Accumulation and phytotoxicity of technical hexabromocyclododecane in maize

To investigate the accumulation and phytotoxicity of technical hexabromocyclododecane（HBCD）in maize,young seedlings were exposed to solutions of technical HBCD at different concentrations.The uptake kinetics showed that the HBCD concentration reached an apparent equilibrium within 96 hr,and the accumulation was much higher in roots than in shoots.HBCD accumulation in maize had a positive linear correlation with the exposure concentration.The accumulation of different diastereoisomers followed the orderγ-HBCD〉β-HBCD〉α-HBCD.Compared with their proportions in the technical HBCD exposure solution,the diastereoisomer contribution increased forβ-HBCD and decreased forγ-HBCD in both maize roots and shoots with exposure time,whereas the contribution ofα-HBCD increased in roots and decreased in shoots throughout the experimental period.These results suggest the diastereomer-specific accumulation and translocation of HBCD in maize.Inhibitory effects of HBCD on the early development of maize followed the order of germination rate〉root biomass≥root elongation〉shoot biomass≥shoot elongation.Hydroxyl radical（OH）and histone H2AX phosphorylation（γ-H2AX）were induced in maize by HBCD exposure,indicative of the generation of oxidative stress and DNA double-strand breaks in maize.An OH scavenger inhibited the expression ofγ-H2AX foci in both maize roots and shoots,which suggests the involvement of OH generation in the HBCD-induced DNA damage.The results of this study will offer useful information for a more comprehensive assessment of the environmental behavior and toxicity of technical HBCD.

Monohalogenated acetamide-induced cellular stress and genotoxicity are related to electrophilic softness and thiol/thiolate reactivity

Haloacetamides（HAMs） are cytotoxic, genotoxic, and mutagenic byproducts of drinking water disinfection. They are soft electrophilic compounds that form covalent bonds with the free thiol/thiolate in cysteine residues through an S_N2 reaction mechanism.Toxicity of the monohalogenated HAMs（iodoacetamide, IAM; bromoacetamide, BAM;or chloroacetamide, CAM） varied depending on the halogen substituent. The aim of this research was to investigate how the halogen atom affects the reactivity and toxicological properties of HAMs, measured as induction of oxidative/electrophilic stress response and genotoxicity. Additionally, we wanted to determine how well in silico estimates of electrophilic softness matched thiol/thiolate reactivity and in vitro toxicological endpoints.Each of the HAMs significantly induced nuclear Rad51 accumulation and ARE signaling activity compared to a negative control. The rank order of effect was IAM 〉 BAM 〉 CAM for Rad51, and BAM ≈ IAM 〉 CAM for ARE. In general, electrophilic softness and in chemico thiol/thiolate reactivity provided a qualitative indicator of toxicity, as the softer electrophiles IAM and BAM were more thiol/thiolate reactive and were more toxic than CAM.