Abstract:
Hexabromocyclododecane (HBCD) is extensively used as an additive brominated flame retardants (BFRs). Due to widespread spectra use of HBCD, it has been found universally in various environmental media including water, sediments, soil, and even in human milk. Moreover, it has multiple toxic effects including developmental toxicity, neurotoxicity and reproductive toxicity. Currently, many toxicological studies of HBCD have been carried out on aquatic organisms and terrestrial species. However, the toxicity of HBCD on soil nematodes is largely unknown. In order to understand toxicological effects along with the changes of stress response by HBCD exposure, the animal model
Caenorhabditis elegans was chosen for toxicity study. To fulfill the tasks, nematodes were exposed to various concentrations of HBCD (0, 0.2, 2, 20, 200 nmol/L) up to 24 h. Multiple endpoints along with the physiological levels (growth, reproduction, and locomotion behaviors), reactive oxygen species (ROS) production, degree of cell apoptosis and stress-related gene expressions, were tested on nematodes. Acute exposure to HBCD at different concentrations domain of 0.2~200 nmol/L did not obviously decrease the body bends and body length on nematodes. In contrast, acute exposure to HBCD at the concentration of 20 nmol/L significantly decreased the locomotion behaviors on nematodes, and the locomotion behaviors were most sensitive among the physiological endpoints. Acute exposure to HBCD at the concentration of 200 nmol/L could significantly increase the ROS production followed by the enhancement in degree of cell apoptosis on nematodes. The integrated gene expression profiles visually revealed that exposure to HBCD at the concentration of 200 nmol/L resulted in obvious change of stress-related gene expressions, and the increased expressions were pronounced in several genes related to oxidative stress and cell apoptotic, e.g.,
hsp-16.2,
hsp-16.48,
sod-1,
sod-3 and
cep-1 gene. Therefore, it was speculated that HBCD exposure induced the oxidative stress and cell apoptosis, which resulted in the adverse physiological effects. The
hsp-16.2,
hsp-16.4,
sod-1,
sod-3 and
cep-1 gene may play important roles in HBCD-induced toxicity, and the oxidative stress and cell apoptosis could be regulated by
hsp-16.2,
hsp-16.4,
sod-1,
sod-3 and
cep-1 gene. The results are helpful for understanding the toxic effects of HBCD and evaluating the potential risk of HBCD.