241 research outputs found
Kolmogorov laws for stratified turbulence
International audienceFollowing the Kolmogorov technique, an exact relation for a vector third-order moment J is derived for three-dimensional incompressible stably stratified turbulence under the Boussinesq approximation. In the limit of a small Brunt-Vaisala frequency, isotropy may be assumed which allows us to find a generalized 4/3-law. For strong stratification, we make the ansatz that J is directed along axisymmetric surfaces parameterized by a scaling law relating horizontal and vertical coordinates. An integration of the exact relation under this hypothesis leads to a generalized Kolmogorov law which depends on the intensity of anisotropy parameterized by a single coefficient. By using a scaling relation between large horizontal and vertical length scales we fix this coefficient and propose a unique law
Performance and limitations of linkage-disequilibrium-based methods for inferring the genomic landscape of recombination and detecting hotspots: a simulation study
Novel approach for characterising archaeological textiles exceptionally preserved in a mineralised form based on 2D and 3D synchrotron micro-imaging
Toxicology of mycotoxins, hazards and risks in human and animal food
Mycotoxins are secondary metabolites produced on plants either in the field or during storage. These
toxins are found as natural contaminants on numerous foods and feeds of plant origin, such as cereals,
fruits, nuts, almonds, grains, fodder, as well as processed foods and feeds using these ingredients.
The toxicity of mycotoxins varies, ranging from hepatotoxic or even carcinogenic (aflatoxins) effects,
to estrogenic (zearalenone), immunotoxic (patulin, trichothecenes, fumonisins), nephrotoxic (ochratoxin
A) and neurotoxic (tremorgens) effects. Their toxicity can also be caused by the presence of mycotoxin
residues in products deriving from animals fed with contaminated feedstuffs. The mycotoxic
risk is difficult to evaluate, as mycotoxin are natural contaminants impossible to eliminate, fungal contaminations
are difficult to control, and one mould may produce several toxins. Consequently, further
research is needed to improve current knowledge on the toxicity of these products, particularly when
various mycotoxins are combined, either together or with other toxins or pathogens.Les mycotoxines sont des
produits du métabolisme secondaire de moisissures pouvant se développer sur la plante au
champ ou en cours de stockage. Ces toxines se retrouvent Ă l'Ă©tat de contaminants naturels
de nombreuses denrées d'origine végétale : céréales, fruits, noix, amandes, grains,
fourrages ainsi que d'aliments composés et manufacturés issus de ces filiÚres. La toxicité
des mycotoxines se révÚle lors des mycotoxicoses des animaux d'élevage. Elle est variable,
certaines exerçant un pouvoir hépa-totoxique voire cancérogÚne (aflatoxines), d'autres se
révélant oestrogÚniques (zéaralénone), immunotoxiques (patuline, trichothécÚnes,
fumonisines), néphrotoxiques (ochratoxine A) ou neurotoxiques (trémorgÚnes). Un autre aspect
de leur toxicité est la prise en compte des résidus présents dans les productions issues
d'animaux ayant consommé une alimentation contaminée. L'évaluation du risque mycotoxique
demeure délicate car ce risque est d'essence naturelle, l'homme n'en maßtrisant pas la
survenue ; il est pernicieux car la contamination fongique est difficilement contrĂŽlable et
enfin il peut ĂȘtre multiple en raison de la possible association d'effets de toxines
produites par une mĂȘme moisissure. Devant ce constat, il convient de poursuivre une activitĂ©
de recherche soutenue afin d'améliorer encore nos connaissances sur la toxicité de ces
dérivés et notamment dans les cas d'associations entre mycotoxines ou entre toxines et
agents pathogĂšnes infectieux
MOLEKULARNE INTERAKCIJE MYCOTOXINA SA JETRENIM ENZIMIMA KOJI SUDJELUJU U METABOLIZMU MEDIKAMENATA U GLODAVCA I DOMAÄIH ĆœIVOTINJA
Mycotoxins are well known for underging liver biotransformation in humans and animal species. Metabolites correspond to either oxydative derivatives such as hydroxymetabolites of aflatoxin B1 or ochratoxin A or hydrolytic derivatives in case of trichothecenes. In some cases, highly reactive epoxides represent the first step in the formation of carcinogenic intermediates like exo-epoxides of aflatoxins. Hepatic phase II enzymes including transferases and hydrolases are involved in the conjugation of such oxidative metabolites. In this respect, they are generally considered as detoxifying enzymes: glucuronidation of deacetylated trichothecenes or hydroxy-aflatoxins, or glutathione conjugation of epoxides. The major metabolism of zearalenone consists of reduction leading to estrogenic zearalenols which is characterized by large interspecies differences. Concerning fumonisin
B1, this toxin would be poorly absorbed from the gastrointestinal tract and metabolised into
hydrolytic products with lower toxic effect as apoptotic compounds. Interactions between mycotoxins and liver drug metabolizing are crucial in terms of detoxication or bioactivation of these toxins in the organism of the human or animal consumers. Most of these interactions are consequences of the metabolic processes occurring in the liver. They result generally from the activity of cytochromes P450 and transferases. In relation to their hepatotoxicity, several studies demonstrate the inhibitory
effects of mycotoxins on certain hepatic biotransformation enzymes, as recently demonstrated in pigs exposed to low doses of aflatoxin B1 or T-2 toxin. In other cases, specific cytochromes P450 or glutathione transferases are significantly increased in terms of both activity and protein expression, namely by aflatoxins, deoxynivalenol or fumonisins. Such results have been obtained in rodents and in farm animals like pigs, rabbits or poultry. The data strengthen the hypothesis that the normal metabolism of endobiotes or xenobiotics by the liver could be altered during chronic exposure to mycotoxins, particularly in farm animals or in humans exposed to aflatoxin B1, ochratoxin A, T-2 toxin,
deoxynivalenol or fumonisin B1.Ulaskom u organizam ljudi i ĆŸivotinja mnogi mikotoksini podlijeĆŸu biotransformaciji u jetri. Njihovi su metaboliti najÄeĆĄÄe oksidativni derivati (hidroksimetaboliti aflatoksina B1 i okratoksina A) ili hidrolitiÄki derivati trihotecena. U nekim sluÄajevima visoko reaktivni epoksidi su prvi korak u stvaranju karcinogenih intermedijera kao ĆĄto su ekso-epoksidi aflatoksina. HepatiÄki enzimi II faze (transferaze i hidrolaze) sudjeluju u konjugaciji tih oksidativnih metabolita tj. njihovoj detoksifikaciji: glukoronidaciji deacetiliranih trihotecena i hidroksi-aflatoksina ili konjugaciji epoksida s glutationom. Zearalenon se reducira u viĆĄe razliÄitih estrogenih zearalenola, ĆĄto ovisi o vrsti organizma koji ga metabolizira. Fumonizin B1 se slabo apsorbira iz probavnog sustava te se metabolizira u hidrolitiÄke produkte koji su manje toksiÄni. Interakcije mikotoksina i hepatiÄkog metabolizma kljuÄni su koraci u njihovoj detoksifikaciji ili bioaktivaciji u organizmu ljudi i ĆŸivotinja. VeÄina tih interakcija posljedica su upravo metaboliÄkog procesa u jetri, posebice aktivnosti citokroma P450 i transferaza. Nedavno je dokazan inhibitorni uÄinak aflatoksina B1 i trihotecena na odreÄene hepatiÄke biotransformacijske enzime u svinja. S druge strane, aktivnost i ekspresija proteina specifiÄnih citokroma P450 i glutation transferaze znaÄajno su poveÄani nakon djelovanja aflatoksina, deoksinivalenola i fumonizina, ĆĄto je zabiljeĆŸeno u glodavaca te domaÄih ĆŸivotinja (svinje, kuniÄi i perad). Ova istraĆŸivanja pokazuju da normalni hepatiÄki metabolizam endobiotika i ksenobiotika moĆŸe biti naruĆĄen tijekom kroniÄnog unosa mikotoksina, posebice u domaÄih ĆŸivotinja i ljudi izloĆŸenih aflatoksinu B1, okratoksinu A, T-2 toksinu, deoksinivalenolu i fumonizinu B1
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Refined exposure assessment of polyethylene glycol (E 1521) from its use as a food additive
The EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion on the refined exposure assessment of polyethylene glycol (E 1521) when used as a food additive. Polyethylene glycols were evaluated by several international bodies and the AFC Panel previously adopted scientific opinions on the safety polyethylene glycol (E 1521). In 2006, the Panel concluded that based on all the data, consumption of PEG through use as plasticisers in filmâcoating formulations for food supplement tablets and/or capsules at the intended use level are not of safety concern. In 2007, in another opinion of the AFC Panel related to dâalphaâtocopheryl polyethylene glycol 1000 succinate (TPGS) in use for food for particular nutritional purposes, the Panel noted that TPGS intakes would correspond to intake to PEG 1000 at levels equivalent to 3.3â8.5 mg/kg body wieght (bw) per day which are within the range of group acceptable daily intakes (ADIs) of the SCF (1997) and JECFA (1980). This assessment could only take into account the use of polyethylene glycol (E 1521) in food supplements and thus the food supplements consumers only scenario was performed. It resulted in exposure estimates of polyethylene glycol (E 1521) up to 3.5 mg/kg bw per day at the mean and up to 6.1 mg/kg bw per day at the high level. The current exposure assessment is based on the methodology used in the reâevaluation of food additives together with reported use levels received following a call for data in 2017. Considering the uncertainties of the exposure assessment, these estimates very likely overestimated the real exposure to polyethylene glycol (E 1521). The Panel also noted that the highest calculated exposure estimate falls within the range of the group ADI previously established by SCF (5 mg/kg bw per day for PEG 300â4000) and of the one set by JECFA (10 mg/kg bw per day for PEG 200â10000)
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Evaluation of diâcalcium malate, used as a novel food ingredient and as a source of calcium in foods for the general population, food supplements, total diet replacement for weight control and food for special medical purposes
The present scientific opinion deals with the evaluation of the safety of diâcalcium malate (DCM) proposed as a novel food ingredient and as a source of calcium for use in foods for the general population, food supplements, total diet replacement for weight control and food for special medical purposes (FSMP), and with the bioavailability of calcium from this source. The structural formula of the proposed complex is based on expert judgement and not supported by any analytical data. On the basis of the available data, the Panel concluded that there was insufficient scientific evidence of a difference between the proposed novel food ingredient named as diâcalcium malate (DCM) and calcium malate already authorised as a source of calcium included in Annex II to Directive 2002/46/EC. Accordingly, the Panel was unable to assess the safety of DCM as a novel food ingredient. On the basis of the results provided, the Panel considered that DCM does not completely dissociate into calcium and malic acid. The Panel concluded that when DCM dissociates, calcium would be available following ingestion of DCM and the bioavailability would appear similar to values reported for other sources of calcium already permitted. Furthermore, the Panel concluded that on the basis of the information available it was not possible to calculate the exposure to DCM as a source of calcium to foods for the general population, food supplements, total diet replacement for weight control and FSMP
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