Organophosphate esters (OPEs) are widespread in various environmental media, and can disrupt thyroid endocrine signaling pathways. Mechanisms by which OPEs disrupt thyroid hormone (TH) signal transduction are not fully understood. Here, we present in vivo-in vitro-in silico evidence establishing OPEs as environmental THs competitively entering the brain to inhibit growth of zebrafish via multiple signaling pathways. OPEs can bind to transthyretin (TTR) and thyroxine-binding globulin, thereby affecting the transport of TH in the blood, and to the brain by TTR through the blood-brain barrier. When GH3 cells were exposed to OPEs, cell proliferation was significantly inhibited given that OPEs are competitive inhibitors of TH. Cresyl diphenyl phosphate was shown to be an effective antagonist of TH. Chronic exposure to OPEs significantly inhibited the growth of zebrafish by interfering with thyroperoxidase and thyroglobulin to inhibit TH synthesis. Based on comparisons of modulations of gene expression with the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases, signaling pathways related to thyroid endocrine functions, such as receptor-ligand binding and regulation of hormone levels, were identified as being affected by exposure to OPEs. Effects were also associated with the biosynthesis and metabolism of lipids, and neuroactive ligand-receptor interactions. These findings provide a comprehensive understanding of the mechanisms by which OPEs disrupt thyroid pathways in zebrafish.

Phytoremediation techniques to clean heavy metal pollution soil depend on identifying plant species that can act as phytoremediators. One important approach to screening potential phytoremediators is to evaluate characteristics of heavy metal accumulation. In this study, we performed firsthand analysis of Cd tolerance and accumulation characteristics of three Sansevieria trifasciata cultivars by pot experiment. Plant growth results showed that all three S. trifasciata cultivars can tolerate 50 mg kg-1 soil Cd concentration. After growth under 50 mg kg-1 soil Cd concentration for 4 months, the Cd bioconcentration factors in the shoots of S. \'Trifasciata\', S. trifasciata \'Laurentii\', and S. trifasciata \'Silver Hahnii\' were 1.26, 1.30, and 1.19, while those in the roots were 12.53, 11.43, and 5.45, respectively. This result reveals the considerably low translocation factors of 0.10, 0.12, and 0.22 for S. \'Trifasciata\', S. trifasciata \'Laurentii\', and S. trifasciata \'Silver Hahnii\', respectively. These results suggest that all three S. trifasciata cultivars had high Cd absorption capacities but low Cd translocation capacities. In combination with total Cd accumulation distribution and plant growth characteristics, S. trifasciata can be designed as a phytostabilizer in Cd-contaminated soils in its cultivation regions. Meanwhile, the mechanism of high Cd tolerance and accumulation characteristics in the roots of S. trifasciata should be explored. This study provides new resources for dealing with Cd-contaminated soils and exploring Cd tolerance and accumulation mechanisms in plants.

Quantitative structure-activity relationship (QSAR) models have been applied to predict a variety of toxicity endpoints. Their performance needs to be validated, in a variety of cases, to increase their applicability to chemical regulation. Using the data set of substances of very high concern (SVHCs), the performance of QSAR models were evaluated to predict the persistence and bioaccumulation of PBT, and the carcinogenicity and mutagenicity of CMR. BIOWIN and Toxtree showed higher sensitivity than other QSAR models - the former for persistence and bioaccumulation, the latter for carcinogenicity. In terms of mutagenicity, the sensitivities of QSAR models were underestimated, Toxtree was more accurate and specific than lazy structure-activity relationships (LAZARs) and Computer Assisted Evaluation of industrial chemical Substances According to Regulations (CAESAR). Using the weight of evidence (WoE) approach, which integrates results of individual QSAR models, enhanced the sensitivity of each toxicity endpoint. On the basis of obtained results, in particular the prediction of persistence and bioaccumulation by KOWWIN, a conservative criterion is recommended of log Kow greater than 4.5 in K-REACH, without an upper limit. This study suggests that reliable production of toxicity data by QSAR models is facilitated by a better understanding of the performance of these models.

Clarifying the mechanisms of heavy metal (HM) accumulation and translocation from soil-root-leaf is crucial to coping with soil HM pollution. In this study, we analysed copper (Cu), manganese (Mn), zinc (Zn) and cadmium (Cd) accumulation characteristics in Chinese turnips and the effect of soil physicochemical properties on both HM accumulation and translocation. Our results indicate that Chinese turnips absorb and translocate Mn, Zn, and Cd at much higher levels than they do Cu. When we measured bioconcentration factors in Chinese turnips for different HMs in the same soil, we found Chinese turnip capacities for HM accumulation decrease from Zn > Mn > Cd > Cu. In addition, the translocation factor for these HMs decreases from Mn > Cd > Zn > Cu. Correlation analysis indicates that soil pH and various soil components are either negatively or positively correlated with Mn, Zn, and Cd accumulation; also, soil properties are correlated with Mn translocation from root to leaf. These findings may help evaluate HM accumulation and translocation mechanisms as well as artificially regulate HM uptake levels from soils to turnips.

Effects of triclosan (5-chloro-2\'-(2,4-dichlorophenoxy)phenol) on mammalian cells were investigated using human peripheral blood mono nuclear cells (PBMC), keratinocytes (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine pancreatic islets (MIN-6) and neuroblastoma cells (MNA) as targets. We show that triclosan (1-10 μg ml-1) depolarised the mitochondria, upshifted the rate of glucose consumption in PMBC, HaCaT, PK-15 and MNA, and subsequently induced metabolic acidosis. Triclosan induced a regression of insulin producing pancreatic islets into tiny pycnotic cells and necrotic death. Short exposure to low concentrations of triclosan (30 min, ≤1 μg/ml) paralyzed the high amplitude tail beating and progressive motility of spermatozoa, within 30 min exposure, depolarized the spermatozoan mitochondria and hyperpolarised the acrosome region of the sperm head and the flagellar fibrous sheath (distal part of the flagellum). Experiments with isolated rat liver mitochondria showed that triclosan impaired oxidative phosphorylation, downshifted ATP synthesis, uncoupled respiration and provoked excessive oxygen uptake. These exposure concentrations are 100-1000 fold lower that those permitted in consumer goods. The mitochondriotoxic mechanism of triclosan differs from that of valinomycin, cereulide and the enniatins by not involving potassium ionophoric activity.