The oriental river prawn, Macrobrachium nipponense, is an important breeding species in China. The ovary development of this prawn is regulated by the genetic factors and external environmental factors and has obvious seasonal regularity. However, the molecular mechanism of regulating ovary degradation in M. nipponense remains unclear. To address this issue, we performed transcriptome sequencing and gene expression analyses of eyestalks, cerebral ganglia (CG) and thoracic ganglia (TG) of female M. nipponense between the full ovary stage and degenerate ovary stage. Differentially expressed genes enrichment analysis results identified several important pathways such as “phototransduction-fly,” “circadian rhythm-fly” and “steroid hormone biosynthesis secretion.” In the period of ovarian degeneration, the expressions of Tim, Per2 and red pigment concentration hormone (RPCH) were significantly decreased in the eyestalk, CG and TG. And expression of 7 genes in the steroid synthesis pathway, including steryl-sulfatase, cytochrome P450 family 1 subfamily A polypeptide 1, estradiol 17β-dehydrogenase 2, glucuronosyltransferase, 3-oxo-5-alpha-steroid 4-dehydrogenase 1, estradiol 17-dehydrogenase 1 and estrone sulfotransferase was significantly decreased in the CG. Food and light signals affect the expression of clock genes and thereby decrease the expression of RPCH and the estradiol synthesis-related genes in the nervous system, which may be the main cause of ovarian degeneration in M. nipponense. The results will contribute to a better understanding of the molecular mechanisms of ovarian development regulation in crustaceans.

Perfluorododecanoic acid (PFDoA), a kind of perfluorinated carboxylic acid (PFCA) with 12 carbon atoms, has an extensive industrial utilization and is widespread in both wildlife and the water environment, and was reported to have the potential to cause a disruption in the thyroid hormone system homeostasis. In this study, zebrafish embryos/larvae were exposed to different concentrations of PFDoA (0, 0.24, 1.2, 6 mg/L) for 96 h post-fertilization (hpf). PFDoA exposure caused obvious growth restriction connected with the reduced thyroid hormones (THs) contents in zebrafish larvae, strengthening the interference effect on the growth of fish larvae. The transcriptional level of genes within the hypothalamic-pituitary-thyroid (HPT) axis was analyzed. The gene expression levels of thyrotropin-releasing hormone (trh) and corticotrophin-releasing hormone (crh) were upregulated upon exposure to 6 mg/L of PFDoA, and iodothyronine deiodinases (dio2) was upregulated in the 1.2 mg/L PFDoA group. The transcription of thyroglobulin (tg) and thyroid receptor (trβ) were significantly downregulated upon exposure to 1.2 mg/L and 6 mg/L of PFDoA. PFDoA could also decrease the levels of sodium/iodide symporter (nis) and transthyretin (ttr) gene expression in a concentration-dependent manner after exposure. A significant decrease in thyroid-stimulating hormoneβ (tshβ), uridinediphosphate-glucuronosyltransferase (ugt1ab) and thyroid receptor (trα) gene expression were observed at 6 mg/L PFDoA exposure. Upregulation and downregulation of iodothyronine deiodinases (dio1) gene expression were observed upon the treatment of 1.2 mg/L and 6 mg/L PFDoA, respectively. All the data demonstrated that gene expression in the HPT axis altered after different PFDoA treatment and the potential mechanisms of the disruption of thyroid status could occur at several steps in the process of synthesis, regulation, and action of thyroid hormones.

Tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) has been demonstrated to be transferred from parental animals to their offspring. However, whether parental exposure to environmental concentrations of TDCIPP show neurodevelopmental toxicity in the F1 generation and the possible underlying mechanism remain unclear. Therefore, in this study, zebrafish embryos were exposed to environmental concentrations of TDCIPP (3, 30 and 300 ng L⁻¹) for 120 days. The effects of exposure on motor behaviors, neurotransmitter levels, DNA methylation, and gene expression of F1 larvae were investigated. Parental exposure left TDCIPP residues in F1 eggs as well as reduced body length of F1 larvae. Moreover, parental exposure significantly reduced swimming activity in F1 5 dpf larvae, although it did not significantly alter serotonin, dopamine, 3,4-dihydroxyphenylacetic acid, γ-aminobutyrate, and acetylcholine levels. Genes encoding DNA methylation transferases (dnmt3aa and dnmt1) were downregulated in F1 larvae. Reduced representation bisulfite sequencing analysis revealed 446 differentially methylated regions and enriched neuronal cell body Gene Ontology term in F1 generation. Correlation analysis between the expression of genes related to neural cell body and swimming speed indicated that solute carrier family 1 member 2b (slc1a2b) downregulation might be responsible for the inhibition of motor behaviors. Furthermore, bisulfite amplicon sequencing analysis confirmed hypermethylation of the promoter region of slc1a2b in F1 larvae following parental exposure to 300 ng L⁻¹ TDCIPP, which might have led to significant downregulation of gene expression and, in turn, influenced the motor behaviors. These results indicate that parental exposure to environmental concentrations of TDCIPP alters DNA methylation, downregulates gene expressions and, thus inducing developmental neurotoxicity, in F1 larvae.

Although triphenyl phosphate (TPHP) has been reported to disrupt lipid metabolism, the effect of TPHP on lipid saturation remains unexplored. In this study, a lipidomic analysis demonstrated decreases in the levels of poly-unsaturated phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS) in RAW264.7 murine macrophage cells exposed to 10 μM TPHP. The expression of the gene encoding lysophosphatidylcholine acyltransferase 3 (Lpcat3) was significantly downregulated by 0.76 ± 0.03 and 0.70 ± 0.08-fold in 10 and 20 μM TPHP exposure groups, relative to the control group. This finding explains the observed decrease in lipid saturation. Correspondingly, exposure to 10 and 20 μM TPHP induced endoplasmic reticulum (ER) stress and inflammatory responses, which have been linked to metabolic dysfunction such as insulin resistance and hypertriglyceridemia. Therefore, TPHP may pose a risk to human health by promoting metabolic diseases.

The abnormality in thyroid hormone modulation in developmental fish, vulnerable to per- and polyfluorinated substances, is of particular concerns for the alternative substances. Juvenile rare minnows, were exposed to chlorinated polyfluoroalkyl ether sulfonates (Cl-PFESAs), the novel alternatives to perfluorooctane sulfonate (PFOS), for 4 weeks followed by 12 weeks of depuration. Half lives were determined to be 33 d, 29 d, and 47 d for total Cl-PFESAs, C8 Cl-PFESA and C10 Cl-PFESA, respectively. Preliminary toxicity test suggested that Cl-PFESAs are moderately toxic to Rare minnow with a LC50 of 20.8 mg/L (nominal concentration） after 96 h of exposure. In the chronic toxicity test, fishes were exposed to Cl-PFESAs at geometric mean measured concentrations of 86.5 μg/L, 162 μg/L and 329 μg/L. In juvenile fishes exposed to Cl-PFESAs for 4 weeks, gene profile sequencing analysis identified 3313 differentially expressed genes, based on which pathways regulating thyroid hormone synthesis and steroid synthesis were enriched. Both whole body total and free 3,5,3′-triiodothyronine (T3) levels were significantly increased. mRNA expression of genes regulating thyroid hormone synthesis (corticotropin-releasing hormone (CRH), thyroid-stimulating hormone (THS), sodium/iodide symporter (NIS), thyroglobulin (TG), and thyroid peroxidase (TPO), transport (transthyretin,TTR), deiodinase (Dio1, Dio2) and receptor (TRα and TRβ) were decreased. Uridinediphosphate glucoronosyl-transferases (UGT1A) gene, regulating THs metabolism, was also decreased. In adult fish, thyroid hormone and genes expression in hypothalamic-pituitary-thyroid axis remained at disturbed levels after 12 weeks of depuration without exposure. Chronic developmental exposure to Cl-PFESAs caused persistent thyroid hormone disrupting effects in fish, highlighting a necessity of comprehensive ecological risk assessment.

Meiobenthic nematodes have been designated as sensitive global models in the development of biomonitoring and ecotoxicology monitoring programs howbeit the sensitivity of these organisms against oxidative stress biomarkers have never been addressed. The present study aimed to decipher this research axis after selecting and culturing a single nematode species from an entire community through original laboratory protocols. The purpose of this investigation was to change the grain size of the sediment into the immediate environment of nematodes by progressively adding a biosubstrate made from Sepia officinalis endoskeletton. At the end of the experiment, Metoncholaimus pristiurus became the unique component of the nematode species when the sediment was enriched with 80% of S. officinalis powder. After the mono-species level had been achieved, the selected species was fed on an another biosubstrate made from bodies of Porcellio scaber under the identical laboratory controlled conditions of light and temperature adopted during the selection process. Accordingly, the bioassay protocol this study layed new foundations for the study of meiobenthic nematodes in the biomarker field. Our results revealed that, in case of M. pritiurus, discernible oxidative stress responses are valid for catalase and gluthatione S-transferase. Indeed, for both enzymes, a clear increase in the activity was recorded, and the response was more reinforced when zinc and permethrin were administrated in combination. The relevance of the protocols proposed in this work parallels their global applicability to reach and maintain the monospecific level in laboratory by using biosubstrates made from animals widely distributed. It is true also that our data provided the first results in terms of biochemical biomarkers for meiobenthic nematodes and showed that the selected taxa, M. pristiurus, could be one of the first marine taxa responding early to the tested stressors, zinc and permethrin, even at very low concentrations.

Tetrabromobisphenol A (TBBPA), one of the most widely used brominated flame retardants (BFRs), is a ubiquitous contaminant in the environment and in the human body. This study demonstrated that zebrafish embryos exposed to TBBPA during a sensitive window of 8–48 h post-fertilization (hpf) displayed morphological malformations and mortality. Zebrafish exposed exclusively between 48 and 96 hpf were phenotypically normal. TBBPA was efficiently absorbed and accumulated in zebrafish embryos, but was eliminated quickly when the exposure solution was removed. Larval behavior assays conducted at 120 hpf indicated that exposure to 5 μM TBBPA from 8 to 48 hpf produced larvae with significantly lower average activity and speed of movement in the normal condition than in those exposed from 48 to 96 hpf. Specifically, 8–48 hpf-exposed larvae spent significantly less time in both activity bursts and gross movements compared to control or 48–96 hpf exposed larvae. Consistent with the motor deficits, TBBPA induced apoptotic cell death, delayed cranial motor neuron development, inhibited primary motor neuron development and loosed muscle fiber during the early developmental stages. To further explore TBBPA-induced developmental and neurobehavioral toxicity, RNA-Seq analysis was used to identify early transcriptional changes following TBBPA exposure. In total, 1969 transcripts were significantly differentially expressed (P < 0.05, FDR < 0.05, 1.5-FC) upon TBBPA exposure. Functional and pathway analysis of the TBBPA transcriptional profile identified biological processes involved in nerve development, muscle filament sliding and contraction, and extracellular matrix disassembly and organization changed significantly. In addition, TBBPA also led to an elevation in the expression of genes encoding uridine diphosphate glucuronyl transferases (ugt), which could affect thyroxine (T4) metabolism and subsequently lead to neurobehavioral changes. In summary, TBBPA exposure during a narrow, sensitive developmental window perturbs various molecular pathways and results in neurobehavioral deficits in zebrafish.

Ocimum basilicum essential oil (EO) was evaluated for its biological effects on M. domestica. Characterization of O. basilicum EO revealed the presence of methyl chavicol (70.93%), linalool (9.34%), epi-α-cadinol (3.69 %), methyl eugenol (2.48%), γ-cadinene (1.67%), 1,8-cineole (1.30%) and (E)-β-ocimene (1.11%). The basil EO and its constituents methyl chavicol and linalool elicited a neuronal response in female adults of M. domestica. Adult female flies showed reduced preference to food source laced with basil EO and methyl chavicol. Substrates treated with EO and methyl chavicol at 0.25% resulted in an oviposition deterrence of over 80%. A large ovicidal effect was found for O. basilicum EO (EC₅₀ 9.74 mg/dm³) followed by methyl chavicol (EC₅₀ 10.67 mg/dm³) and linalool (EC₅₀ 13.57 mg/dm³). Adults exposed to EO (LD₅₀ 10.01 μg/adult) were more susceptible to contact toxicity than to methyl chavicol and linalool (LD₅₀ 13.62 μg/adult and LD₅₀ 43.12 μg/adult respectively). EO and its constituents methyl chavicol and linalool also induced the detoxifying enzymes Carboxyl esterase (Car E) and Glutathione S – transferases (GST).

Ester-functionalized pyridinium ionic liquids (ILs), 1-decyloxycarbonylmethylpyridinium chloride (PyrСOOC₁₀-Cl), and 1-dodecyloxycarbonylmethylpyridinium chloride (PyrСOOC₁₂-Cl) have been synthesized and studied for their environmental toxicity. Simple long-chain pyridinium ILs, 1-dodecylpyridinium chloride (PyrC₁₂-Cl), and commercial disinfectant cetylpyridinium chloride (CPC) were used as reference compounds. Both ester-functionalized ILs and CPC showed significantly reduced antibacterial activity compared to PyrC₁₂-Cl. However, ester-functionalized ILs were found to have excellent antifungal activity towards Candida albicans fungus strains, similar to PyrC₁₂-Cl and much higher than for CPC. The molecular docking of ILs in the active site of the known antifungal target N-myristoyltransferase (Nmt) C. albicans has been conducted. The obtained results indicate the possibility of ILs binding into the Nmt pocket. The high stability of the complexes, especially for PyrCOOC₁₀-Cl, is ensured by hydrogen bonding, electrostatic anion-pi interactions, as well as hydrophobic pi-alkyl and alkyl interactions that was confirmed by calculated binding energy values. The acute toxicity studies of ester-functionalized ILs on D. rerio (zebrafish) hydrobiont have shown their dramatically reduced ecotoxicity compared to PyrC₁₂-Cl and CPC. Thus, LD₅₀ values of 15.2 mg/L and 16.8 mg/L were obtained for PyrCOOC₁₀-Cl and PyrCOOC₁₂-Cl, respectively, whereas CPC had LD₅₀ value of 0.018 mg/L. The primary biodegradation test CEC L-33-A93 of ILs indicated an improved biodegradability of ester-functionalized compounds compared to simple long-chain ILs. Based on the obtained results, PyrCOOC₁₀-Cl may be considered as very promising cationic biocide due to the combination of soft antimicrobial activity and reduced ecotoxicity, as well as improved biodegradability.