Plastic, as a form of marine litter, is found in varying quantities and sizes around the globe from surface waters to deep-sea sediments. Identifying patterns of microplastic distribution will benefit an understanding of the scale of their potential effect on the environment and organisms. As sea ice extent is reducing in the Arctic, heightened shipping and fishing activity may increase marine pollution in the area. Microplastics may enter the region following ocean transport and local input, although baseline contamination measurements are still required. Here we present the first study of microplastics in Arctic waters, south and southwest of Svalbard, Norway. Microplastics were found in surface (top 16 cm) and sub-surface (6 m depth) samples using two independent techniques. Origins and pathways bringing microplastic to the Arctic remain unclear. Particle composition (95% fibres) suggests they may either result from the breakdown of larger items (transported over large distances by prevailing currents, or derived from local vessel activity), or input in sewage and wastewater from coastal areas. Concurrent observations of high zooplankton abundance suggest a high probability for marine biota to encounter microplastics and a potential for trophic interactions. Further research is required to understand the effects of microplastic-biota interaction within this productive environment.

海洋环境是海洋渔业资源赖以生存和发展的重要物质基础，为海洋生物的生长和繁殖提供了必要的生存空间和适宜的环境条件，对水产养殖等渔业生产活动起着决定性的作用。微塑料由于分布广、粒径小、难降解和持久性等特点已成为威胁海洋环境和渔业生产的新型污染物。本文通过归纳和总结微塑料在海洋渔业方面的研究进展，理清了海洋环境中微塑料的主要来源，阐明了微塑料对海洋环境和渔业生产影响的主要机制，并提出相应的防控措施，以期为有效防控海洋环境及渔业生产过程中微塑料污染问题提供科学依据和技术指导。

Metabolomics, the research area studying chemical processes involving metabolites, finds its utility in inflammasome biomarker discovery, thus representing a novel approach for cardiometabolic syndrome pathogeny acknowledgements. Metabolite biomarkers discovery is expected to improve the disease evolution and outcome. The activation of abundantly expressed NLRP3 inflammasome represents the background process of the diabetes mellitus disturbances like hyperglycemia and insulin resistance, as well as for myocardial cell death and fibrosis, all of them being features characteristic for cardiometabolic syndrome. Many molecules like troponins, brain natriuretic protein (BNP), ST2/IL-33, C-reactive protein (CRP), TNF, IL-1β, and IL-18 cytokines have been already examined as molecular markers for diagnosing or predicting different cardiac disturbances like myocardial infarction, heart failure, or myocarditis. In addition, metabolomics research comes with new findings arguing that NLRP3 inflammasome becomes a promising molecular tool to use for clinical and therapeutical management providing new targets for therapies in cardiometabolic syndrome. Inflammasome markers analyses, along with other molecular or genetic biomarkers, will result in a better understanding of cardiometabolic syndrome pathogenesis and therapeutic targets. Screening, diagnostic, and prognostic biomarkers resulted from inflammasome biomarker research will become standard of care in cardiometabolic syndrome management, their utility becoming the first magnitude.

Schizothorax o’connori (S. o’connori) is a representative tetraploid species in the subfamily Schizothoracinae and an important endemic fish in the Qinghai-Tibet Plateau. However, the domestication of S. o’connori remains challenging due to the lack of basic research. Here, we investigated the effects of artificial feeding on the oocytes and liver of S. o’connori by comparing the histological, metabolomic, and transcriptomic data. Histological results showed that the oocytes and liver of captive-reared S. o’connori had abnormal cell morphology. After comparison with the self-built database, a total of 233 metabolites were annotated. In oocytes, a total of 37 differentially accumulated metabolites (DAMs) were detected and two pathways were significantly enriched. There were obvious differences in the metabolites related to ovarian development, including pregnenolone and arachidonic acid. In liver, a total of 70 DAMs were detected and five pathways were significantly enriched. Based on the transcriptomic data, a total of 159 differentially expressed genes (DEGs) were significantly related with cell growth and death pathway in oocytes, while a total of 2841 DEGs were significantly related with 102 pathways in liver. Comparing the metabolomic and transcriptomic data showed that there were three common significant enrichment pathways in liver, including biosynthesis of unsaturated fatty acids, starch and sucrose metabolism, and fatty acid biosynthesis. These results showed that special attention should be given to the composition and intake of fatty acids during the artificial breeding of S. o’connori. In addition, many of metabolite-gene pairs were related to adenosine 5′-diphosphate, adenosine monophosphate, and pregnenolone. In summary, these data provide an overview of global metabolic and transcriptomic resources and broaden our understanding of captive-reared S. o’connori.

In a previous study, the authors reported that madecassoside (MA) exerted a potent neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury in rats, mediated by anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. However, the cellular and molecular bases for its neuroprotective effects have not been fully elucidated. In this study, an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD/R) was used to investigate the role of the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway in the neuroprotective and anti-inflammatory effects of MA. BV2 microglia viability after OGD/R, treated with or without MA, was measured using the MTT assay. Messenger RNA and protein expression of pro-inflammatory cytokines (tumor necrosis factor α [TNF-α], interleukin-1β [IL-1β], interleukin-6 [IL-6]) were measured using real-time polymerase chain reaction (RT-PCR) and ELISA after OGD/R or lipopolysaccharide treatment. Expression of TLR4/MyD88 and NF-κB p65 were measured using RT-PCR, Western blotting, and immunofluorescence analysis. MA significantly rescued OGD/R-induced cytotoxicity in BV2 microglia. Meanwhile, MA suppressed the secretion of pro-inflammatory mediators, including TNF-α, IL-1β, and IL-6, induced by OGD/R or lipopolysaccharide in BV2 microglia. The mechanism of its neuroprotection and anti-inflammation from OGD/R may involve the inhibition of activation of TLR4 and MyD88 in BV2 microglia, and the blockage of NF-κB p65 nuclear translocation. MA exhibited a significant neuroprotective effect against I/R injury in both in vivo and in vitro experiments by attenuating microglia-mediated neuroinflammation via inhibition of the TLR4/MyD88/NF-κB signaling pathway.Copyright © 2017 Elsevier B.V. All rights reserved.

Methylmalonic acidemia can be secondary to a deficiency of methylmalonyl CoA mutase or to a defect of cobalamin metabolism that is classified by complementation group. We report on a new patient with cblF complementation group that is associated with an elevation of both methylmalonic acid and homocysteine, and her outcome in response to routine therapy and a dietary restriction.

The cerebral computed tomographic findings in two infants with methylmalonic acidemia and one infant and one adult with propionic acidemia are presented. Pertinent metabolic, clinical, and pathologic features of these genetic disorders of vitamin B12 (cobalamin) and biotin metabolism are reviewed briefly. Computed tomographic abnormalities consist of focal or diffuse deep cerebral hemisphere lucencies and diffuse loss of brain substance. These findings correlated well with the clinical and pathologic findings. The leukoencephalopathy in these uncommon autosomal recessive conditions appears to be due to ketoacidosis, which in some cases may be managed by vitamin supplementation.

A comprehensive literature search was performed to collate evidence of mitochondrial dysfunction in autism spectrum disorders (ASDs) with two primary objectives. First, features of mitochondrial dysfunction in the general population of children with ASD were identified. Second, characteristics of mitochondrial dysfunction in children with ASD and concomitant mitochondrial disease (MD) were compared with published literature of two general populations: ASD children without MD, and non-ASD children with MD. The prevalence of MD in the general population of ASD was 5.0% (95% confidence interval 3.2, 6.9%), much higher than found in the general population (≈ 0.01%). The prevalence of abnormal biomarker values of mitochondrial dysfunction was high in ASD, much higher than the prevalence of MD. Variances and mean values of many mitochondrial biomarkers (lactate, pyruvate, carnitine and ubiquinone) were significantly different between ASD and controls. Some markers correlated with ASD severity. Neuroimaging, in vitro and post-mortem brain studies were consistent with an elevated prevalence of mitochondrial dysfunction in ASD. Taken together, these findings suggest children with ASD have a spectrum of mitochondrial dysfunction of differing severity. Eighteen publications representing a total of 112 children with ASD and MD (ASD/MD) were identified. The prevalence of developmental regression (52%), seizures (41%), motor delay (51%), gastrointestinal abnormalities (74%), female gender (39%), and elevated lactate (78%) and pyruvate (45%) was significantly higher in ASD/MD compared with the general ASD population. The prevalence of many of these abnormalities was similar to the general population of children with MD, suggesting that ASD/MD represents a distinct subgroup of children with MD. Most ASD/MD cases (79%) were not associated with genetic abnormalities, raising the possibility of secondary mitochondrial dysfunction. Treatment studies for ASD/MD were limited, although improvements were noted in some studies with carnitine, co-enzyme Q10 and B-vitamins. Many studies suffered from limitations, including small sample sizes, referral or publication biases, and variability in protocols for selecting children for MD workup, collecting mitochondrial biomarkers and defining MD. Overall, this evidence supports the notion that mitochondrial dysfunction is associated with ASD. Additional studies are needed to further define the role of mitochondrial dysfunction in ASD.

Organic acidurias represent a group of inherited disorders resulting from deficient activity of specific enzymes of the catabolism of amino acids, carbohydrates or lipids, leading to tissue accumulation of one or more carboxylic (organic) acids. Patients affected by organic acidurias predominantly present neurological symptoms and structural brain abnormalities, of which the aetiopathogenesis is poorly understood. However, in recent years increasing evidence has emerged suggesting that oxidative stress is possibly involved in the pathology of some organic acidurias and other inborn errors of metabolism. This review addresses some of the recent developments obtained mainly from animal studies indicating oxidative damage as an important determinant of the neuropathophysiology of some organic acidurias. Recent data showing that various organic acids are capable of inducing free radical generation and decreasing brain antioxidant defences is presented. The discussion focuses on the relatively low antioxidant defences of the brain and the vulnerability of this tissue to reactive species. This offers new perspectives for potential therapeutic strategies for these disorders, which may include the early use of appropriate antioxidants as a novel adjuvant therapy, besides the usual treatment based on removing toxic compounds and using special diets and pharmacological agents, such as cofactors and L-carnitine.

Lipid and immune pathways are crucial in the pathophysiology of metabolic and cardiovascular disease. Arachidonic acid (AA) and its derivatives link nutrient metabolism to immunity and inflammation, thus holding a key role in the emergence and progression of frequent diseases such as obesity, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease. We herein present a synopsis of AA metabolism in human health, tissue homeostasis, and immunity, and explore the role of the AA metabolome in diverse pathophysiological conditions and diseases.

Systemic administration of 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP) produces parkinsonism in experimental animals by a mechanism involving impaired energy production. MPTP is converted by monoamine oxidase B to 1-methyl-4-phenylpyridinium (MPP+), which blocks complex I of the electron transport chain. Oral supplementation with creatine or cyclocreatine, which are substrates for creatine kinase, may increase phosphocreatine (PCr) or cyclophosphocreatine (PCCr) and buffer against ATP depletion and thereby exert neuroprotective effects. In the present study we found that oral supplementation with either creatine or cyclocreatine produced significant protection against MPTP-induced dopamine depletions in mice. Creatine protected against MPTP-induced loss of Nissl and tyrosine hydroxylase immunostained neurons in the substantia nigra. Creatine and cyclocreatine had no effects on the conversion of MPTP to MPP+ in vivo. These results further implicate metabolic dysfunction in MPTP neurotoxicity and suggest a novel therapeutic approach, which may have applicability for Parkinson's disease.Copyright 1999 Academic Press.

Membrane biology seeks to understand how lipids and proteins within bilayers assemble into large structures such as organelles and the plasma membranes. Historically, lipids were thought to merely provide structural support for bilayer formation and membrane protein function. Research has now revealed that phospholipid metabolism regulates nearly all cellular processes. Sophisticated techniques helped identify >10,000 lipid species suggesting that lipids support many biological processes. Here, we highlight the synthesis of the most abundant glycerophospholipid classes and their distribution in organelles. We review vesicular and nonvesicular transport pathways shuttling lipids between organelles and discuss lipid regulators of membrane trafficking and second messengers in eukaryotic cells.© 2018 by The American Society for Biochemistry and Molecular Biology, Inc.

Arachidonic acid (AA)-derived eicosanoids belong to a complex family of lipid mediators that regulate a wide variety of physiological responses and pathological processes. They are produced by various cell types through distinct enzymatic pathways and act on target cells via specific G-protein-coupled receptors. Although originally recognized for their capacity to elicit biological responses such as vascular homeostasis, protection of the gastric mucosa and platelet aggregation, eicosanoids are now understood to regulate immunopathological processes ranging from inflammatory responses to chronic tissue remodelling, cancer, asthma, rheumatoid arthritis and autoimmune disorders. Here, we review the major properties of eicosanoids and their expanding roles in biology and medicine.

Grass carp (Ctenopharyngodon idellus) is an important aquaculture species in China that is affected by serious diseases, especially hemorrhagic disease caused by grass carp reovirus (GCRV). Grass carp have previously shown age-dependent susceptibility to GCRV, however, the mechanism by which this occurs remains poorly understood. Therefore, we performed transcriptome and metabolome sequencing on five-month-old (FMO) and three-year-old (TYO) grass carp to identify the potential mechanism. Viral challenge experiments showed that FMO fish were susceptible, whereas TYO fish were resistant to GCRV. RNA-seq showed that the genes involved in immune response, antigen presentation, and phagocytosis were significantly upregulated in TYO fish before the GCRV infection and at the early stage of infection. Metabolome sequencing showed that most metabolites were upregulated in TYO fish and downregulated in FMO fish after virus infection. Intragroup analysis showed that arachidonic acid metabolism was the most significantly upregulated pathway in TYO fish, whereas choline metabolism in cancer and glycerophospholispid metabolism were significantly downregulated in FMO fish after virus infection. Intergroup comparison revealed that metabolites from carbohydrate, amino acid, glycerophospholipid, and nucleotide metabolism were upregulated in TYO fish when compared with FMO fish. Moreover, the significantly differentially expressed metabolites showed antiviral effects both in vivo and in vitro. Based on these results, we concluded that the immune system and host biosynthesis and metabolism, can explain the age-dependent viral susceptibility in grass carp.

Ethylbenzene is classified as a priority pollutant; however, toxicity data, especially those regarding sublethal toxicity, are rarely reported on gastropods. The present work was performed to elucidate the sublethal effects of ethylbenzene using a freshwater snail, Bellamya aeruginosa (Reeve), exposed to ethylbenzene for 21 days followed by a 17-day recovery period. Superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), reduced glutathione (GSH), and malonyldialdehyde (MDA) were used as biomarkers to evaluate oxidative stress in hepatopancreas of snails. In addition, alkaline comet assay was applied to determine the genotoxicity of ethylbenzene in hepatopancreas of snails. These biomarkers and DNA damage exhibited various responses to ethylbenzene in the tested snails. SOD and CAT activities were almost significantly stimulated during the exposure period. As exposure time was prolonged beyond 7 days, CAT activity gradually became significantly increased at higher doses of ethylbenzene. GSH concentration was positively and linearly related with exposure dose. MDA concentration was significantly greater than that in the control only under the lowest treatment after a 7-day exposure. Alkaline comet assay showed that ethylbenzene could significantly induce DNA damage in hepatopancreas of snails, and there was a good dose- and time-response in DNA damage, indicating potential genotoxicity of ethylbenzene on snails. At the end of the recovery period, the repair of DNA damage was not yet completed, showing that DNA repair requires more time. The findings from this study could indicate that SOD, GST, and GSH seem to be effective oxidative biomarkers for snails exposed to ethylbenzene in the short term. CAT proved to be a valuable discriminating biomarker in subchronic exposure to ethylbenzene, but MDA was not a suitable oxidative biomarker for exposure to ethylbenzene in either the short or long term. Alkaline comet assay was efficient tool with which to evaluate the potential genotoxicity of ethylbenzene.

Diet greatly influences gene expression and physiology. In mammals, elucidating the effects and mechanisms of individual nutrients is challenging due to the complexity of both the animal and its diet. Here, we used an interspecies systems biology approach with Caenorhabditis elegans and two of its bacterial diets, Escherichia coli and Comamonas aquatica, to identify metabolites that affect the animal's gene expression and physiology. We identify vitamin B12 as the major dilutable metabolite provided by Comamonas aq. that regulates gene expression, accelerates development, and reduces fertility but does not affect lifespan. We find that vitamin B12 has a dual role in the animal: it affects development and fertility via the methionine/S-Adenosylmethionine (SAM) cycle and breaks down the short-chain fatty acid propionic acid, preventing its toxic buildup. Our interspecies systems biology approach provides a paradigm for understanding complex interactions between diet and physiology.Copyright © 2014 Elsevier Inc. All rights reserved.