The enantioselective toxic effect and environmental behavior of chiral pesticides have attracted increasing research attention. In this study, the enantioselective toxicity and residues of hexaconazole (HEX) in earthworms (Eisenia fetida) were investigated. In the present study, significant enantioselective degradation characteristics were observed in artificial soil with the R-enantiomer preferentially degrading (p < 0.05); however, no significant enantioselective bioaccumulation was observed in the earthworms (p > 0.05). The acute toxicity of S-(+)-HEX was higher than that of R-(−)-HEX in earthworms, with 48-h LC₅₀ values of 8.62 and 22.35 μg/cm², respectively. At 25 mg/kg, enantiospecific induction of oxidative stress was observed in earthworms; moreover, S-(+)-HEX had a greater influence on the contents of malonaldehyde, cytochrome P450, and 8-hydroxy-2-deoxyguanosine than R-(−)-HEX. These results were consistent with those of the enrichment analysis of differentially expressed genes. The transcriptome sequencing results showed that S-(+)-HEX had a more significant influence on steroid biosynthesis, arachidonic acid metabolism, and cell cycle processes than R-(−)-HEX, leading to abnormal biological function activities. These results indicate that S-(+)-HEX may pose a higher risk to soil organisms than R-(−)-HEX. This study suggests that the environmental risk of chiral pesticides to nontarget organisms should be assessed at the enantiomeric level.

The mechanisms contributing to toxic effects of airborne lower-chlorinated PCB congeners (LC-PCBs) remain poorly characterized. We evaluated in vitro toxicities of environmental LC-PCBs found in both indoor and outdoor air (PCB 4, 8, 11, 18, 28 and 31), and selected hydroxylated metabolites of PCB 8, 11 and 18, using reporter gene assays, as well as other functional cellular bioassays. We focused on processes linked with endocrine disruption, tumor promotion and/or regulation of transcription factors controlling metabolism of both endogenous compounds and xenobiotics. The tested LC-PCBs were found to be mostly efficient anti-androgenic (within nanomolar – micromolar range) and estrogenic (at micromolar concentrations) compounds, as well as inhibitors of gap junctional intercellular communication (GJIC) at micromolar concentrations. PCB 8, 28 and 31 were found to partially inhibit the aryl hydrocarbon receptor (AhR)-mediated activity. The tested LC-PCBs were also partial constitutive androstane receptor (CAR) and pregnane X receptor (PXR) agonists, with PCB 4, 8 and 18 being the most active compounds. They were inactive towards other nuclear receptors, such as vitamin D receptor, thyroid receptor α, glucocorticoid receptor or peroxisome proliferator-activated receptor γ. We found that only PCB 8 contributed to generation of oxidative stress, while all tested LC-PCBs induced arachidonic acid release (albeit without further modulations of arachidonic acid metabolism) in human lung epithelial cells. Importantly, estrogenic effects of hydroxylated (OH-PCB) metabolites of LC-PCBs (4-OH-PCB 8, 4-OH-PCB 11 and 4′-OH-PCB 18) were higher than those of the parent PCBs, while their other toxic effects were only slightly altered or suppressed. This suggested that metabolism may alter toxicity profiles of LC-PCBs in a receptor-specific manner. In summary, anti-androgenic and estrogenic activities, acute inhibition of GJIC and suppression of the AhR-mediated activity were found to be the most relevant modes of action of airborne LC-PCBs, although they partially affected also additional cellular targets.

Animal studies have suggested that phthalate exposure alters the fatty acid composition of blood plasma. Therefore, we conducted an epidemiological study to examine whether urinary concentrations of phthalates are correlated with circulating fatty acids in the general US population. The 2003–2004 and 2011–2012 National Health and Nutrition Examination Survey were used in this study. Ten urinary phthalate metabolites and 23 fatty acids were measured. Fatty acid patterns were identified using principal component analysis (PCA) with an eigenvalue greater than 1. A two-step analysis was performed. We first performed multivariable linear regressions to evaluate whether urinary phthalate metabolites were related to the PCA-derived components of blood fatty acid levels. Then we performed multivariable linear regressions to investigate each of the fatty acids that were suggestively correlated with some of the phthalates in PCA. There were 994 participants (51.91% women). As for men, after adjustments for potential confounding factors, MECPP, MEHHP, and ∑DEHP were all positively correlated with gamma-linolenic, myristoleic, and myristic acids; both MEHHP and ∑DEHP were positively correlated with stearic acid; MMP was positively correlated with docosahexaenoic acid. As for women, MMP was negatively correlated with docosanoic, lignoceric, and arachidic acids; MBzP was negatively correlated with docosahexaenoic acid; both MEHP and MCPP were negatively correlated with docosatetraenoic acid; MEHP was negatively correlated with arachidonic acid, and MCPP was negatively correlated with docosapentaenoic-6 acid. Our findings support that phthalates may be correlated with circulating fatty acids.

Individuals with metabolic disorders exhibit enhanced susceptibility to the cardiovascular health effects of particulate air pollution, but the underlying mechanisms are not yet understood. We aim to assess whether changes in proinflammatory lipid signals are associated with fine particulate matter (PM₂.₅) exposure in individuals with and without prediabetes. A longitudinal panel study was conducted in Beijing, China, and included 120 participants followed up over 589 clinical visits from August 2013 to February 2015. We measured 12 lipids derived from arachidonic acid pathways in blood samples of the participants via targeted lipidomic analyses. Ambient PM₂.₅ concentrations were continuously monitored at a station for associations with the lipids. Among the 120 participants, 110 (mean [SD] age at recruitment, 56.5 [4.2] years; 31 prediabetics) who visited the clinic at least twice over the follow-up period were assigned exposure values of the outdoor residential PM₂.₅ concentrations during the 1–14 days preceding each clinical visit. With an interquartile range increase in the 1-day-lag PM₂.₅ exposure (64.0 μg/m³), the prediabetic group had consistently greater increases in the concentration of arachidonate metabolites derived from the cytochrome P450 (CYP450) pathway (5,6-DHET, 15.8% [95% CI, 3.5–29.7%]; 8,9-DHET, 9.7% [95% CI, 0.6–19.6%]; 11,12-DHET, 8.3% [95% CI, 1.9–15.1%]; 14,15-DHET, 7.4% [95% CI, 0.9–14.4%]; and 20-HETE, 8.9% [95% CI, 1.0–17.5%]), compared with the healthy group. Among CYP450-derived lipids, 14,15-DHET and 20-HETE significantly mediated 8% and 8% of the PM₂.₅-associated increase in white blood cells, 10% and 13% of that in neutrophils, and 20% and 23% of that in monocytes, respectively, in the prediabetic group. In conclusion, proinflammatory lipid signals from CYP450 pathways triggered the health effects of particulate air pollution in individuals with prediabetes, suggesting that targeting lipid metabolism has therapeutic potential to attenuate or prevent the cardiovascular effects of air pollution in susceptible populations.

The wide ecological relevance of lipid homeostasis modulators in the environment has been increasingly acknowledged. Tributyltin (TBT), for instance, was shown to cause lipid modulation, not only in mammals, but also in fish, molluscs, arthropods and rotifers. In vertebrates, TBT is known to interact with a nuclear receptor heterodimer module, formed by the retinoid X receptor (RXR) and the peroxisome proliferator-activated receptor (PPAR). These modulate the expression of genes involved in lipid homeostasis. In the present work, we isolated for the first time the complete coding region of the Echinodermata (Paracentrotus lividus) gene orthologues of PPAR and RXR and evaluated the ability of a model lipid homeostasis modulator, TBT, to interfere with the lipid metabolism in this species. Our results demonstrate that TBT alters the gonadal fatty acid composition and gene expression patterns: yielding sex-specific responses in fatty acid levels, including the decrease of eicosapentaenoic acid (C20:5 n-3, EPA) in males, and increase of arachidonic acid (20:4n-6, ARA) in females, and upregulation of long-chain acyl-CoA synthetase (acsl), ppar and rxr. Furthermore, an in vitro test using COS-1 cells as host and chimeric receptors with the ligand binding domain (LBD) of P. lividus PPAR and RXR shows that organotins (TBT and TPT (Triphenyltin)) suppressed activity of the heterodimer PPAR/RXR in a concentration-dependent manner. Together, these results suggest that TBT acts as a lipid homeostasis modulator at environmentally relevant concentrations in Echinodermata and highlight a possible conserved mode of action via the PPAR/RXR heterodimer.

Maternal 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) serum levels during pregnancy have been negatively linked to child neurodevelopment in contrast to intake of omega-3 and -6 (ω-3 and ω-6) fatty acids.To assess whether maternal dietary intake of ω-3 and ω-6 during pregnancy modifies the association between exposure to DDE and child neurodevelopment from age 42–60 months.Prospective cohort study with 142 mother–child pairs performed in Mexico. DDE serum levels were determined by electron capture gas chromatography. Dietary ω-3 and ω-6 intake was estimated by questionnaire. Child neurodevelopment was assessed by McCarthy Scales.Docosahexaenoic (DHA) fatty acid intake significantly modified the association between DDE and motor component: increased maternal DDE was associated with lower motor development in children whose mothers had lower DHA intake (βlog2DDE = −1.25; 95% CI: −2.62, 0.12), in contrast to the non-significant increase among children whose mothers had higher DHA intake (βlog2DDE-motor = 0.50; 95% CI: 0.55, 1.56). Likewise, arachidonic fatty acid (ARA) intake modified the association between DDE and memory component: increased maternal DDE was associated with a significantly larger reduction in the memory component in children whose mothers had lower ARA intake (βlog2DDE = −1.31; 95% CI: −2.29, −0.32) than children whose mothers had higher ARA intake (βlog2DDE-memory = 0.17; 95% CI: −0.78, 1.11).Dietary intake of DHA and ARA during pregnancy may protect against child neurodevelopment damage associated with prenatal maternal DDE levels.

In this study, we aim to explore the allelochemicals of marine brown algae Sargassum fusiforme and the mechanism of allelopathy effect on Heterosigma akashiwo. Six potential allelopathic substances, palmitic acid, arachidonic acid, α-linolenic acid (ALA), fucosterol, 24-hydroperoxy-24-vinylcholesterol, and saringosterowere, were isolated and identified from S. fusiforme by column chromatography, NMR, TOF-MS and GC‐MS analyses. The ALA and 24-hydroperoxy-24-vinylcholesterol showed remarkable inhibitory activities on H. akashiwo growth. Besides, the allelopathic mechanism between the ALA and H. akashiwo was preliminarily investigated. The results indicated that the activities of SOD and POD of H. akashiwo gradually decreased under high ALA concentration. The reduction of photosynthetic pigments and chlorophyll fluorescence parameters, as well as apparent electron transport rate in H. akashiwo cells, aggravated gradually with increasing the concentration of the ALA. In summary, this study revealed the responses of morphology and physiology of H. akashiwo when exposed by ALA, while revealing the potential of macroalgae in red tide control.

Vetiver has a broad history of traditional medicinal uses, but only a handful of research article has reported its utility in treating diseases. But unfortunately, no work has been reported on the anti-inflammatory activity of its plant extract and inflammatory-linked diseases. Hence, the present review focuses on investigating the several presumptions which can be put forward to explain its anti-inflammatory property. Thus, for ensuring the same, all the databases like science direct, PubMed, book chapters, and other authenticated papers were thoroughly studied to present a connection between inflammation and the plant potential. After gaining enough knowledge on pathogenesis of inflammation, it has been observed that the release of mediators from the arachidonic acid metabolism pathway and generation of oxidative and nitrogen species are presented as the main reason for the occurrence of inflammation condition. The stimulation of antioxidant enzyme system network by the plant extract reduces the level of oxidative stress, creating a balance between oxidant and antioxidant system. Moreover, its antimicrobial activity will prevent the biological source of stimulation towards injury and the CNS depressant effect will subside the pain of inflammation. Amalgamating all the factors together, the plant can be utilized as anti-inflammatory can be and also can be proved as a beneficial perspective in the treatment of inflammation-linked disorders.

Cadmium (Cd) pollution is a serious heavy metal pollution in paddy fields, but its effect and underlying mechanism on soil arthropod overwintering and cold resistance are still unclear. In the present study, adult females of the wolf spider Pirata subpiraticus exposed to Cd stress underwent a simulated temperature process (25℃ → 16℃ → 8℃ → 4℃). The mortality rate and content of nutrients in the Cd-treated spiders were dramatically elevated after low-temperature treatment compared to those in the Cd-free control spiders under the same temperature condition. To uncover the putative modulatory mechanism of Cd on cold tolerance in P. subpiraticus, we employed an in-depth RNA sequencing analysis and yielded a total of 888 differentially expressed genes (DEGs). Besides, we characterized genes that participate in multiple cryoprotectant syntheses, including arginine, cysteine, glucose, glycerol, heat shock protein, and mannose. The enrichment analyses found that most of the DEGs involved in biological processes and pathways were related to carbohydrate, lipid, and protein metabolism. Notably, ten Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, such as starch and sucrose metabolism, arachidonic acid metabolism, amino acid metabolism, mineral absorption, and vitamin digestion and absorption, were distinctively enriched with downregulated genes. Meanwhile, we also identified that seven DEGs might inhibit the KEGG pathway of ovarian steroidogenesis and potentially cripple ovarian function and fecundity in the spider. The decreased egg sac weight, number of hatched spiderlings, and vitellin concentration further supported the view that Cd exposure vitiates the overwintering spider’s fecundity. Collectively, the comparative analysis provides a novel perspective regarding the survival response and fecundity on the cold tolerance of spiders under Cd stress and offers a profound insight for evaluating Cd-induced toxicity on overwintering arthropods.

Ibuprofen is one of the most commonly detected pharmaceuticals in wastewater effluent; however, the effects of ibuprofen on aquatic organisms are poorly understood. This study presents the transcriptome-wide response of the inland silverside, Menidia beryllina, to chronic exposure to ibuprofen. At the lowest exposure concentration (0.0115 mg/L), we detected a downregulation of many genes involved in skeletal development, aerobic respiration, and immune function. At the highest exposure concentration (1.15 mg/L), we detected increased expression of regulatory genes in the arachidonic acid metabolism pathway and several immune genes involved in an inflammatory response. Additionally, there was differential expression of genes involved in oxidative stress responses and a downregulation of genes involved in osmoregulation. This study provides useful information for monitoring the effects of this common wastewater effluent contaminant in the environment and for the generation of biomarkers of exposure to ibuprofen that may be transferable to other fish species.