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It has been verified that, as an emerging contaminant, microplastics are capable of adsorbing certain traditional contaminants like the heavy metal Cd. However, the majority of previous studies only focused on certain types of virgin microplastics, especially for PE and PS. In addition, this adsorption process might be affected by microplastics inevitably undergoing aging and consequent changes in the natural environment. Unfortunately, the relevant reports on aging effects were mainly about organic pollutants, rather than heavy metals. By far, there have been few comprehensive and mechanistic studies on the key aging effects on the Cd adsorption by various types of microplastics. In this study, five representative types of microplastics (i.e., PS, ABS, PP, PVC, and PET) were selected for aging by ultraviolet radiation, and the physicochemical properties of virgin and aged microplastics were thoroughly compared, including specific surface area, crystallinity, surface functional groups, and surface elements. Accordingly, the changes in adsorption isotherms of Cd by microplastics were discussed. The results showed that:① aging induced non-significant changes in specific surface area but a significant decrease in crystallinity. Surface functional groups also changed, including the emergence of a C=O functional group on PS and ABS, the decrease in C=C absorption peak intensity on ABS, and the increase in absorption peak intensities of C=O, C-O, and polar ester groups on PET. Regarding surface C content, C=C/C-C decreased, whereas C-O and O-C=O increased. The total O content and O/C significantly increased as well. ② The Langmuir model well-fitted the adsorption isotherms of Cd by virgin and aged microplastics. Aging significantly expanded the adsorption capacity of Cd by microplastics, as the order of saturated adsorption capacity before aging was ABS (0.2284 mg·g -1 )>PVC (0.1360 mg·g -1 )>PS (0.1286 mg·g -1 )>PP (0.1005 mg·g -1 )>PET (0.0462 mg·g -1 ) and then became PS (0.2768 mg·g -1 )>ABS (0.2586 mg·g -1 )>PVC (0.1776 mg·g -1 )>PP (0.1721 mg·g -1 )>PET (0.0951 mg·g -1 ) after aging. ③ Both crystallinity and surface functional groups played key roles in the adsorption of Cd by microplastics. As for virgin microplastics, crystallinity was negatively correlated with the saturated adsorption capacity of Cd, because the amorphous regions contributed most to Cd adsorption. Aging brought about the decrease in crystallinity and the increase in amorphous regions, which further promoted the oxidation reaction on microplastics. Consequently, oxygen-containing functional groups increased on the surface and eventually expanded the adsorption capacity of Cd by microplastics. Note that certain specific functional groups of various microplastics also had impacts on the adsorption process. These results provide valuable information about the environmental behaviors and interactions of microplastics and heavy metals in nature.

Aging is a risk factor in the development of many diseases, including liver-related diseases. The two aims of the present study were 1 ) to determine how aging affects liver health in mice in the absence of any interventions and 2 ) if degenerations observed in relation to blood endotoxin levels are critical in aging-associated liver degeneration. Endotoxin levels and markers of liver damage, mitochondrial dysfunction, insulin resistance, and apoptosis as well as the Toll-like receptor 4 (Tlr-4) signaling cascade were studied in liver tissue and blood, respectively, of 3- and 24-mo-old male C57BL/6J mice. In a second set of experiments, 3- to 4-mo-old and 14-mo-old female lipopolysaccharide-binding protein (LBP) -/- mice and littermates fed standard chow, markers of liver damage, insulin resistance, and mitochondrial dysfunction were assessed. Plasma activity of aspartate aminotransferase and histological signs of hepatic inflammation and fibrosis were significantly higher in old C57BL/6J mice than in young animals. The number of neutrophils, CD8α-positive cells, and mRNA expression of markers of apoptosis were also significantly higher in livers of old C57BL/6J mice compared with young animals, being also associated with a significant induction of hepatic Tlr-4 and LBP expression as well as higher endotoxin levels in peripheral blood. Compared with age-matched littermates, LBP -/- mice display less signs of senescence in liver. Taken together, our data suggest that, despite being fed standard chow, old mice developed liver inflammation and beginning fibrosis and that bacterial endotoxin may play a critical role herein. NEW & NOTEWORTHY Old age in mice is associated with marked signs of liver degeneration, hepatic inflammation, and fibrosis. Aging-associated liver degeneration is associated with elevated bacterial endotoxin levels and an induction of lipopolysaccharide-binding protein (LBP) and Toll-like receptor 4-dependent signaling cascades in liver tissue. Furthermore, in old aged LBP -/- mice, markers of senescence seem to be lessened, supporting the hypothesis that bacterial endotoxin levels might be critical in aging-associated decline of liver.

Purpose: Impairments of intestinal barrier function are discussed as risk factors for the development and progression of non-alcoholic fatty liver disease (NAFLD). Studies suggest an association between arginine/citrulline homeostasis and the development of liver damages. Here, the effect of an oral L-citrulline (Cit) supplement on the development of a Western-style diet (WSD)-induced NAFLD was determined in mice., Methods: Female 6- to 8-week-old C57BL/6J mice were either pair-fed a liquid Western-style or control diet (C) ± 2.5 g/kg bodyweight Cit for 6 weeks (C + Cit or WSD + Cit). Indices of liver damage, glucose metabolism, intestinal barrier function and NO synthesis were measured., Results: While bodyweight gain was similar between groups, markers of glucose metabolism like fasting blood glucose and HOMA index and markers of liver damage like hepatic triglyceride levels, number of neutrophils and plasminogen activator inhibitor-1 protein levels were significantly lower in WSD + Cit-fed mice when compared to WSD-fed mice only. Protein levels of the tight junction proteins occludin and zonula occludens-1 in duodenum were significantly lower in mice fed a WSD when compared to those fed a WSD + Cit (-~70 and -~60 %, respectively, P < 0.05), whereas portal endotoxin levels, concentration of 3-nitrotyrosine protein adducts in duodenum and toll-like receptor-4 mRNA expression in livers of WSD + Cit-fed mice were markedly lower than in WSD-fed mice (-~43 %, P = 0.056; -~80 and -~48 %, respectively, P < 0.05)., Conclusion: Our data suggest that the protective effects of supplementing Cit on the development of NAFLD in mice are associated with a decreased translocation of endotoxin into the portal vein.

Intestinal microbiota and barrier functions seem to play an important role in the development of non-alcoholic fatty liver disease (NAFLD). However, whether these changes are an early event in the development of NAFLD or are primarily associated with later stages of the disease, has not yet been clarified. Using a pair-feeding model, we determined the effects of a short-term intake of a fat-, fructose- and cholesterol-rich diet (FFC) on the development of early hepatic steatosis and markers of intestinal barrier function in mice treated with and without non-resorbable antibiotics (AB). For four days, C57BL/6J mice were either pair-fed a control diet or a FFC diet ± AB (92 mg/kg body weight (BW) polymyxin B and 216 mg/kg BW neomycin). Hepatic steatosis and markers of inflammation, lipidperoxidation and intestinal barrier function were assessed. Lipid accumulation and early signs of inflammation found in the livers of FFC-fed mice were markedly attenuated in FFC + AB-fed animals. In FFC-fed mice the development of NAFLD was associated with a significant loss of tight junction proteins and an induction of matrix metalloproteinase-13 in the upper parts of the small intestine as well as significantly higher portal endotoxin levels and an induction of dependent signaling cascades in the liver. As expected, portal endotoxin levels and the expression of dependent signaling cascades in liver tissue were almost at the level of controls in FFC + AB-fed mice. However, FFC + AB-fed mice were also protected from the loss of zonula occludens-1 and partially of occludin protein in small intestine. Our data suggest that the development of early diet-induced hepatic steatosis in mice at least in part results from alterations of intestinal barrier function., Competing Interests: I.B. received financial support from Yakult for another, unrelated research project. A.B., C.J.J., K.N., C.S. and A.J.E. declare no conflict of interest.

Objective: Increased fasting blood ethanol levels, suggested to stem from an increased endogenous ethanol synthesis in the GI tract, are discussed to be critical in the development of non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to further delineate the mechanisms involved in the elevated blood ethanol levels found in patients with NAFLD., Design: In 20 nutritionally and metabolically screened children displaying early signs of NAFLD and 29 controls (aged 5-8 years), ethanol plasma levels were assessed. Ethanol levels along the GI tract, in vena cava and portal vein, intestinal and faecal microbiota, and activity of alcohol dehydrogenase (ADH) and cytochrome P450 2E1 (CYP2E1) were measured in wild-type, ob/ob and anti-TNFα antibody (aT) treated ob/ob mice., Results: Despite not differing in dietary pattern or prevalence of intestinal overgrowth, fasting ethanol levels being positively associated with measures of insulin resistance were significantly higher in children with NAFLD than in controls. Ethanol levels were similar in portal vein and chyme obtained from different parts of the GI tract between groups while ethanol levels in vena cava plasma were significantly higher in ob/ob mice. ADH activity was significantly lower in liver tissue obtained from ob/ob mice in comparison to wild-type controls and ob/ob mice treated with aT., Conclusions: Taken together, our data of animal experiments suggest that increased blood ethanol levels in patients with NAFLD may result from insulin-dependent impairments of ADH activity in liver tissue rather than from an increased endogenous ethanol synthesis., Trial Registration Number: NCT01306396., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)