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In a context of global changes, a foresight study is helpful to look into the future, anticipate possible scenarios and take appropriate decisions to face emerging risks for food and feed safety. Considering that an increased use of the ocean is expected for the next decades, it is essential to explore its possible impact on the safety of food and feed from the oceans. A scoping study was carried out to analyse drivers of change that may impact/promote the future uses of the ocean and its resources. From bibliographic search, different ocean uses were identified: coastal and open‐sea mining, marine aquaculture, sea transport and trade, energy production and related infrastructures, fisheries, ocean crops, saline farming, desalination, extraction of bioresources, marine protected areas and conservation of the ocean. Through the information gathered in the scoping study and the input of several experts, three key ocean uses were prioritised to proceed to a participatory foresight exercise: (i) coastal and open‐sea mining; (ii) marine aquaculture; and (iii) sea transport and trade. The foresight exercise produced three possible scenarios for 2050 for each prioritised use of the ocean. On the basis of these scenarios, possible implications and potential emerging issues for the safety of food and feed from the oceans were identified and characterised through bibliographic data. This document also provides a description of the methodology followed in the scoping study and in the foresight exercise, and recommendations that could help EFSA to prepare to the challenges posed by the future exploitation of ocean resources. [ABSTRACT FROM AUTHOR]

Telangiectatic osteosarcoma is a rare variant of osteosarcoma histologically and clinically similar to hemangiosarcoma (HSA). This case series describes the imaging and cytologic features of four histologically confirmed telangiectatic osteosarcomas, including the use of cytochemical stains. Alkaline phosphatase (ALP) was applied to Wright–Giemsa‐stained cytology slides, and Factor VIII immunohistochemistry was evaluated. Cytologic characteristics included atypical mesenchymal cells with evidence of acute and chronic hemorrhage. Telangiectatic osteosarcoma cases had positive ALP cytochemical staining, while control HSA cases were negative. Factor VIII immunohistochemistry was negative in telangiectatic osteosarcoma and positive in HSA. Cytologic diagnosis of telangiectatic osteosarcoma with positive ALP cytochemical staining can help differentiate this neoplasm from HSA. [ABSTRACT FROM AUTHOR]

A 13‐year‐old, male neutered domestic short‐haired cat was diagnosed with multiple biliary duct hamartomas after liver lobectomy for a suspected malignant hepatic mass. Distinguishing ultrasonographic findings included a lobular, mostly well‐defined, heterogeneous, predominantly hyperechoic, left hepatic mass. Computed tomography (CT) confirmed the presence of a lobular, well‐defined, fluid to soft tissue attenuating, heterogeneously hypoenhancing left divisional hepatic mass. Grossly, a large left sided multilobular pale pink gelatinous hepatic mass was surgically excised. Histopathologically, the mass was composed of irregular cystic spaces lined by cuboidal epithelium and separated by mature regular fibrous tissue. Three months following surgery there was no evidence of recurrence or progression of disease on repeat abdominal ultrasound (AUS). [ABSTRACT FROM AUTHOR]

Summary: Fish consumption is an important part of a healthy and sustainable diet. However, smoked fish can provide significant amounts of salt (NaCl), which is inadequate considering that the reduction of its intake is a priority for public health authorities worldwide. The aim of this study was to develop smoked rainbow trout with reduced NaCl content without compromising its quality and safety. In Experiment I, optimal salting parameters (2% NaCl and 4 h) were selected. In Experiment II, different combinations of NaCl, KCl (with and without bitterness masking agent), or microencapsulated spices and aromatic plants were evaluated. In general, products prepared with different formulations showed similar microbiological and physicochemical characteristics. Nevertheless, the most desirable ratio of sodium/potassium and sensory scores was attributed to the formulations prepared with 50% NaCl + 50% KCl (with and without bitterness masking agent). [ABSTRACT FROM AUTHOR]

BACKGROUND Natural products are currently in the spotlight due to the increasing awareness of consumers. Among these products is phycocyanin (C‐PC), a blue colorant that can be extracted from cyanobacteria – a poorly explored feedstock – and applied in several fields, due to its argued health benefits. Arthropira (previously called Spirulina) is the major source of C‐PC nowadays, but within the scope of pursuing alternative sources, the cyanobacterium Anabaena cylindrica was used in the present study to extract this colorant. RESULTS: The biological activities of two types of extracts (raw and purified, both in fresh and in lyophilized forms) were analysed. The raw extracts produce better results than their pure counterparts by presenting a higher antioxidant activity and better biocompatibility and antitumor activity. However, when compared to literature records, C‐PC extracts from A. cylindrica produced less impressive results. This leads to a new hypothesis and a simple comparison between the antioxidant activities of C‐PC extracts from different biomass sources. These second‐stage results showed that different cyanobacteria species produced different C‐PC extracts with different antioxidant profiles; these results highlight that, even when the extracts are blue, they may present differential compositions and, therefore, different biological activities. CONCLUSION: This study proves that the direct link often made between biological activities and C‐PC can be speculative, and thus, should be avoided. © 2021 Society of Chemical Industry (SCI). [ABSTRACT FROM AUTHOR]

This study employed NMR metabolomics to characterize macrophage responses to subtoxic concentrations of silver nanoparticles (AgNPs ca. 30 nm) and ionic silver (Ag+), with a view to further elucidate their immunomodulatory activity at the cell metabolism level. Exposure to AgNPs caused RAW 264.7 macrophages to decrease intracellular glucose utilization, possibly due to interference with glycolytic enzymes, and to reprogram the TCA cycle towards anaplerotic fueling and production of anti‐inflammatory metabolites (e.g. itaconate and creatine). Moreover, AgNPs‐exposed cells were able to control the levels of reactive oxygen/nitrogen species (ROS/RNS), likely through upregulation of glutathione synthesis. On the other hand, macrophages exposed to Ag+ at equivalent subtoxic concentrations showed reduced metabolic activity, lower ability to counterbalance ROS/RNS and alterations in membrane‐related lipids. Overall, the metabolomics approach hereby employed provided novel insights into the differential effects of AgNPs and Ag+, which help explain the lower toxic potential of nanosilver than silver ions. [ABSTRACT FROM AUTHOR]

New onset of diabetes is associated with the use of statins. We have recently demonstrated that pravastatin‐treated hypercholesterolemic LDL receptor knockout (LDLr−/−) mice exhibit reductions in insulin secretion and increased islet cell death and oxidative stress. Here, we hypothesized that these diabetogenic effects of pravastatin could be counteracted by treatment with the antioxidant coenzyme Q 10 (CoQ 10), an intermediate generated in the cholesterol synthesis pathway. LDLr −/− mice were treated with pravastatin and/or CoQ 10 for 2 months. Pravastatin treatment resulted in a 75% decrease of liver CoQ 10 content. Dietary CoQ 10 supplementation of pravastatin‐treated mice reversed fasting hyperglycemia, improved glucose tolerance (20%) and insulin sensitivity (>2‐fold), and fully restored islet glucose‐stimulated insulin secretion impaired by pravastatin (40%). Pravastatin had no effect on insulin secretion of wild‐type mice. In vitro, insulin‐secreting INS1E cells cotreated with CoQ 10 were protected from cell death and oxidative stress induced by pravastatin. Simvastatin and atorvastatin were more potent in inducing dose‐dependent INS1E cell death (10–15‐fold), which were also attenuated by CoQ 10 cotreatment. Together, these results demonstrate that statins impair β‐cell redox balance, function and viability. However, CoQ 10 supplementation can protect the statins detrimental effects on the endocrine pancreas. Statins impair β‐cell redox balance, function, and viability. CoQ10 supplementation can protect the statins detrimental effects on the endocrine pancreas. [ABSTRACT FROM AUTHOR]

Occupational environments are major exposure routes to Cr(VI). However, Cr(VI) may also establish in bone tissues by ingestion or through Cr containing orthopaedic prostheses that, due to wear and corrosion, may release metal particles and ions potentially affecting bone tissue. The aim of this work was to evaluate the effects of clinically relevant concentrations of Cr(VI) in human osteoblasts, by integrating genotoxic effects, evaluated by the comet assay and cytokinesis‐blocked micronucleus assay (scoring the presence of micronucleus, nucleoplasmic bridges and nuclear division index), with the effects on cell cycle and cell viability. Human osteoblasts MG‐63 were in vitro exposed to Cr(VI) at concentrations ranging from 0.1 to 5 μm, for 24 and 48 hours. Results pointed out to a decrease of cell viability for both time exposures in a time‐ and dose‐dependent manner, which was related to cell cycle arrest and DNA damage. Chromosome abnormalities were also observed. Hence, these data suggest that cells arrested in the cell division with DNA damage may have followed cell death pathways, while some surviving ones still revealed DNA damage at chromosome level indicating abnormal cell division progression. In conclusion, Cr(VI) induced cytotoxic and genotoxic effects in human bone cells at concentrations that could be found in patients with metal‐on‐metal prostheses. In addition, the early onset of genotoxic damage induced by Cr(VI) at low concentrations after 24 hours of cell exposure alert to the relevance of periodic monitoring of patients for genotoxicity diagnosis after implantation of prostheses before clinical symptoms appear. Cr containing orthopaedic prostheses may, due to wear and corrosion, release metal particles and ions that may affect bone tissue formation. In this study, the effects of clinically relevant concentrations of Cr(VI) in human osteoblasts were assessed by integrating genotoxic endpoints with the effects on cell cycle and cell viability. The results pointed to a decrease on cell viability, cell cycle arrest and DNA damage with chromosome breakage/loss by Cr(VI) at low concentrations 24 hours after exposure. [ABSTRACT FROM AUTHOR]

Our previous studies show that cafeteria diet increases body adiposity, plasma insulin levels, and sympathetic activity to brown adipose tissue (BAT) and white adipose tissue (WAT) of Wistar rats, leading to rapid and progressive changes in the metabolic profile. The identification of suitable reference genes that are not affected by the experimental conditions is a critical step in accurate normalization of the reverse transcription quantitative real‐time PCR (qRT‐PCR), a commonly used assay to elucidate changes in the gene expression profile. In the present study, the effects of the cafeteria diet and sympathetic innervation on the gene expression of adrenoceptor beta 3 (Adrb3) from BAT and WAT were assessed using one of the most stable and one of the least stable genes as normalizers. Rats were fed the cafeteria diet and on the 17th day, interscapular BAT or retroperitoneal WAT was denervated and, 7 days after surgery, the contralateral innervated tissue was used as control. Ten reference genes were evaluated (18S, B2m, Actb, CypA, Gapdh, Hprt1, Rpl32, Tbp, Ubc, and Ywhaz) and ranked according to their stability using the following algorithms: geNorm, NormFinder, BestKeeper, and comparative delta threshold cycle (ΔCt) method. According to the algorithms employed, the normalization of Adrb3 expression by the least stable genes produced opposite results compared with the most stable genes and literature data. In cafeteria and control diet‐fed rats, the three most stable genes were Hprt1, Tbp, and Rpl32 for interscapular BAT and Tbp, B2m, and Hprt1 for retroperitoneal WAT, while the least stable genes were 18S, Actb, and Gapdh for both tissues. [ABSTRACT FROM AUTHOR]

Olive anthracnose causes fruit rot leading to its drop or mummification, resulting in yield losses and the degradation of oil quality. Taxonomy and distribution: The disease is caused by diverse species of Colletotrichum, mostly clustering in the C. acutatum species complex. Colletotrichum nymphaeae and C. godetiae are the prevalent species in the Northern Hemisphere, whereas C. acutatum sensu stricto is the most frequent species in the Southern Hemisphere, although it is recently and quickly emerging in the Northern Hemisphere. The disease has been reported from all continents, but it attains higher incidence and severity in the west of the Mediterranean Basin, where it is endemic in traditional orchards of susceptible cultivars. Life cycle: The pathogens are able to survive on vegetative organs. On the fruit surface, infections remain quiescent until fruit maturity, when typical anthracnose symptoms develop. Under severe epidemics, defoliation and death of branches can also occur. Pathogen species differ in virulence, although this depends on the cultivar. Control: The selection of resistant cultivars depends strongly on pathogen diversity and environmental conditions, posing added difficulties to breeding efforts. Chemical disease control is normally achieved with copper-based fungicides, although this may be insufficient under highly favourable disease conditions and causes concern because of the presence of fungicide residues in the oil. In areas in which the incidence is high, farmers tend to anticipate harvest, with consequences in yield and oil characteristics. Challenges: Olive production systems, harvest and postharvest processing have experienced profound changes in recent years, namely new training systems using specific cultivars, new harvest and processing techniques and new organoleptic market requests. Changes are also occurring in both the geographical distribution of pathogen populations and the taxonomic framework. In addition, stricter rules concerning pesticide use are likely to have a strong impact on control strategies. A detailed knowledge of pathogen diversity, population dynamics and host-pathogen interactions is basal for the deployment of durable and effective disease control strategies, whether based on resistance breeding, agronomic practices or biological or chemical control. [ABSTRACT FROM AUTHOR]

This commentary introduces the subject, the context and the history of the Brazilian annually held meeting on Mitochondrial Research by the occasion of its 10th anniversary. Mitomeetings gather people interested in all aspects of mitochondrial biology in diverse species, including protists, animals, plants, and fungi. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are major causes of death worldwide. Beyond the classical cholesterol risk factor, other conditions such as oxidative stress are well documented to promote atherosclerosis. The Mangifera indica L. extract (Vimang1) was reported to present antioxidant and hypocholesterolemic properties. Thus, here we evaluate the effects of Vimang treatment on risk factors of the atherosclerosis prone model of familial hypercholesterolemia, the LDL receptor knockout mice. Mice were treated with Vimang during 2 weeks and were fed a cholesterol-enriched diet during the second week. The Vimang treated mice presented significantly reduced levels of plasma (15%) and liver (20%) cholesterol, increased plasma total antioxidant capacity (10%) and decreased reactive oxygen species (ROS) production by spleen mononuclear cells (50%), P<0.05 for all. In spite of these benefits, the average size of aortic atherosclerotic lesions stablished in this short experimental period did not change significantly in Vimang treated mice. Therefore, in this study we demonstrated that Vimang has protective effects on systemic and tissue-specific risk factors, but it is not sufficient to promote a reduction in the initial steps of atherosclerosis development. In addition, we disclosed a new antioxidant target of Vimang, the spleen mononuclear cells that might be relevant for more advanced stages of atherosclerosis. [ABSTRACT FROM AUTHOR]

Mitochondrial redox imbalance and high Ca2+ uptake induce the opening of the permeability transition pore (PTP) that leads to disruption of energy-linked mitochondrial functions and triggers cell death in many disease states. In this review, we discuss the major results from our studies investigating the consequences of NAD(P)-transhydrogenase (NNT) deficiency, and of statins treatment for mitochondrial functions and susceptibility to Ca2+-induced PTP. We highlight the aggravation of high fat diet-induced fatty liver disease in the context of NNT deficiency and the role of antioxidants in the prevention of statins toxicity to mitochondria. [ABSTRACT FROM AUTHOR]

Chromium (Cr) contamination in arable soils and irrigating water remains a priority, particularly due to the challenges posed to crop production and food safety. Long-term Cr(VI) effects remain less addressed than short-term ones, particularly regarding organ-specific genotoxic profiles. Here we used the crop Lactuca sativa growing in a protected horticultural system and irrigated for 21 days with Cr(VI) (up to 200 mg/L). Besides the oxidative stress, the genotoxicity was evaluated. Shoots and roots showed distinctive oxidative stress status and genotoxic effects, in a dose-dependent manner. While 50 mg/L stimulated antioxidant activities and no major genotoxic effects were found, plants exposed to ≥150 showed an increase of oxidative disorders, together with cytostatic and DNA damage effects, and some mitotic impairment. Leaves showed less oxidative signs at 50 mg/L, while at 150/200 mg/L the antioxidant battery was stimulated. In Cr treated plants, the highest dose increased the DNA damage, reinforcing the idea that DNA breaks were related to mitotic disorders in higher doses. In conclusion, long-term exposure data show a highly responsive root, with a quadratic response meaning higher defenses at lower Cr doses, and higher oxidative and DNA damage and cytostatic effect at a higher dose. [ABSTRACT FROM AUTHOR]

Regular exercise and anabolic androgenic steroids have opposing effects on the plasma lipoprotein profile and risk of cardio-metabolic diseases in humans. Studies in humans and animal models show conflicting results. Here, we used a mice model genetically modified to mimic human lipoprotein profile and metabolism. They under-express the endogenous LDL receptor gene (R1) and express a human transgene encoding the cholesteryl ester transfer protein (CETP), normally absent in mice. The present study was designed to evaluate the independent and interactive effects of testosterone supplementation, exercise training and CETP expression on the plasma lipoprotein profile and CETP activity. CETP/R1 and R1 mice were submitted to a 6-week swimming training and mesterolone (MEST) supplementation in the last 3 weeks. MEST treatment increased markedly LDL levels (40%) in sedentary CETP/R1 mice and reduced HDL levels in exercised R1 mice (18%). A multifactorial ANOVA revealed the independent effects of each factor, as follows. CETP expression reduced HDL (21%) and increased non-HDL (15%) fractions. MEST treatment increased the VLDL concentrations (42%) regardless of other interventions. Exercise training reduced triacylglycerol (25%) and free fatty acids (20%), increased both LDL and HDL (25-33%), and reduced CETP (19%) plasma levels. Significant factor interactions showed that the increase in HDL induced by exercise is explained by reducing CETP activity and that MEST blunted the exercise-induced elevation of HDL-cholesterol. These results reinforce the positive metabolic effects of exercise, resolved a controversy about CETP response to exercise and evidenced MEST potency to counteract specific exercise benefits. [ABSTRACT FROM AUTHOR]

BACKGROUND: The aim of this studywas to analyse the influence of desalting temperature, fish thickness and desalting time on themass transfer kinetics during the cod desalting process by physico-chemical analyses. RESULTS: Both water uptake and salt loss increased with increasing temperature (15 °C>10 °C>5 °C) up to 24h in 'thicker' pieces. The equilibrium achievementwas faster in 'thinner' pieces and alsowith increasing temperature. Longer desalting times at 10 °C can be a good practice to be used during cod desalting at an industrial scale in order to obtain commercial products with higher yields. The fastermass transfer during desalting of 'thinner' pieces appears to followthree periods as a result of diffusion of the components (water, NaCl, and soluble proteins) because of the concentration differences, and pressure gradients due to expansion/shrinkage of the proteinmatrix, which is dependent on theNaCl content. The refractive index can be used by industry as an indirect measurement to determine themoment at which the 'thicker' samples are near the ZNaCl = YNaCl equilibrium. CONCLUSION: Optimum combinations between the process variables analysed are essential in order to speed up the mass transfer kinetics during cod desalting at an industrial scale. [ABSTRACT FROM AUTHOR]

Abstract: Plasmonic nanostructures concentrate light and heat within a small volume at the nanoscale, offering potential applications in nanotechnology and biomedicine (e.g., hyperthermia). However, the precise quantification of the actual temperature rise in the vicinity of such nanosystems poses considerable challenges. Here, we present a new heater–thermometer nanoplatform capable of measuring the plasmon‐induced local temperature increase of Au nanorods via the ratiometric upconversion of (Gd,Yb,Er)2O3 nanothermometers upon 980 nm laser excitation (up to 102.0 W cm−2). The local temperature rise, 302–548 K (maximum temperature sensitivity 1.22 % K−1, uncertainty 0.32 K and repeatability >99 %), is assessed using Boltzmann's distribution of the Er3+ 2H11/2→4I15/2/ 4S3/2→4I15/2 intensity ratio. The nanoplatforms are biocompatible with MG‐63 and A549 cells and were mapped within the former using hyperspectral imaging, opening up an avenue to monitor the cellular uptake of Ln3+‐based nanoplatforms. [ABSTRACT FROM AUTHOR]

BACKGROUND To advise consumers and manufacturers regarding decreasing the time needed to desalt salted cod (a time-consuming process), there is a need to develop knowledge about quality changes at different desalting temperatures. The objective of this work was to evaluate the physico-chemical, microbiological and sensory quality changes and their causes during cod desalting at 5, 10 and 15 °C, using a cod/water ratio of 1:9 without water changes. The influence of slices with different thickness and different desalting times was also evaluated. RESULTS Desalting promoted a decrease in the levels of total volatile basic nitrogen, thiobarbituric acid reactive substances and free amino acids nitrogen ( FAA-N). The highest FAA-N values were found in 'thicker' samples desalted at 15 °C due to the higher proteolytic bacteria number observed in these samples, which activity compensated the leaching of soluble components to the desalting solution. The water uptake and the salt leaching out of the muscle found during the processes created conditions for the bacterial growth, contributing to the spoilage at 15 °C. Based on fresh odour and 'off'-flavours results, 'thicker' samples desalted at 15 °C after 72 h were close to spoilage and on microbial levels were spoiled. CONCLUSION In order to extend the shelf life and safety of cod desalted products, desalting at temperatures above 10 °C is not advisable. © 2014 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

This review focuses on the photoprotection conferred by lycopene, one of the most potent anti-oxidants. Lycopene has been recently proposed to play a critical role on anticarcinogenic action at different levels. The photoprotective properties of lycopene remain contradictory. Some studies point out a positive and others a negative effect in both in vitro and in vivo models. Currently, researchers recognise that crucial gaps exist in understanding the role of carotenoids as effective modulators of apoptosis, cell cycle dynamics and/or of their in vivo behaviour as cellular anti-oxidants. The development of novel therapeutic strategies for skin disorders depends on our understanding of the molecular mechanism of UV damage on skin cells. The use of several effective phytocompounds, including lycopene, working through preventive and/or corrective pathways in the cell, may be an approach for reducing UV-B-generated damage. [ABSTRACT FROM AUTHOR]

In this study, we investigated the effect of low density lipoprotein receptor (LDLr) deficiency on gap junctional connexin 36 (Cx36) islet content and on the functional and growth response of pancreatic beta-cells in C57 BL/6 mice fed a high-fat ( HF) diet. After 60 days on regular or HF diet, the metabolic state and morphometric islet parameters of wild-type ( WT) and LDLr−/− mice were assessed. HF diet-fed WT animals became obese and hypercholesterolaemic as well as hyperglycaemic, hyperinsulinaemic, glucose intolerant and insulin resistant, characterizing them as prediabetic. Also they showed a significant decrease in beta-cell secretory response to glucose. Overall, LDLr−/− mice displayed greater susceptibility to HF diet as judged by their marked cholesterolaemia, intolerance to glucose and pronounced decrease in glucose-stimulated insulin secretion. HF diet induced similarly in WT and LDLr−/− mice, a significant decrease in Cx36 beta-cell content as revealed by immunoblotting. Prediabetic WT mice displayed marked increase in beta-cell mass mainly due to beta-cell hypertrophy/replication. Nevertheless, HF diet-fed LDLr−/− mice showed no significant changes in beta-cell mass, but lower islet-duct association (neogenesis) and higher beta-cell apoptosis index were seen as compared to controls. The higher metabolic susceptibility to HF diet of LDLr−/− mice may be explained by a deficiency in insulin secretory response to glucose associated with lack of compensatory beta-cell expansion. [ABSTRACT FROM AUTHOR]

The main objective of this review is to summarize the present state of knowledge of different ways of processing cod, giving emphasis to salting, drying, and desalting steps. As an introduction, a description of the main characteristics of the Gadidae family and cod species, the general chemical composition of fresh cod, and a reference to farmed cod is included. Statistics on world fishery and aquaculture cod production are also reviewed. It is expected that this review will contribute to build a current picture of the technical and scientific knowledge on the cod processing situation, helping to move forward and to support future developments in this important seafood industry. [ABSTRACT FROM AUTHOR]

Congenitally analbuminaemic individuals and rats (NARs) exhibit several metabolic abnormalities, including hypertriglyceridaemia and plasma free fatty acid deficiency. Our aim was to study glucose homeostasis and insulin secretion in NARs. Plasma concentrations of lipids, glucose and insulin and secretion of insulin from the pancreatic islets were measured in female NARs and control animals (Sprague-Dawley rats; SDRs). Glucose homeostasis tests were also performed. Plasma glucose levels were similar between NARs and SDRs, irrespective of feeding status. However, fed insulinaemia was ∼37% higher ( P≤ 0.05) in NARs than in SDRs. The NARs displayed a markedly increased glucose tolerance, i.e. the integrated glycaemic response was one-third that of the control animals. Enhanced glucose tolerance was associated with threefold higher insulinaemia at peak glycaemia after a glucose load than in the control animals. Similar peripheral insulin sensitivity was observed between groups. Isolated pancreatic islets from NARs secreted significantly more insulin than islets from SDRs in response to a wide range of glucose concentrations (2.8-33.3 m m). Despite having similar liver glycogen contents in the fully fed state, NARs had ∼40% ( P≤ 0.05) lower glycogen contents than SDRs after 6 h fasting. The injection of a gluconeogenic substrate, pyruvate, elicited a faster rise in glycaemia in NARs compared with SDRs. Overall , NARs displayed enhanced glucose tolerance, insulin secretion and gluconeogenic flux. The higher glucose tolerance in NARs compared with SDRs is attributed to enhanced islet responsiveness to secretagogues, while peripheral insulin sensitivity seems not to be involved in this alteration. We propose that the enhanced glucose metabolism is a chronic compensatory adaptation to decreased free fatty acid availability in NARs. [ABSTRACT FROM AUTHOR]

In the past decades the increased use of chromium (Cr) in several anthropogenic activities and consequent contamination of soil and water have become an increasing concern. Cr exists in several oxidation states but the most stable and common forms are Cr(0), Cr(III) and Cr(VI) species. Cr toxicity in plants depends on its valence state. Cr(VI) as being highly mobile is toxic, while Cr(III) as less mobile is less toxic. Cr is taken up by plants through carriers of essential ions such as sulphate. Cr uptake, translocation, and accumulation depend on its speciation, which also conditions its toxicity to plants. Symptoms of Cr toxicity in plants are diverse and include decrease of seed germination, reduction of growth, decrease of yield, inhibition of enzymatic activities, impairment of photosynthesis, nutrient and oxidative imbalances, and mutagenesis. [ABSTRACT FROM AUTHOR]

Cholesteryl ester transfer protein (CETP) exerts a profound impact on high-density lipoprotein (HDL) metabolism and, consequently, on the risk of atherosclerosis development and cardiovascular mortality. Here, we review the complex relationship between CETP and atherosclerosis based upon the experimental, clinical, and epidemiological studies. In addition, we discuss the recent findings that expand the functions of CETP to new areas of interest such as Alzheimer's disease, inflammation, and obesity. © 2011 IUBMB IUBMB Life, 63(4): 272-276, 2011 [ABSTRACT FROM AUTHOR]

This work investigated the effects of butylscopolamine bromide, a drug present in the pharmaceutical formulation Buscopan®, on the development of Chrysomya megacephala, a blow fly species of considerable forensic and medical importance in Brazil. Larvae exposed to the drug showed a decreased rate of development, with higher drug concentrations further retarding the development. Besides, larvae reared on the presence of the drug showed smaller body weight and body length when compared with larvae reared on the absence of Buscopan®. The drug also affected the mortality of the species. [ABSTRACT FROM AUTHOR]

Abuse of anabolic–androgenic steroids (AAS) for improving physical performance is associated with serious, sometimes fatal, adverse effects. The aim of the present work was to investigate the effects of AAS on the cardiac structure and the plasma lipoprotein profile isolated and in combination with exercise. Transgenic mice with a human lipaemic phenotype (expressing cholesteryl ester transfer protein on the LDL receptor knockout background) were used in this study. Sedentary and exercised mice (treadmill running, five times per week for 6 weeks) were treated with mesterolone (2 μg/g body weight) or vehicle (control-C) in the last 3 weeks. Four groups were compared: (i) exercise + mesterolone (Ex-M), (ii) exercise + vehicle (Ex-C), (iii) sedentary + mesterolone (Sed-M) and (iv) sedentary + vehicle (Sed-C). Arterial blood pressure and body mass increased in all groups along time, but Sed-M reached the highest values and Ex-C the lowest. Treatment with mesterolone increased total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-c) and very LDL-c (VLDL-c) plasma levels. However, exercise blunted some of these deleterious effects by increasing high-density lipoprotein cholesterol and decreasing LDL-c, VLDL-c and triglycerides. Exercise training induced beneficial effects, such as physiological cardiomyocyte hypertrophy, increase in myocardial circulation and decrease in cardiac interstitium. However, mesterolone impaired such physiological gains and in addition increased troponin T plasma levels both in sedentary and exercised mice. Thus, while mesterolone induced pro-atherogenic lipoprotein profile and pathogenic cardiac hypertrophy, exercise counteracted these effects and modified favourably both the lipoprotein profile and the cardiac remodelling induced by mesterolone. [ABSTRACT FROM AUTHOR]

Changes in mitochondrial function are intimately associated with metabolic diseases. Here, we review recent evidence relating alterations in mitochondrial energy metabolism, ion transport and redox state in hypercholesterolemia and hypertriglyceridemia. We focus mainly on changes in mitochondrial respiration, K+ and Ca2+ transport, reactive oxygen species generation and susceptibility to mitochondrial permeability transition. IUBMB Life, 59: 263-268, 2007 [ABSTRACT FROM AUTHOR]

1. The hepatic mechanisms involved in the simultaneous regulation of plasma cholesterol concentration and cholesteryl ester transfer protein (CETP) activity were investigated by sharply modifying the hepatic rates of cholesterol synthesis. This was accomplished by cholestyramine, lovastatin and cholesterol feeding in human CETP transgenic mice cross-bred with low-density lipoprotein receptor (LDLr)-knockout mice, generating CETP+/–/LDLr+/– mice, which present a plasma lipoprotein profile resembling that of humans. 2. Analyses of pooled data showed that the plasma CETP activity correlated positively with plasma total cholesterol concentration, hepatic CETP mRNA and the liver microsomal cholesterol content; a negative correlation was found between plasma CETP activity and the liver 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and LDLr mRNA levels. These coordinated events represent an efficient control system that stabilizes the cell cholesterol content. 3. Nonetheless, not all cholesterol metabolism regulatory systems seem to fit into a coherent pattern of responses, suggesting that other unknown cellular mechanisms play roles depending on the type of pharmacological intervention. 4. For example, microsomal cholesterol content was not affected by cholestyramine, but was increased on cholesterol feeding (as predicted), and, surprisingly, on lovastatin treatment. Furthermore, although both plasma cholesterol-lowering drugs increased CYP7A1 mRNA and had no effect on CYP27 mRNA, other metabolic components were differentially modified. Cholestyramine and lovastatin, respectively, did not modify and increased both HMG-CoA and sterol responsive element binding protein 1c mRNA, did not modify and lowered liver X receptor α mRNA, lowered and increased ATP binding cassette A1 mRNA and lowered and did not modify scavenger receptor B1 mRNA. 5. That is, different to unabsorbed cholestyramine, lovastatin, as an absorbed plasma cholesterol-lowering drug, may have modified the activity of other unknown genes that play roles in the interaction of CETP with the metabolism of hepatic cholesterol. [ABSTRACT FROM AUTHOR]

Berti JA, Salerno AG, Bighetti EJB, Casquero AC, Boschero AC, Oliveira HCF. Effects of diabetes and CETP expression on diet-induced atherosclerosis in LDL receptor-deficient mice. APMIS 2005;113:37–44.The role of CETP expression and diabetes in atherogenesis was investigated in mice with heterozygous disruption of the LDL receptor gene (LDLR1). LDLR1 mice with and without CETP expression were treated with streptozotocin (STZ) and maintained on a standard diet for one month before switching to an atherogenic diet for an additional month. STZ-sensitive mice had∼2.5-fold higher glycemia and 7.5- to 8.0-fold higher cholesterolemia. Factorial analysis of variance showed no significant effect of diabetes, CETP or diabetes-CETP interaction on the size of the atherosclerotic lesions. CETP expression in non-diabetic mice resulted in a 50% reduction in the area of the atherosclerotic lesions. Multiple regression analysis showed a positive and independent atherogenic effect of triglyceridemia in LDLR1 mice and of cholesterolemia in diabetic mice. Logistic analysis showed that elevated plasma cholesterol level significantly increased the risk of developing large lesion size (>75th percentile). In conclusion, CETP expression did not alter the lesion formation in response to diabetes, although it may be protective in the euglycemic state; the triglyceride level was an independent risk factor for LDL receptor-deficient mice but not for CETP-expressing mice; and elevated plasma cholesterol levels increased the risk of developing large atherosclerotic lesions, independently of CETP and diabetes. [ABSTRACT FROM AUTHOR]

The mechanism by which ω3 fatty acids lower plasma triacylglycerol levels was investigated. Rats were fed fish oil, olive oil (10% fat by weight) or a nonpurified diet 4% fat by weight) for 15 days. Lipoprotein lipase was inhibited by intra-arterial administration of Triton WR 1339 to estimate hepatic triacylglycerol output. Rats fed the olive oil diet showed a higher rate of triacylglycerol formation than rats fed the ω3 fatty acid diet or the low-fat diet. All three groups showed identical rates of removal from plasma of intraarterially administered artificial chylomicrons that had simultaneously been labeled with cholesteryl [1-C]oleate and [9,10(n)-H]triolein. Liver radioactivity and total fat content were lowest in rats fed the fish oil diet, indicating that ω3 fatty acids were preferentially metabolized in liver. Chylomicrons obtained from donor rats fed either fish oil containg [C]cholesterol or olive oil containing [H]cholesterol were removed at similar rates when infused together intraarterially into recipient animals. A slower formation of plasma very low density lipoprotein triacylglycerols in rats fed fish oil is probably due to a faster rate of oxidation of the fatty acid chains in the liver resulting in decreased plasma triacylglycerol concentrations. [ABSTRACT FROM AUTHOR]

Presents a study which examined the mitochondrial function and production of reactive oxygen species in the atherosclerosis-susceptible, hypercholesterolemic low density lipoprotein (LDL) receptor knockout mice. Results of the isolation of mitochondria from the LDL mice; Oxidizing of pyridine nucleotides in LDL receptor knockout mouse; Secretion and synthesis of triglycerides and cholesterol in the livers of hypercholesterolemic low density lipoprotein (LDL) receptor knockout mice.

An introduction is presented in which the editors discuss various papers within the issue on topics including soil contamination, plant interactions, and valorization of halophyte crops.

1. The hepatic mechanisms involved in the simultaneous regulation of plasma cholesterol concentration and cholesteryl ester transfer protein (CETP) activity were investigated by sharply modifying the hepatic rates of cholesterol synthesis. This was accomplished by cholestyramine, lovastatin and cholesterol feeding in human CETP transgenic mice cross-bred with low-density lipoprotein receptor (LDLr)-knockout mice, generating CETP(+/-)/LDLr(+/-) mice, which present a plasma lipoprotein profile resembling that of humans. 2. Analyses of pooled data showed that the plasma CETP activity correlated positively with plasma total cholesterol concentration, hepatic CETP mRNA and the liver microsomal cholesterol content; a negative correlation was found between plasma CETP activity and the liver 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and LDLr mRNA levels. These coordinated events represent an efficient control system that stabilizes the cell cholesterol content. 3. Nonetheless, not all cholesterol metabolism regulatory systems seem to fit into a coherent pattern of responses, suggesting that other unknown cellular mechanisms play roles depending on the type of pharmacological intervention. 4. For example, microsomal cholesterol content was not affected by cholestyramine, but was increased on cholesterol feeding (as predicted), and, surprisingly, on lovastatin treatment. Furthermore, although both plasma cholesterol-lowering drugs increased CYP7A1 mRNA and had no effect on CYP27 mRNA, other metabolic components were differentially modified. Cholestyramine and lovastatin, respectively, did not modify and increased both HMG-CoA and sterol responsive element binding protein 1c mRNA, did not modify and lowered liver X receptor alpha mRNA, lowered and increased ATP binding cassette A1 mRNA and lowered and did not modify scavenger receptor B1 mRNA. 5. That is, different to unabsorbed cholestyramine, lovastatin, as an absorbed plasma cholesterol-lowering drug, may have modified the activity of other unknown genes that play roles in the interaction of CETP with the metabolism of hepatic cholesterol.