RESUMEN
Antibiotics in aqueous environments can have extremely adverse effects on non-targeted organisms. However, many research projects have only focused on the toxicological evaluation of individual antibiotics in various environments. In the present work, individual and binary mixture toxicity experiments have been conducted with the model organism Raphidocelis subcapitata (R. subcapitata), and a mixture concentration-response curve was established and contrasted with the estimated effects on the basis of both the concentration addition (CA) and the independent action (IA) models. In addition, different risk assessment methods were used and compared to evaluate the environmental risk of binary mixtures. The toxic ranking of the selected antibiotics to R. subcapitata was erythromycin (ERY) > sulfamethoxazole (SMX) > sulfamethazine (SMZ). In general, the conclusion of this study is that the adverse effects of binary mixtures are higher than the individual antibiotics. The CA model and RQSTU are more suitable for toxicity prediction and risk assessment of binary mixtures. This study reveals the potential ecological risks that antibiotics and their mixtures may pose to water ecosystems, thus providing scientific information for environmental quality regulation.
RESUMEN
Haloacetonitriles (HANs) are nitrogenous disinfection byproducts (N-DBPs) detected in drinking water that have high toxicity and are a high risk to human health. The cytotoxicity and genotoxicity as well as the oxidative stress of five HANs, namely chloroacetonitrile (CAN), dichloroacetonitrile (DCAN), trichloroacetonitrile (TCAN), bromoacetonitrile (BAN), and dibromoacetonitrile (DBAN) on a hepatoma cell line (HepG2) were determined by single, binary or ternary exposure. The median effective concentrations, based on cell viability, ranged from 0.8360â¯mg/L for BAN to 256.9â¯mg/L for DCAN, with a cytotoxicity order of BANâ¯>â¯DBANâ¯>â¯CANâ¯>â¯TCANâ¯>â¯DCAN. The lowest observed effective concentrations regarding DNA damage were 0.01â¯mg/L for CAN and DCAN, 0.1â¯mg/L for DBAN and TCAN, and 1â¯mg/L for BAN. The DNA damage induced by CAN, DCAN and TCAN was repaired to about 80% in 30â¯min, and when induced by BAN and DBAN, it was repaired completely in 60â¯min. The intracellular reactive oxygen species (ROS) levels were significantly increased by the five HANs, and bromo-acetonitrile produced a stronger oxidative stress than chloro-acetonitrile. Co-exposure of DCAN, TCAN and DBAN significantly inhibited cell viability, induced DNA damage and facilitated ROS generation in HepG2 cells. However, the interactive effects were inconsistent for the different endpoints, which seemed to be antagonism for cell viability but synergy for ROS generation.