The toxic effects induced by benzethonium chloride on Daphnia carinata over two generations: Resistance and higher sublethal toxicity.

With the widespread utilization of the sanitizing product benzethonium chloride (BEC) throughout the coronavirus pandemic, concerns have emerged regarding its potential hazards. Nevertheless, the long-term and multigenerational toxic effects of BEC on aquatic organisms remains unexplored. This study investigates acute and chronic toxicity, oxidative stress, mitochondrial membrane potential, ATP concentrations, and gene expression using Daphnia carinata as the model organism. Meanwhile, hierarchical clustering analysis was utilized to investigate phenotypic effects among different treatment groups. The integrated biomarker response index version 2 (IBRv2) was employed to estimate the deviation in toxic effects over two generations. These results indicated that D. carinata in the second generation exhibited higher survival rate and lower levels of oxidative stress than the first generation. However, the higher sublethal effects were found in the second generation as follows, the weakened growth performance, mitochondrial membrane potential depolarization, reduced ATP concentrations, and down-regulated gene expression. The mitochondrial toxicity induced by BEC may account for the distinct toxic effects exhibited in two generations. The findings here can assist with the evaluation of potential risk for BEC on aquatic organisms, and provide new insight into the cross-generational toxicity mechanisms of pollutants in aquatic ecosystems.

Toxicity of benzethonium chloride and polyhexamethylene guanidine hydrochloride mixtures on Daphnia carinata: synergistic and antagonistic effects at specific ratios.

Throughout the coronavirus (COVID-19) pandemic, the sanitizing products benzethonium chloride (BEC) and polyhexamethylene guanidine hydrochloride (PHMG-H) were widely used; however, few studies have investigated their combined toxicity to organisms. In the present study, acute toxicity and genotoxicity of BEC, PHMG-H, and the combination of the two were investigated as endpoints using Daphnia carinata as the model organism. For individual reagents, PHMG-H was found to be more toxic than BEC in terms of both mortality and genotoxicity. DNA damage and survival rate were used as toxicity endpoints. The interaction was evaluated with the concentration addition (CA) model via toxic unit (TU) approach and additive index (AI) method in mixtures at different ratios in TU. Only the binary mixture BEC + PHMG-H at the ratio 1:9 in TU was regarded as synergistic, while all others indicated increased antagonistic effects as the proportion of BEC increased over the PHMG-H concentration. The findings here benefit understanding surrounding precisely how BEC and PHMG-H interact at different mixing ratios, and can assist with the evaluation of risk assessments for binary mixtures in aquatic ecosystems.

Transcriptome profiles of red swamp crayfish Procambarus clarkii hematopoietic tissue in response to WSSV challenge.

The crayfish Procambarus clarkii could achieve a high cumulative mortality after WSSV infections. To better understand the immune response to WSSV in hematopoietic tissue, the present study investigated the immunological response of P. clarkii and analyzed the expression of some hematopoietic cytokines. After assembly, there was an average of 47,712,411 clean reads were obtained in control and treatment groups. A total of 35,945 unigenes were discovered with N50 length of 1554 bp. Under functional classification, enrichment, and pathway analysis using different database, there were about 257 differentially expressed genes (DEGs) identified, of which 139 were up-regulated and 118 were down-regulated. The GO function analysis of these DEGs were mostly participated in activation of immune response, complement activation, complement binding, negative regulation of humoral immune response and secretory granule membrane. Under KEGG analysis, these DEGs were involved in ECM-receptor interaction, HIF-1 signaling pathway, Glycolysis/Gluconeogenesis, Thyroid hormone signaling pathway and Glucagon signaling pathway. The real-time quantitative PCR (RT-qPCR) analysis of 9 selected genes confirmed the reliability of RNA-Seq results. The present research provide for the first time the transcriptomic profile of P. clarkii hematopoietic tissue in response to WSSV infection and reveals the astakines may play important roles in antiviral immune response. The results of the present study will further enrich the theoretical basis of the crayfish immune system and provide new ideas for disease prevention and control.

Body mass index change in relation to longitudinal systolic blood pressure: An age- and sex-matched and repeated measures study.

BACKGROUND AND AIMS: The positive association between mean systolic blood pressure (SBP) and body mass index (BMI) diminished or reversed over the past four decades. The primary aim of this study was to evaluate effects of BMI change on longitudinal SBP. METHODS AND RESULTS: A total of 3638 participants who had annual health examination from 2015 to 2019 were included and matched by age and sex according to BMI levels. BMI and SBP were measured annually and their association were assessed by a linear mixed-effects regression model. The normal weight participants had a sustained weight gain as well as SBP increase during the study period (all Ptrend <0.001). The obese participants had a sustained weight loss but SBP did not decrease simultaneously. If BMI change was considered, the obese participants with BMI loss had a significant decrease of SBP during the study period (Ptrend = 0.0012). Mixed-effects models showed that weight gain was more influential on longitudinal SBP in the normal weight participants and weight loss was in the obese participants. The obese group with BMI loss had a decrease of SBP by 5.01 mmHg (95% confidence interval: 2.56 mmHg, 7.46 mmHg) compared to their counterparts with BMI maintenance from 2015 to 2019. CONCLUSIONS: The effect of weight change on longitudinal SBP was varied among BMI groups. With the increase of baseline BMI level, the positive effect of weight loss on SBP became greater and the negative effect of weight gain on SBP were attenuated.

Long-term BPA exposure leads to bone malformation and abnormal expression of MAPK/Wnt/FoxO signaling pathway genes in zebrafish offspring.

Bisphenol A (BPA) is one of the world's most widely used plasticizer, and its hazardous impacts have been well studied. However, few studies focused on the effects of parental long-term BPA exposure on the bone development of offspring. In the present study, the bone development of offspring was studied following long-term exposure of parental zebrafish to environmentally relevant 15 and 225 µg/L BPA. The results showed that BPA increased the mortality and deformity rate of offspring and caused craniofacial deformities characterized by changes in various cartilage angles and lengths. The alizarin red and calcein staining showed that BPA could delay bone mineralization and reduce bone mass accumulation. The results of acridine orange staining indicated that BPA induced apoptosis of the skull. The degree of harm of BPA presented a dose-dependent pattern. The results of the comparative transcriptome showed that there were 380 different expression genes (DEGs) in the 15 µg/L BPA group, and 645 DEGs in the 225 µg/L BPA group. MAPK/Wnt/FoxO signaling pathway-related genes were significantly down-regulated in the BPA-exposed groups. The present study demonstrates that long-term parental BPA exposure would severely affect cartilage development and bone mineralization of fish offspring, and MAPK/Wnt/FoxO signaling pathways may be involved in this process.

Bisphenol A disrupts apolipoprotein E expression through estrogen-related receptor gamma and DNA methlylation in the liver of male rare minnow Gobiocypris rarus.

An increasing number of studies show that bisphenol A (BPA) can cause lipid metabolism disorder. However, few studies focused on the effect of BPA on lipid transport. Apolipoprotein E (ApoE) plays important roles in triglyceride (TG) transportation. Our previous study found that ApoE was a sensitive gene in response to BPA exposure in male rare minnow. To investigate the effect and mechanism of BPA on hepatic ApoE, adult male rare minnow Gobiocypris rarus were exposed to environmentally relevant concentrations of BPA (15 µg/L) for 1, 3 and 5 weeks. Results showed that BPA inhibited ApoE expression at week 1 and 5, while induced its expression at week 3. A positive estrogen-related receptor gamma (Esrrg) response element was identified in the promoter region of ApoE. The change of the Esrrg recruitment was consistent with ApoE mRNA expression. Moreover, the methylation status of the CpG sites near and on the Esrrg binding sites changed opposite to the ApoE mRNA level, which may be the main cause for the change in Esrrg recruitment. The expression of ApoE protein was significantly enhanced following long-term BPA exposure. Consistently, the TG accumulation was significantly increased in the plasma. The present study demonstrates that BPA could affect rare minnow ApoE expression, which is probably one of the ways for BPA disturbing fish lipid metabolism.

Bisphenol A induces hepatic triglyceride level in adult male rare minnow Gobiocypris rarus.

Bisphenol A (BPA), an endocrine disruptor, exist in almost all waters. In the present study, we expose adult male Gobiocypris rarus rare minnow to 15 µg/L BPA to study the effect BPA on fish hepatic lipid metabolism. Following 1, 3 and 5 weeks exposure, the liver tissue of rare minnow was separated. The change of the hepatic morphology, hepatosomatic index, lipid composition and expression of lipid metabolism related genes were analyzed through paraffin section, oil red O staining, lipidomic analysis, and quantitative real-time PCR. BPA can cause significant hepatic lipid deposition in male rare minnow, leading to an increase in triglyceride (TG) level (1.84-22.87-fold), but it is also accompanied by a decrease in diglyceride level (1.67-4.78-fold). The expression of lipid metabolism related genes showed that BPA exposure can up-regulate TG synthesis related genes expression, and down-regulate TG degradation genes expression. Expression of TG transport related genes were also disrupted by BPA. It suggests that BPA can up-regulate rare minnow hepatic TG level through multi-path, and ultimately lead to lipid accumulation in the liver. The results of the present study enrich the mechanisms of environmental endocrine disruptors affecting lipid accumulation in fish.

Acute BPA exposure-induced oxidative stress, depressed immune genes expression and damage of hepatopancreas in red swamp crayfish Procambarus clarkii.

Bisphenol A is a typical endocrine disrupting chemicals (EDCs) and produce various toxic effects on animals due to its potential endocrine disruption, oxidative damage effect, mutagenic effect and hypomethylation. To study its effect on the immune system of crustaceans, the Procambarus clarkii were utilized to detect the immune related indicators after 225 µg/L BPA exposure for 1 week. Hepatopancreatic histology and ultrastructure analysis showed that the brush border disappeared, the lumen increased, and the connection between the hepatic tubules fade away in BPA treated group. BPA could significantly increase the level of ROS, inhibit the activities of antioxidant-related enzymes (SOD, POD, and CAT), and thereby cause the oxidative stress. The enzyme activities of AKP, ACP and lysozyme in hepatopancreas after BPA exposure were also depressed even after Aeromonas hydrophila infections. The relative expression profiles of immune-related genes after BPA exposure and bacterial infection showed suppressed trends of most selected genes. Under A. hydrophila infections, the cumulative mortality of 225 µg/L BPA-treated crayfish was significantly higher than other groups. All these results indicated that BPA exposure had adverse effects on the immune ability of P. clarkii. The present study will provide an important foundation for further understanding the effects of EDCs on crustacean immune functions.

Diversity of the Bosmina (Cladocera: Bosminidae) in China, revealed by analysis of two genetic markers (mtDNA 16S and a nuclear ITS).

BACKGROUND: China is an important biogeographical zone in which the genetic legacies of the Tertiary and Quaternary periods are abundant, and the contemporary geography environment plays an important role in species distribution. Therefore, many biogeographical studies have focused on the organisms of the region, especially zooplankton, which is essential in the formation of biogeographical principles. Moreover, the generality of endemism also reinforces the need for detailed regional studies of zooplankton. Bosmina, a group of cosmopolitan zooplankton, is difficult to identify by morphology, and no genetic data are available to date to assess this species complex in China. In this study, 48 waterbodies were sampled covering a large geographical and ecological range in China, the goal of this research is to explore the species distribution of Bosmina across China and to reveal the genetic information of this species complex, based on two genetic markers (a mtDNA 16S and a nuclear ITS). The diversity of taxa in the Bosmina across China was investigated using molecular tools for the first time. RESULTS: Two main species were detected in 35 waterbodies: an endemic east Asia B. fatalis, and the B. longirostris that has a Holarctic distribution. B. fatalis had lower genetic polymorphism and population differentiation than B. longirostris. B. fatalis was preponderant in central and eastern China, whereas B. longirostris was dominated in western China. The third lineage (B. hagmanni) was only detected in a reservoir (CJR) of eastern China (Guangdong province). Bosmina had limited distribution on the Tibetan plateau. CONCLUSIONS: This study revealed that the biogeography of Bosmina appear to be affected by historical events (Pleistocene glaciations) and contemporary environment (such as altitude, eutrophication and isolated habitat).

Effects of microcystin-LR on the immune dysfunction and ultrastructure of hepatopancreas in giant freshwater prawn Macrobrachium rosenbergii.

Microcystins (MCs), produced by cyanobacteria, can strongly inhibit the activity of protein phosphatase, and exhibit strong hepatotoxicity. Macrobrachium rosenbergii is an important aquaculture economic species. Cyanobacterial blooms occur frequently during the culture of M. rosenbergii. However, the effects of MCs on the M. rosenbergii immune function have not been studied. In the present study, M. rosenbergii were exposed to environment-related concentrations of MC-LR type (0.5 and 5 µg/L) for 3 weeks. Hepatopancreatic histology was investigated, and antioxidant enzymes activity, acid phosphatase, alkaline phosphatase and lysozyme activity in hepatopancreas were also analyzed. Results showed that MC-LR could damage M. rosenbergii hepatopancreas, induce hepatopancreatic apoptosis and antioxidant dysfunctions. The expression profiles of major immune-related genes after MC-LR exposure were also detected. Some genes with antibacterial functions were suppressed, and the expression of apoptosis-related genes were up-regulated. After MC-LR exposure, the cumulative mortality of M. rosenbergii infected with Vibrio vulnificus and Aeromonas hydrophila were much higher than the control in a time-dose dependent manner. These results indicated the potential negative influence of MC-LR on the immune function of M. rosenbergii.

MDA5 and LGP2 acts as a key regulator though activating NF-κB and IRF3 in RLRs signaling of mandarinfish.

RIG-I-like receptors (RLRs), as key cytoplasmic sensors of viral pathogen-associated molecular patterns, can recognise viral RNA and enhance the antiviral response. Some investigations have focused on the roles of RLRs in the innate immune response in grass carp, large yellow croaker, and rainbow trout. However, little is known about the function of RLRs in mandarinfish (Siniperca chuatsi), an important economic fish in Perciformes. Here, we functionally characterized the RLRs involved in the immune responses of mandarinfish (Siniperca chuatsi), by evaluating three RLRs, namely, RIG-I, MDA5, and LGP2. The results revealed that MDA5 and LGP2 were present in mandarinfish, whereas RIG-I was absent. The MDA5 and LGP2 cDNA sequences contained 2976 and 2046 bp and encoded 991 and 681 amino acids, respectively. Multiple sequence alignments showed that MDA5 and LGP2 of mandarinfish were clustered together with their homologs from other teleost fishes and shared high similarities with those from other vertebrates, and RIG-I of mandarinfish was absent. Moreover, quantitative real-time PCR (qPCR) analysis suggested that MDA5 and LGP2 were constitutively expressed in all tissues tested, and MDA5 mRNA expression was relatively high in the gill, and spleen, whereas LGP2 mRNA expression was high in the liver, gill, and head kidney. After stimulation with lipopolysaccharide or poly I:C, the expression of MDA5 and LGP2 was upregulated in spleen, gill and head kidney, but the pattern was not exactly the same, MDA5 transcripts generally increased and then declined with the prolonged infection, while LGP2 transcripts went up continuously, which showed that mandarinfish MDA5 and LGP2 may play independent roles in antiviral response. Besides, it is further revealed that the MDA5 could activate NF-κB and IRF3 to inducing the production of IFN-ß by constructing tet-on stable strain of 293T cell, however over-expression of LGP2 resulted in decreased NF-κB, IRF3 and IFN-ß production in cells challenged with LPS and polyI:C Taken together, our results demonstrated that MDA5 and LGP2, as a positive and negative regulator, respectively, played an important role in modulating antibacterial andantiviral immune responses though activating NF-κB and IRF3 in RLRs signaling of mandarinfish.

Excessive use of enrofloxacin leads to growth inhibition of juvenile giant freshwater prawn Macrobrachium rosenbergii.

Giant freshwater prawn Macrobrachium rosenbergii is an economically important species. However, its growth retardant have brought serious economic losses in recent years. Antibiotics abuse is suggested as a reason for M. rosenbergii's growth retardant, while few studies focused on the toxic effect of antibiotics on M. rosenbergii. To investigate the effect of enrofloxacin, a widely used antibiotic, on juvenile M. rosenbergii, a 14 days exposure study was carried out within 0.2, 1 and 5 mg/L enrofloxacin and followed by 7 days decontamination. Results showed that during the test period, enrofloxacin had the largest accumulation in juvenile shrimp at day 3, and gradually decreased at day 7 and 14, and almost all the drugs are cleared after 3 days decontamination. Short-term exposure to low dose enrofloxacin can promote the growth of juveniles. High dose enrofloxacin inhibited the growth of juvenile shrimp, to gill and liver damage, and induced apoptosis of the hepatopancreatic cells. These adverse effects was possibly caused by enrofloxacin-induced oxidative stress. Moreover, we also found the damage caused by high concentrations of enrofloxacin was irreversible in the short term. Collectively, these data indicated that enrofloxacin did affect the juvenile shrimp growth and development, and high level enrofloxacin abuse may contributed to M. rosenbergii's growth retardant.

The NOD1 and NOD2 in mandarinfish (Siniperca chuatsi): molecular characterization, tissue distribution, and expression analysis.

BACKGROUND: NOD-like receptors (NLRs) are a family of cytoplasmic pattern recognition receptors (PRRs), of which NOD1 and NOD2, are the main representative members. Many investigations have focused on the role of NOD1 and NOD2 in the innate immune response in Cypriniformes and Siluriformes. As an important economic fish in Perciformes, little is known about the function of NOD1 and NOD2 in mandarinfish (Siniperca chuatsi). RESULTS: The full-length NOD1 and NOD2 cDNA sequence was obtained using reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends (RACE). The mandarinfish NOD1 and NOD2 cDNA sequences contain 3247 bp and 3257 bp, and encode 918 amino acids and 988 amino acids, respectively. Multiple sequence alignments showed that mNOD1 and mNOD2 share high similarity with that from other vertebrates. RT-PCR analysis revealed that relatively high levels of mNOD1 and mNOD2 mRNA were detected in gill and head kidney tissues, compared with the heart, spleen, liver, muscle, and intestine. In addition, the relative levels of mNOD1 and mNOD2 transcripts were significantly upregulated in three tissues when the fishes were challenged with LPS and Poly I:C, interestingly, the NOD1 mRNA got peaked earlier than NOD2 after LPS induction in the spleen, gill, and head kidney, and during Poly I:C treatment, the NOD2 mRNA got peaked at 8 h in spleen and gill, while NOD1 showed significant higher expression at 24 h post infection, besides, in head kidney, the NOD2 mRNA showed a great increasing trend and NOD1 got peaked at 16 h. Therefore the mNOD1 and mNOD2 may act differently within different tissues in different time during antiviral and antibacterial defense. CONCLUSIONS: These results revealed the dynamic mNOD1 and mNOD2 expression during viral and bacterial infections, which suggested the NOD1 and NOD2 play important roles in innate immune of mandarinfish.

MicroRNA-194 promotes osteoblast differentiation via downregulating STAT1.

Osteoblast differentiation is a vital process in maintaining bone homeostasis in which various transcriptional factors, signaling molecules, and microRNAs (miRNAs) are involved. Recently, signal transducer and activator of transcription 1 (STAT1) has been found to play an important role in regulating osteoblast differentiation. Here, we identified that STAT1 expression was regulated by miR-194. Using mouse bone mesenchymal stem cells (BMSCs), we found that miR-194 expression was significantly increased following osteoblast differentiation induction. Overexpression of miR-194 by lentivirus-mediated gene transfer markedly increased osteoblast differentiation, whereas inhibition of miR-194 significantly suppressed osteoblast differentiation of BMSCs. Using a dual-luciferase reporter assay, a direct interaction between miR-194 and the 3'-untranslated region (UTR) of STAT1 was confirmed. Additionally, miR-194 regulated mRNA and protein expression of STAT1 in BMSCs. Further analysis showed that miR-194 overexpression promoted the nuclear translocation of runt-related transcription factor 2 (Runx2), which is critical for osteoblast differentiation. In contrast, inhibition of miR-194 blocked the nuclear translocation of Runx2. Moreover, overexpression of STAT1 significantly blocked Runx2 nuclear translocation and osteoblast differentiation mediated by miR-194 overexpression. Taken together, our data suggest that miR-194 regulates osteoblast differentiation through modulating STAT1-mediated Runx2 nuclear translocation.

NF-κB Inhibitor Myrislignan Induces Ferroptosis of Glioblastoma Cells via Regulating Epithelial-Mesenchymal Transformation in a Slug-Dependent Manner.

Glioblastoma (GBM) is the most common malignant tumor of the adult central nervous system. Aberrant regulation of cell death is an important feature of GBM, and investigating the regulatory mechanisms of cell death in GBM may provide insights into development of new therapeutic strategies. We demonstrated that myrislignan has ferroptosis-promoting activity. Myrislignan is a lignan isolated from Myristica fragrans Houtt and an inhibitor of NF-κB signaling pathway. Ferroptosis is an iron-dependent form of programmed cell death characterized by the accumulation of intracellular lipid peroxidation products. Interestingly, ferroptosis was associated with other biological processes in tumor cells such as autophagy and necroptosis. Recently, the crosstalk between epithelial-mesenchymal transition (EMT) and ferroptosis has also been reported, but the mechanisms underlying the crosstalk have not been identified. Our results indicated that myrislignan suppressed growth of GBM through EMT-mediated ferroptosis in a Slug-dependent manner. Myrislignan inhibited the activation of NF-κB signaling by blocking the phosphorylation of p65 protein and induced ferroptosis through the Slug-SLC7A11 signaling pathway in GBM cells. In addition, myrislignan suppressed the progression of GBM in xenograft mouse model. Hence, our findings contribute to the understanding of EMT-induced ferroptosis and provide targets for the development of targeted therapy against GBM.

Polyester microplastic fibers induce mitochondrial damage, apoptosis and oxidative stress in Daphnia carinata, accompanied by changes in apoptotic and ferroptosis pathway.

With the widespread utilization of plastic products, microplastics (MPs) have merged as a newfound environmental contaminant in the United States, and the bulk of these MPs in the environment manifest as fibrous structures. Concerns have also been voiced regarding the potential hazards posed by microplastic fibers (MFs). However, research examining the toxicity of MFs, particularly in relation to planktonic organisms, remains severely limited. Meanwhile, polyester fiber materials find extensive applications across diverse industries. As a result, this investigation delved into the toxicology of polyester microplastic fibers (PET-MFs) with a focus on their impact on Daphnia carinata (D. carinata), a freshwater crustacean. Newly hatched D. carinata were subjected to varying concentrations of PET-MFs (0, 50, and 500 MFs/mL) to scrutinize the accumulation of PET-MFs within these organisms and their resultant toxicity. The outcomes revealed that D. carinata was capable of ingesting PET-MFs, leading to diminished rates of survival and reproduction. These effects were accompanied by mitochondrial impairment, heightened mitochondrial count, apoptosis, escalated generation of reactive oxygen species, augmented activity of antioxidant enzymes, and distinct patterns of gene expression. Interestingly, when comparing the group exposed to 50 MFs/mL with the one exposed to 500 MFs/mL, it was observed that the former triggered a more pronounced degree of mitochondrial damage, apoptosis, and oxidative stress. This phenomenon could be attributed to the fact that brief exposure to 500 MFs/mL resulted in greater mortality, eliminating individuals with lower adaptability. Those that survived managed to regulate elevated in vivo reactive oxygen species levels through an increase in glutathione S-transferase content, thereby establishing an adaptive mechanism. Low concentrations did not induce direct mortality, yet PET-MFs continued to inflict harm within the organism. RNA-seq analysis unveiled significant alterations in 279 and 55 genes in the 50 MFs/mL and 500 MFs/mL exposure groups, respectively. Functional enrichment analysis of the 50 MFs/mL group indicated involvement of the apoptosis pathway and ferroptosis pathway in the toxic effects exerted by PET-MFs on D. carinata. This study imparts valuable insights into the toxicological ramifications of PET-MFs on D. carinata, underscoring their potential risks within aquatic ecosystems.

Bisphenol A disturbs hepatic apolipoprotein A1 expression and cholesterol metabolism in rare minnow Gobiocypris rarus.

Bisphenol A (BPA) is a well-known plasticizer, which is widely distributed in the aquatic environment. Lots of studies showed that BPA could lead to lipid metabolism disorder in fish, but few studies studied the mechanism from the perspective of lipid transport. Apolipoprotein A1 (ApoA1) is the main component of high-density lipoprotein (HDL), and plays important roles in reverse cholesterol transport (RCT). In this study, we investigated the effect and molecular mechanism of BPA on ApoA1 and its effect on cholesterol in adult male rare minnow. Results showed that BPA could disturb hepatic ApoA1 expression through regulating Esrrg recruitment and DNA methylation in its promoter region, and ultimately up-regulated ApoA1 protein levels. The increased hepatic ApoA1 improved HDL-C levels, enhanced RCT, and disrupted cholesterol levels. The present study reveals the effect and mechanism of BPA on fish cholesterol metabolism from the perspective of cholesterol transport.

The toxic effects of polystyrene microplastics on freshwater algae Chlorella pyrenoidosa depends on the different size of polystyrene microplastics.

Microplastics (MPs) are persistent environmental contaminants. The toxic effects of MPs on aquatic organisms have raised increasing concerns, but their toxic effects on aquatic phytoplankton has not been thoroughly investigated. In the present study, the toxic effects of two sizes MPs (1 µm and 5 µm) on Chlorella pyrenoidosa at 2, 10, 50 mg/L were explored for 1, 5, 10 days. The growth ratio, photosynthetic pigments content, extracellular polymeric substances content, soluble protein content, MDA content and relative expression of genes related to photosynthesis and energy metabolism were measured. These results indicated that 1 µm MP could significantly inhibit the growth of C. pyrenoidosa. Compared with the control group, 1 µm MP significantly reduced the photosynthetic pigment content, induced oxidative stress and disrupted the cell membrane integrity of C. pyrenoidosa. At the molecular level, 1 µm MP altered the transcript levels of genes related to photosynthesis and energy metabolism. Scanning electron microscopy and fluorescent images showed that MPs aggregation with C. pyrenoidosa may be the main reason for the toxic effects of MPs. These results will provide new insight into the toxicity of different MPs on aquatic phytoplankton, and evaluate the risks caused by MPs in aquatic environments.

Single and binary-combined toxic effects of acetochlor and Cu2+ on goldfish (Carassius auratus) larvae.

Acetochlor and copper are common freshwater pollutants and pose a severe threat to aquatic animals. The toxicity of acetochlor (Ac) and Cu2+ toward goldfish larvae was investigated by subjecting the larvae to different concentrations of acetochlor, Cu2+, and mixed solutions for 1, 3, and 7 days. The length of goldfish larvae exposed to the 100 µg/L Ac + 100 µg/L Cu2+ mixed solution was considerably lower than that of the control on day 3, but there were no significant differences among the other groups. The heart rates of the larvae in 100 µg/L Ac + 100 µg/L Cu2+ mixed solution were higher than those of the control group on days 3 and 7. Acetochlor and Cu2+ also caused severe damage to the liver and intestine of the larvae, especially in the 100 µg/L Ac + 100 µg/L Cu2+ mixed solution group. Indicators related to oxidative stress (hydrogen peroxide, catalase, glutathione peroxidase, and total superoxide dismutase) that could potentially be induced by acetochlor or Cu2+ began to increase on day 7, and the enzyme activities of the larvae in the mixed groups were significantly lower than those in the control group. In contrast, the expression levels of the genes related to antioxidant stress were rapidly down-regulated in all groups on the 7th day after exposure. Briefly, the combined toxicity of acetochlor and Cu2+ was stronger than that of the single toxicity treatments. Furthermore, toxicity toward larvae in the mixed solution group (100 µg/L Ac + 100 µg/L Cu2+) was more obvious.

Complete mitochondrial genome of Bosmina fatalis (Cladocera: Bosminidae) and its phylogenetic analysis.

Bosmina is a globally distributed zooplankton that adapts to a eutrophic environment. In this study, we cultivated monoclonal Bosmina fatalis and determined its complete mitochondrial gene sequence using the Illumina HiSeq 4000 platform. It was 15,209 bp in length, including 13 protein-coding genes, 22 tRNA genes, and 2 rRNA genes, with the A + T content (69.2%) significantly higher than the G + C content (30.9%). All 22 typical tRNA genes had a classical cloverleaf structure, except for tRNAIle. The complete mitochondrial genome of nine other cladoceran species was used to reconstruct a phylogenetic tree, showing that B. fatalis has a closer relationship with Daphnia than other cladocerans.