Investigation of membrane fouling and mechanism induced by extracellular organic matter during long-term exposure to pharmaceuticals and personal care products.

This study investigated ultrafiltration membrane fouling by extracellular organic matter (EOM) and the mechanism operating during long-term exposure to pharmaceuticals and personal care products. The results indicated that carbamazepine and diclofenac in algal-laden water altered the filtration flux and membrane fouling by EOM. Exposure to low-concentration carbamazepine (0.25 µg/L) improved the filtration flux and the total (Rtot) and reversible fouling resistance (Rc), whereas the filtration flux and Rtot and Rc were reduced when EOM was used during long-term exposure to high carbamazepine concentrations (>1 µg/L). Both Rtot and Rc were increased when algae were exposed to 0.25 µg/L diclofenac, whereas the filtration flux and Rtot and Rc were alleviated when algae were exposed to >1 µg/L diclofenac. Moreover, carbamazepine and diclofenac (0.25 µg/L - 1000 µg/L) in water enhanced the irreversible fouling resistance (Rb) when ultrafiltration was used to treat algal-laden waters. The mechanism indicated that membrane fouling induced by standard blocking was transformed to complete blocking when EOM was exposed to high levels of carbamazepine (>0.25 µg/L) in the initial filtration process, whereas cake layer formation played an important role during the later filtration process; with low carbamazepine levels (0.25 µg/L), standard blocking of EOM was dominant during the entire filtration process. The membrane fouling mechanism also changed when algal-laden waters were exposed to diclofenac, the membrane fouling was transformed from complete blocking to standard blocking when DFC was present in the initial filtration process, whereas cake layer formation exerted an important role during the late filtration process. This research provides important information on the long-term risks caused by pharmaceutical and personal care products and potential threats to membrane treatment.

Polystyrene nanospheres-induced hepatotoxicity in swamp eel (Monopterus albus): From biochemical, pathological and transcriptomic perspectives.

As ubiquitous emerging pollutants, microplastics (MPs) in aquatic environments have aroused critical global concerns. Despite the occurrence and characteristics of MPs in freshwater agroecosystems well-described by our previous study, their ecotoxicological implications in Monopterus albus remains unfathomed. Herein, we dissected toxic effects and mechanisms of PS-NPs exposure against M. albus hepatic tissues at concentrations of 0.5 (L), 5 (M), 10 (H) mg/L for 28 days using physiochemical measurements, histopathological analysis and transcriptomic sequencing. Results showed that upon PS-NPs treatments, levels of ROS, MDA, 8-OHdG and MFO activity were significantly enhanced relative to the control (C) group, while SP content and T-AOC activity were dramatically suppressed, suggesting ROS burst, lipid peroxidation and DNA damage may occur in liver tissues. This oxidative damage further triggered impaired hepatic function and histopathology, disordered lipid metabolism and hepatocyte apoptosis, as reflected by significantly diminished activities of GPT, GOT, ACP, AKP and LDH, paralleled with augmented levels of TG, TC and HSI as well as Cytc and Caspase-3,8,9 activities. Noticeably, concentration-dependent rises of apoptotic rate, vacuolar degeneration and lipid deposition were manifest in TUNEL, H&E and ORO staining. In addition, a total of 375/475/981 up-regulated as well as 260/611/1422 down-regulated DEGs in C vs L, C vs M and C vs H categories were identified based on RNA-seq, respectively. These DEGs were significantly annotated and enriched into GO terms (membrane, cytoplasm, response to stimuli, oxidation-reduction process) as well as KEGG pathways (ether lipid metabolism, apoptosis, chemical carcinogenesis-reactive oxygen species, non-alcoholic fatty liver disease). Moreover, signaling cascades Keap1-Nrf2, p53 and PPAR were either substantially initiated or dysregulated to orchestrate PS-NPs hepatotoxicity featuring oxidative damage, hepatocyte apoptosis and lipid steatosis. Collectively, this study not only expounded on toxicological mechanisms whereby PS-MPs exerted deleterious effects on M. albus, but also pointed to ecological risks of PS-MPs-induced hepatoxicity and lipid steatosis in this commercially-important species.

Dietary polystyrene nanoplastics exposure alters hepatic glycolipid metabolism, triggering inflammatory responses and apoptosis in Monopterus albus.

Microplastics and nanoplastics (MPs and NPs) are abundant, persistent, and widespread environmental pollutants that are of increasing concern as they pose a serious threat to ecosystems and aquatic species. Identifying the ecological effects of NPs pollution requires understanding the effects of changing nanoplastics concentrations in aquatic organisms. Monopterus albus were orally fed three different concentrations of 100 nm polystyrene nanoplastics (PS-NPs): 0.05 %, 0.5 %, and 1 % of the feed for 28 days. Nanoplastics significantly activated the PPAR signaling pathway, Acyl-CoA oxidase 1 (ACOX1), carnitine palmitoyltransferase 1a (CPT1A), angiopoietin-like 4 (ANGPTL4), and phosphoenolpyruvate carboxykinase (PCK) at the mRNA level, resulting in disturbed lipid metabolism. Glutathione peroxidase (GSH-px) activity, catalase (CAT) activity, and malondialdehyde (MDA) were significantly elevated in the high nanoplastics-feeding exposure group, leading to oxidative stress in the liver. Overexpression of the cytokines genes Interleukin 1 (IL1B) and Interleukin-8 (IL8), Tumor necrosis factor alpha (TNF-α), activation of MAPK signaling pathway, and increased gene expression of c-Jun amino-terminal kinases (JNK) and p38 indicate that exposure to NPs may lead to hepatopancreas apoptosis through oxidative stress and inflammation. In summary, dietary PS-NPs exposure alters hepatic glycolipid metabolism, triggering inflammatory responses and apoptosis in M. albus. The results of this study provide valuable ecotoxicological data for a better understanding of the biological fate and effects of nanoplastics in M. albus.

Effects of exposure to waterborne polystyrene microspheres on lipid metabolism in the hepatopancreas of juvenile redclaw crayfish, Cherax quadricarinatus.

Previous research has identified microplastics as new environmental pollutants that are widely distributed in a variety of environments, including aquaculture environments. However, the potential hazard of microplastics to aquaculture animals, especially toward lipid metabolism involved with the survival and growth of aquatic animal, has not yet been investigated. In the present study, redclaw crayfish (Cherax quadricarinatus) were exposed to different concentrations of 200 nm-sized polystyrene microspheres (0, 0.5, and 5 mg/L) for 21 days, to investigate the effects of microplastics on lipid metabolism. After ingestion, the microplastics were distributed in the intestines and hepatopancreas, and appeared to inhibit the growth of Cherax quadricarinatus. Subsequently, the lipid levels in the hepatopancreas and hemolymph was detected, and found that after 21 days of exposure, the lipid content and free fatty acids in the hepatopancreas and hemolymph decreased significantly, and total cholesterol and triglycerides levels increased significantly in the hemolymph. This might have been caused by insufficient intake of exogenous fat. A significant decrease in lipase activity also supported this view. The activity of lipoprotein lipase related to lipolysis in the hepatopancreas increased significantly, while the activity of fatty acid synthase related to fat synthesis increased, and the activity of acetyl-CoA carboxylase decreased. These results indicated disturbed lipid metabolism in the hepatopancreas. The significant increase of lipid transport-related low-density lipoprotein indicated that the lipolytic capacity was higher than the lipid synthesis capacity. The expression levels of fatty acid metabolism-related genes FAD6 and FABP decreased significantly, indicating that the fatty acid utilization ability of hepatopancreas cells was inhibited, which was consistent with the results of enzyme activities. Thus, microplastics represent a potential hazard to redclaw crayfish, at least on lipid metabolism. This study provided basic data on the ecotoxicological effects of microplastics on crustaceans.

Microplastic pollution in rice-fish co-culture system: A report of three farmland stations in Shanghai, China.

Microplastics are emerging contaminants of increasing concern. Despite the occurrence of microplastics in farmland soils, the knowledge on microplastics in rice-fish co-culture ecosystems is limited. In this study, we investigated the distribution of microplastics in three rice-fish culture stations in Shanghai. During non-rice and rice-planting periods, microplastics in water, soils and aquatic animals (eel, loach and crayfish) were systematically assayed using methods of NaCl density extraction, H2O2 digestion and micro-fourier transform infrared spectroscopy. Results showed that average microplastic abundances were 0.4 ±â€¯0.1 items L-1, 10.3 ±â€¯2.2 items kg-1, 1.7 ±â€¯0.5 items individual-1 in water, soils and aquatic animal samples, respectively. We found an increasing trend in microplastic abundances in water, soil and animal samples from non-rice period to rice-planting period. Almost all of microplastics were found in digestive tracts of animals. Major microplastics were small (<1 mm) polyethylene and polypropylene fibers, with color of white and translucent. Size, shape, color and polymer type distributions of microplastics were similarly found in environmental and animal samples. Moreover, microplastic abundances in aquatic animals correlated to abundance in farmland soils. This study, for the first time, reveals the occurrence and characteristics of microplastic pollution in rice-fish culture ecosystem which suggests the potential ecological risks of microplastics in the agroecosystem.

Accumulation of polystyrene microplastics in juvenile Eriocheir sinensis and oxidative stress effects in the liver.

As a widespread and ubiquitous pollutant of marine ecosystems, microplastic has the potential to become an emerging global threat for aquatic organisms. The present study aims to elucidate the effects of microplastics on the growth, accumulation and oxidative stress response in the liver of Eriocheir sinensis. Fluorescent microplastic particles (diameter = 0.5 µm) accumulated in the gill, liver and gut tissues of E. sinensis were investigated when crabs were exposed to a concentration of 40000 µg/L for 7 days. A 21 day toxicity test suggested that the rate of weight gain, specific growth rate, and hepatosomatic index of E. sinensis decreased with increasing microplastic concentration (0 µg/L, 40 µg/L, 400 µg/L, 4000 µg/L and 40000 µg/L). The activities of AChE and GPT in crabs exposed to microplastics were lower than those in control group. GOT activity increased significantly after exposure to a low concentration of microplastics and then decreased continuously with increasing microplastic concentrations. The activities of superoxide dismutase (SOD), aspartate transaminase (GOT), glutathione (GSH), and glutathione peroxidase (GPx) increased in specimens exposed to low concentrations of microplastics (40 and 400 µg/L) compared to the control and decreased in organisms exposed to high concentrations (4000 and 40000 µg/L). In contrast, the activities of acetylcholinesterase, catalase (CAT), and alanine aminotransferase were significantly lower in the organisms exposed to microplastics compared to control animals. Upon exposure to increasing microplastic concentrations, the expression of genes encoding the antioxidants SOD, CAT, GPx and glutathione S-transferase in the liver decreased after first increasing. Exposure to microplastics increased the expression of the gene encoding p38 in the MAPK signaling pathway and significantly decreased the expressions of genes encoding ERK, AKT, and MEK. The results of this study demonstrate that microplastics can accumulate in the tissues of E. sinensis and negatively affect growth. In addition, exposure to microplastics causes damage and induces oxidative stress in the hepatopancreas of E. sinensis. The findings provide basic biological data for environmental and human risk assessments of microplastics of high concern.

Microplastic and mesoplastic pollution in farmland soils in suburbs of Shanghai, China.

Microplastics are emerging pollutants which have been extensively detected in water environments. However, little is known about microplastic pollution in soil environments. In this study, we investigated microplastics and mesoplastics in farmland soils from twenty vegetable fields around the suburbs of Shanghai. In each site, three duplicate soil samples were collected from shallow (0-3 cm) and deep soils (3-6 cm), respectively. Microplastics (sizes of 20 µm - 5 mm) and mesoplastics (5 mm - 2 cm) were detected using methods of density extraction, 30% H2O2 digestion and micro-fourier transform infrared spectroscopy. The abundance of microplastics was 78.00 ±â€¯12.91 and 62.50 ±â€¯12.97 items kg-1 in shallow and deep soils, respectively. While, mesoplastics were found with abundance of 6.75 ±â€¯1.51 and 3.25 ±â€¯1.04 items kg-1 in shallow and deep soils. Among these micro(meso)plastics, 48.79% and 59.81% were in size of <1 mm in shallow and deep soils. The main morphotypes of microplastics included fiber, fragment and film, mostly in color of black or transparent. Moreover, we found that topsoil contained higher concentrations and larger sizes of micro(meso)plastics than deep soil. In addition, the vast majority of micro(meso)plastics were polypropylene (50.51%) and polyethylene (43.43%). This study reveals occurrence and characteristics of microplastic pollution in typical farmland soils. It provides important data for subsequent research on microplatics in the terrestrial ecosystem.