. Overall, the FeAB sorbent down-regulates the antioxidant mechanism, and this, together with the inefficient mitochondria, increases the ROS generation, leading to mitochondrial dysfunction again. The potential oxidative stress of FeAB on D. manga observed in this study suggests that the environmental application of FeAB needs to adopt a method that can minimize the direct contact between FeAB and organisms.

Automated summary

This study reveals that FeAB may induce oxidative stress in Daphnia, inhibiting their antioxidant system. Exposure to low concentrations of FeAB results in higher ROS/RNS levels, indicating antioxidant mechanism failure, while exposure to relatively high concentrations leads to reduced ROS/RNS levels possibly due to decreased production from cell damage.