Transcriptome reveals overview of Ca^(2+) dose-dependent metabolism disorders in zebrafish larvae after Cd^(2+) exposure

Cadmium (Cd),a ubiquitous environmental hazardous heavy metal,poses a significant threat to the health of aquatic organisms,including teleosts.Although the toxic profile of Cd is well recognized,little is known regarding the overall view of toxic responses to varying aquatic environmental parameters (e.g.,water hardness) at an individual level.Herein,differences in water hardness were partially mimicked by adjusting Ca^(2+)levels in E3 medium.As an in vivo model,zebrafish embryos were exposed to variable Ca^(2+)levels (NV,normal Ca^(2+);LV,low Ca^(2+);HV,high Ca^(2+)) alone or combined with 30.7μg/L Cd^(2+)(NC,LC,and HC,respectively) until 144 hr post-fertilization.The genome-wide transcriptome revealed differentially expressed genes between groups.Functional enrichment analysis found that biological processes related to metabolism,particularly lipid metabolism,were significantly disrupted in NC and LC treatments,while a remission was observed in the HC group.Biochemical assays confirmed that the decrease in Ca^(2+)enhanced synthesis,inhibited mobilization and increased the storage of lipids in Cd^(2+)treatments.This study suggests that the toxic effect of Cd on biological pathways will be influenced by Ca^(2+),which will improve the toxicological understanding and facilitate accurate assessment of Cd.

Effects of Exogenous Carbon Monoxide Releasing Molecules on the Development of Zebrafish Embryos and Larvae

The use of exogenous carbon monoxide releasing molecules（CORMs）provides promise for clinical application;however,the hazard potential of CORMs in vivo remains poorly understood.The developmental toxicity of CORM-3 was investigated by exposure to concentrations ranging from 6.25 to400μmol/L during 4-144 h post fertilization.Toxicity endpoints of mortality,spontaneous movement,heart rate,hatching rate,malformation,body length,and larval behavior were measured.

An In Vitro and In Vivo Study of Thyroid Disruption of 1,2-Bis(2,4,6-tribromophenoxy)ethane(BTBPE)�A Novel Brominated Flame Retardant

The novel brominated flame retardant,1,2-bis-(2,4,6-tribromophenoxy)ethane(BTBPE),is an emerging environ-mental pollutant with undetermined toxicity.We investigated how BTBPE causes thyroid endocrine disruption with integrated in silico,in vitro,and in vivo assays.In yeast two-hybrid and T-Screen assays,BTBPE interacted with zebrafish thyroid hormone receptors with binding energies weaker than the TR agonist-3,3′,5-Triiodo-L-thyronine(T3),and disrupted thyroid function as a thyroid receptor(TR)agonist.We examined the bioconcentra-tion,developmental toxicity,and thyroid endocrine disruption in zebrafish after a 14-day exposure to BTBPE(1,3,10μg/L).Thyroxine(T4)was lower in BTBPE-treated larvae,whereas corticotropin-releasing hormone(CRH)and thyroid-stimulating hormone(TSH)were higher.The gene transcription alterations along the hypothalamic-pituitary-thyroid(HPT)axis were observed.Furthermore,reduced locomotion suggested that BTBPE imparts developmental neurotoxicity at zebrafish early developmental stage.Establishing that BTBPE has thyroid endocrine-disrupting effects is an important step for understanding and managing BTBPE toxicity.