Polybrominated diphenyl ethers (PBDEs) have been used as flame retardants (FRs) in China for decades, even after they were identified as persistent organic pollutants. In this study, serum samples were collected from 172 adults without occupational exposure who were residents of a well-known FR production region (Laizhou Bay, north China), and PBDE congeners were measured to assess their occurrence, congener profile and influencing factors in serum. Moreover, the relationships between serum concentrations of PBDEs and thyroid/liver function indicators were analyzed to evaluate whether human exposure to PBDEs would lead to thyroid/liver injury. All 8 PBDE congeners were detected at higher frequencies and serum concentrations than those found in general populations. The median levels of ∑PBDEs, BDE-209 and ∑₃₋₇PBDEs (sum of tri-to hepta-BDEs) were 64.5, 56.9 and 7.2 ng/g lw (lipid weight), respectively, which indicated that deca-BDE was the primarily produced PBDE in Laizhou Bay and that the lower brominated BDEs were still ubiquitous in the environment. Gender was a primary influencing factor for some BDE congeners in serum; their levels in female serum samples were significantly lower than those in male serum samples. Serum PBDE levels showed a downward trend with increased body mass index (BMI), which might reflect the increasing serum lipid contents. Serum levels of some BDE congeners were significantly positively correlated with certain thyroid hormones and antibodies, including free triiodothyronine (fT3), total triiodothyronine (tT3), total thyroxine (tT4) and thyroid peroxidase antibody (TPO-Ab). Levels of some congeners were significantly negatively correlated with some types of serum lipid, including cholesterol (CHOL), low density lipoprotein (LDL) and total triglyceride (TG). Other than serum lipids, only two liver function indicators, total protein (TP) and direct bilirubin (DBIL), were significantly correlated with certain BDE congeners (BDE-100 and BDE-154). Our results provide new evidence on the thyroid-disrupting and hepatotoxic effects of PBDEs.

Combining hydrothermal treatment and composting is an effective method to dispose of penicillin fermentation residue (PFR), but the safety and related mechanism are still unclear. In this study, penicillin solution was hydrothermally treated to decipher its degradation mechanism, and then hydrothermally treated PFR (HT-PFR) was mixed with bulking agents at ratios of 2:0 (CK), 2:1.5 (T1), and 2:5 (T2) to determine the absolute abundance of antibiotic resistance genes (ARGs) and the succession of bacterial community. Results showed that penicillin was degraded to several new compounds without the initial lactam structure after hydrothermal treatment. During composting, temperature and pH of the composts increased with the raising of HT-PFR proportion, except the pH at days 2. After 52 days of composting, the absolute copies of ARGs (blaTEM, blaCMY2, and blaSFO) and the relative abundance of bacteria related to pathogens were reduced significantly (P < 0.05). Especially, the total amount of ARGs in the samples of CK and T1 were decreased to equal level (around 5 log₁₀ copies/g), which indicated that more ARGs were degraded in the latter by the composting process. In the CK samples, Bacteroidetes and Proteobacteria accounted for ~69.8% of the total bacteria, but they were gradually replaced by Firmicutes with increasing proportions of HT-PFR, which can be caused by the high protein content in PFR. Consisting with bacterial community, more gram-positive bacteria were observed in T1 and T2, and most of them are related to manganese oxidation and chitinolysis. As composting proceeded, bacteria having symbiotic or pathogenic relationships with animals and plants were reduced, but those related to ureolysis and cellulolysis were enriched. Above all, hydrothermal treatment is effective in destroying the lactam structure of penicillin, which makes that most ARGs and pathogenic bacteria are eliminated in the subsequent composting.

In steroidogenic cells, steroids are synthesized de novo from cholesterol stored in lipid droplets (LDs). The size of LDs regulated by adipose differentiation-related protein (ADRP) is closely related to cholesterol ester hydrolysis. Many studies reported that cadmium (Cd) had dual effects on steroidogenesis in granulosa cells (GCs). However, the role of LD and its regulation in abnormal steroidogenesis caused by Cd exposure remain unknown. In current study, female rats were exposed to CdCl₂ during gestation and lactation, and influence of such exposure was investigated in ovarian GCs of female offspring. The size of LDs was found much smaller than normal in GCs; ADRP was down-regulated and hormone-sensitive lipase (HSL) phosphorylation was increased, followed by up-regulation of steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage enzyme (CYP11A1); the expression of 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase beta-2 (PLCβ2) and protein kinase C alpha type (PKCα) were both decreased accompanying the ADRP down-regulation. This series of events resulted in a high level of progesterone in serum. Similar results were demonstrated in GCs treated with 20 μM CdCl₂ for 24 h in vitro. The protein level of ADRP was decreased after gene silencing of PLCβ2/PKCα, and the knockdown of PLCβ2/PKCα/ADRP led to micro-sized LD formation. We found that Cd exposure down-regulated ADRP by inhibiting the PLCβ2-PKCα signaling pathway, reduced the size of LDs, and promoted HSL phosphorylation. StAR and CYP11A1 were both up-regulated following the hydrolysis of cholesterol ester, which led to a high production of progesterone. LD thereby is a target subcellular organelle for Cd to affect steroid hormone synthesis in ovarian GCs. These findings might help to uncover the mechanism of ovarian dysfunction and precocious puberty caused by Cd pollution.

A chemical contaminant of growing concern to freshwater aquatic organisms, including many amphibians, is chloride ion. The salinization of freshwater ecosystems is likely caused, in part, by the application of massive amounts of road de-icing salts to roadways during winter months. The issue of freshwater salinization has become the subject of many toxicity studies and is often investigated in conjunction with other chemical stressors. However, few published studies attempt to investigate the interactions of elevated chloride concentration and increased temperature. Further, no studies have investigated the gap between the recommended feeding conditions typically used in standard toxicity tests and those that may exist in natural amphibian habitats. This study addressed the critical issues of elevated chloride, increased temperature, and variation in food quality. We conducted a 96-h acute toxicity test to investigate acute chloride toxicity as impacted by different diets, as well as a chronic toxicity test to investigate the impacts of chloride, temperature, and resource quality on the survival and development of larval Lithobates sylvaticus (wood frogs). Chloride LC₅₀s ± 1 SE were 3769.22 ± 589.05, 2133.00 ± 185.95, and 2644.69 ± 209.73 mg Cl⁻/L were for non-fed, low-protein diet, and high-protein diet, respectively. For the chronic toxicity study, elevated chloride decreased tadpole survival. Increased temperature, and lower resource quality, were found negatively impacted survival of tadpoles and altered time-to-metamorphosis. This study shows that environmentally relevant concentrations of chloride, temperatures, and the protein content of the diet all exert critical effects on larval wood frogs.

Lipid metabolism could be used as a biomarker for environmental monitoring of metal pollution, including Cu. Given the potential role of the Wnt/β-catenin signaling pathway and acetylation in lipid metabolism, the aim of this study was to investigate the mechanism of Wnt signaling and acetylation mediating Cu-induced lipogenesis. Grass carp Ctenopharyngodon idella, widely distributed freshwater teleost, were used as the model. We found that waterborne Cu exposure increased the accumulation of Cu and lipid, up-regulated lipogenesis, suppressed Wnt signaling, reduced β-catenin protein level and its nuclear location, reduced the sirt1 mRNA levels and up-regulated the β-catenin acetylation level. Further investigation found that Cu up-regulated lipogenesis through Wnt/β-catenin pathway; Cu regulated the β-catenin acetylation, and K311 was the key acetylated residue after Cu incubation. SIRT1 mediated Cu-induced changes of acetylated β-catenin and played an essential role in nuclear accumulation of β-catenin and Cu-induced lipogenesis. Cu facilitated lipid accumulation via the regulation of Wnt pathway by SIRT1. For the first time, our study uncovered the novel mechanism for Wnt/β-catenin pathway and β-catenin acetylation levels mediating Cu-induced lipid deposition, which provided insights into the association between Cu exposure and lipid metabolism in fish and had important environmental implications for monitoring metal pollution in the water by using new biomarkers involved in lipid metabolism.

Antibiotics used in global aquaculture production cause various side effects, which impair fish health. However, the use of dietary composition such as carbohydrate, which is one of the dominant components in fish diets to attenuate the side effects induced by antibiotics, remains unclear. We determined the ability of high carbohydrate diet to protect Nile tilapia (Oreochromis niloticus) from oxytetracycline-induced side effects. Triplicate groups of thirty O. niloticus (9.50 ± 0.08 g) were fed on medium carbohydrate (MC; 335 g/kg) and high carbohydrate (HC; 455 g/kg) diets without and with 2.00 g/kg diet of oxytetracycline (80 mg/kg body weight/day) hereafter, MCO and HCO for 35 days. Thereafter, we assessed growth performance, hepatic nutrients composition and metabolism, microbiota abundance, immunity, oxidative and cellular stress, hepatotoxicity, lipid peroxidation and apoptosis. To understand the possible mechanism of carbohydrate protection on oxytetracycline, we assessed the binding effects and efficiencies of mixtures of medium and high starch with oxytetracycline as well as the MCO and HCO diets. The O. niloticus fed on the MCO and HCO diets had lower growth rate, nutrients utilization and survival rate than those fed on the MC and HC diets, respectively. Dietary HCO increased hepatosomatic index and hepatic protein content of O. niloticus than MCO diet. The O. niloticus fed on the HCO diet had lower mRNA expression of genes related to protein, glycogen and lipid metabolism compared to those fed on the MCO diet. Feeding O. niloticus on the HCO diet increased innate immunity and reduced pathogenic bacteria, pro-inflammation, hepatotoxicity, cellular stress and apoptosis than the MCO diet. The high starch with oxytetracycline and HCO diet had higher-oxytetracycline binding effects and efficiencies than the medium starch with oxytetracyline and MCO diet, respectively. Our study demonstrates that, high carbohydrate partially protects O. niloticus from oxytetracycline-induced side effects by binding the antibiotic. Incorporating high carbohydrate in diet formulation for omnivorous fish species alleviates some of the side effects caused by antibiotics.

Polyacrylonitrile polymer (PAN), a common representative textile material and a microplastic, has significant influence on phytoplankton algae, especially with co-exposure with other pollutants, e.g. Cu²⁺. In the present study, we carried out experiments to reveal the population size variation trends of Chlorella pyrenoidosa over time (during a whole growth cycle of 6 days) under PAN and/or Cu²⁺. The levels of pigments (chlorophyll a, b, total chlorophyll and carotenoids), chlorophyll a fluorescence parameters, and other physiological and biochemical indices, containing total protein measurements of H₂O₂, catalase (CAT), and malondialdehyde (MDA) under different treatment groups were measured to explain the physio-ecological mechanism of the effect of PAN and/or Cu²⁺ on the growth of C. pyrenoidosa. The results showed that PAN, Cu²⁺ and the combination of PAN and Cu²⁺ inhibited the growth of C. pyrenoidosa. Chlorophyll a and b decreased significantly with increasing levels of pollutants (PAN and/or Cu²⁺); however, the carotenoid levels increased with increasing levels of pollutants (PAN and/or Cu²⁺) for the first three cultivation days. The oxygen-evolving complexes (OECs) of C. pyrenoidosa had been damaged under Cu²⁺ pollution. The results also showed that CAT activity, MDA content and H₂O₂ activity of C. pyrenoidosa increased with increasing levels of pollutants (PAN and/or Cu²⁺); however, total protein content decreased with increasing levels of pollutants (PAN and/or Cu²⁺) at the first cultivation day. These results indicate that pollutants (PAN and/or Cu²⁺) are harmful to the growth of the C. pyrenoidosa population and negatively affect the levels and function of the pigments in C. pyrenoidosa by decreasing chlorophyll a and b levels, increasing carotenoid levels, and increasing antioxidant enzyme activity.

The frequent outbreaks of cyanobacteria bloom are often accompanied by the generation and release of reduced phosphorus species (e.g., phosphine), which raises interesting questions regarding their potential algae-related effects. To clarify the physiological and biochemical responses of cyanobacteria to phosphine, Microcystis aeruginosa was treated with different concentrations of phosphine. Net photosynthetic rate, total antioxidant capacity (T-AOC), catalase (CAT) activity, and the concentrations of chlorophyll a, carotenoid and total protein were investigated and scanning electron microscopy (SEM) was conducted to elucidate the physiological and biochemical responses of M. aeruginosa to phosphine. The results showed that phosphine was beneficial to the growth of algal cells after M. aeruginosa acclimatized to the treatment of phosphine, and treatment with 2.48 × 10⁻² mg/L phosphine had a greater positive effect on the growth and reproduction of M. aeruginosa than 7.51 × 10⁻³ mg/L phosphine, in which most algal cells were smooth and flat on day 16. Treatment with the high concentration of phosphine (7.51 × 10⁻² mg/L) for 16 d reduced T-AOC, CAT activity, net photosynthetic rate, and the concentrations of chlorophyll a, carotenoid and total protein of M. aeruginosa to the minimums, resulting in the lysis and death of M. aeruginosa cells, which indicates phosphine has a toxic effect on the growth of algal cells. However, the high concentration of phosphine (7.51 × 10⁻² mg/L) had a greater positive effect on the growth of M. aeruginosa cells than the lower two (7.51 × 10⁻³ mg/L and 2.48 × 10⁻² mg/L) from 3 d to 12 d. Our findings provide insight into how phosphine potentially affects the growth of M. aeruginosa cells and the important roles of elevated phosphine on the outbreak of cyanobacteria bloom.

Bisphenol S (BPS) has been widely used as a bisphenol alternative in recent few years. However, with mounting evidence suggesting that the presence of BPS in the environment also poses risks to ecosystems and human health, we decided to use the juvenile common carp (Cyprinus carpio) and its primary macrophages as in vivo and in vitro models to examine if BPS is a safe substitute of BPA. The present study evaluated the immune responses of chronic BPS exposure and their mechanisms of action associated with peroxisome proliferator-activated receptor (PPAR) signaling pathway. Potential oxidative stress and pro-inflammatory effects of BPS exposure were identified in fish liver after 60-day exposure, based on the increased reactive oxygen species (ROS) production, antioxidant capacity, NO production, lipid peroxidation, and induction of inflammatory cytokine expression, as well as acute phase protein levels of C-reactive protein, immunoglobulin M, lysozyme, and complement component 3. Moreover, pparγ, PPAR pathway-associated genes retinoid x receptor α (rxrα) and nuclear factor-κb (nfκb) presented a rough concentration-dependent alteration after BPS exposure. An acute BPS exposure to the isolated primary macrophages from juvenile common carp was performed to help elucidate gene expression patterns of pparγ, rxrα, and nfκb in a typical immune cell model, the results were consistent with what we found in vivo experiments for long-term BPS exposure. Furthermore, with coexposure to BPS and a PPARγ antagonist, the restriction of PPAR signaling pathway significantly inhibited the induction of ROS and the mRNA level of interleukin-1β, confirming the involvement of PPAR pathway in BPS-induced chronic inflammatory stress in liver.

Cadmium (Cd), a ubiquitous environmental pollutant, is known to impair placental development. However, the underlying mechanisms remain unclear. The present study used in vivo and in vitro models to investigate the effects of Cd on apoptosis and autophagy in placental trophoblasts and its mechanism. Pregnant mice were exposed to CdCl₂ (4.5 mg/kg) on gestational day (GD) 9. Human JEG-3 cells were exposed to CdCl₂ (0–40 μM) for different time points. Gestational Cd exposure obviously lowered the weight and diameter of mouse placentas. Number of TUNEL-positive cells was markedly elevated in Cd-administered mouse placentas and JEG-3 cells. Correspondingly, Cd significantly up-regulated cleaved caspase-3 protein level, a key indicator of apoptosis, in murine placentas and JEG-3 cells. Simultaneously, Cd also triggered autophagy, as determined by an elevation of LC3B-II and p62 protein, and accumulation of LC3-positive puncta, in placental trophoblasts. Chloroquine an autophagy inhibitor, obviously aggravated Cd-induced apoptosis in JEG-3 cells. By contrast, rapamycin, a specific autophagy inducer, significantly alleviated Cd-triggered apoptosis in JEG-3 cells. Mechanistically, autophagy inhibited Cd-induced apoptosis mainly via degrading caspase-9. Co-localizations of p62, a classical autophagic receptor, and caspase-9 were observed in Cd-stimulated human JEG-3 cells. Moreover, p62 siRNAs pretreatment markedly blocked the degradation of caspase 9 proteins via Cd-activated autophagy in JEG-3 cells. Collectively, our data suggest that activation of autophagy inhibits Cd-induced apoptosis via p62-mediated caspase-9 degradation in placental trophoblasts. These findings provide a new mechanistic insight into Cd-induced impairments of placental and fetal development.