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Dietetics, Nutrition and Biological Sciences

Permanent URI for this collectionhttps://eresearch.qmu.ac.uk/handle/20.500.12289/23

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End date: 2009Has files: No

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    The influence of moderate red wine consumption on antioxidant status and indices of oxidative stress associated with CHD in healthy volunteers
    (Cambridge University Press, 2007-03-08) Tsang, Catherine; Higgins, Siobhan; Duthie, Garry G.; Duthie, Susan J.; Howie, Moira; Mullen, William; Lean, Michael E. J.; Crozier, Alan
    The effects of moderate red wine consumption on the antioxidant status and indices of lipid peroxidation and oxidative stress associated with CHD were investigated. A randomised, controlled study was performed with twenty free-living healthy volunteers. Subjects in the red wine group consumed 375 ml red wine daily for 2 weeks. We measured the total concentration of phenolics and analysed the individual phenolics in the wine and plasma by HPLC with tandem MS. The antioxidant capacity of plasma was measured with electron spin resonance spectroscopy while homocysteine and fasting plasma lipids were also determined. The production of conjugated dienes and thiobarbituric acid-reactive substances (TBARS) were measured in Cu-oxidised LDL. Plasma total phenolic concentrations increased significantly after 2 weeks of daily red wine consumption (P≤0·001) and trace levels of metabolites, mainly glucuronides and methyl glucuronides of (+)-catechin and (−)-epicatechin, were detected in the plasma of the red wine group. These flavan-3-ol metabolites were not detected in plasma from the control group. The maximum concentrations of conjugated dienes and TBARS in Cu-oxidised LDL were reduced (P≤0·05) and HDL cholesterol concentrations increased (P≤0·05) following red wine consumption. The findings from the present study provide some evidence for potential protective effects of moderate consumption of red wine in healthy volunteers.
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    The absorption, metabolism and excretion of flavan-3-ols and procyanidins following the ingestion of a grape seed extract by rats
    (Cambridge University Press, 2007-03-08) Tsang, Catherine; Auger, Cyril; Mullen, William; Bornet, Aurélie; Rouanet, Jean-Max; Crozier, Alan; Teissedre, Pierre-Louis
    Rats were fed a grape seed extract (GSE) containing (+)-catechin, (−)-epicatechin and dimers, trimers, tetramers and polymeric procyanidins. Liver, kidney, brain and gastrointestinal (GI) tract together with plasma, urine and faeces were collected over a 24 h period and their flavan-3-ol content was analysed by HPLC with tandem mass spectrometry and diode array detection. Small amounts of the GSE flavan-3-ols moved out of the stomach and into the duodenum/jejunum, and to a greater extent the ileum 1 h after ingestion, and into the caecum after 2 h with relatively small amounts being detected in the colon after 3 h. The GI tract contained the parent GSE flavan-3-ols and procyanidins with only trace amounts of metabolites and there were no indications that proanthocyanidins were depolymerised in the GI tract releasing monomeric flavan-3-ols. Plasma contained exclusively catechin glucuronides and methylated glucuronide metabolites which were also detected in the liver and kidneys. These metabolites were also present in urine together with sulphated metabolites and low amounts of the procyanidin dimers B1, B2, B3 and B4 as well as the trimer C2 and an unknown GSE trimer. The amounts of (+)-catechin and (−)-epicatechin metabolites excreted in urine relative to the quantity of the monomers ingested were 27 and 36 %, respectively, after 24 h. This is similar to the levels of urinary excretion reported to occur by other investigators after feeding (−)-epicatechin to rats and provides further, albeit indirect, evidence that the procyanidin oligomers in the GSE were not depolymerised to monomers to any extent after ingestion. No convincing analytical data were obtained for the presence of flavan-3-ol metabolites in the brain.
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    A gene-targeted mouse model of P102L Gerstmann-Sträussler-Scheinker syndrome
    (Elsevier, 2003-03) Barron, Rona; Manson, Jean C.
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    The 101L mutation in murine PrP can alter transmission across three species barriers
    (2002) Barron, Rona; Jamieson, Elizabeth; Thomson, Val; Melton, David W.; Will, Robert; Ironside, James; Manson, Jean C.
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    Gene Targeting the PrP Gene
    (Horizon Bioscience, 2004) Barron, Rona; Manson, Jean C.
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    Knockouts, Knockins, Transgenics and Transplants in Prion Research
    (Cold Spring Harbor Laboratory Press, 2004) Weissman, C; Fleschig, E; Barron, Rona; Aguzzi, A; Manson, Jean C.
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    The transmissible spongiform encephalopathies.
    (Cambridge University Press, 2005-04) Manson, Jean C.; Barron, Rona; Diggard, P.; Nash, A.A.; Randall, R.E.
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    The role of host PrP in control of incubation time
    (Springer Verlag, 2005) Manson, Jean C.; Barron, Rona; Hart, Patricia; Tuzi, Nadia L.; Bishop, Matthew T.
    PrP is central to TSE disease and has been hypothesised to be the infectious agent. Polymorphisms in the PrP gene are associated with different incubation times of disease following exposure to an infectious agent and mutations in the human PrP gene can apparently lead to spontaneous genetic disease. Strains of TSE agent are proposed to be generated and maintained through differences in glycosylation or conformation of PrP and the barrier to infection between species is thought to be due to the differences in the sequence of PrP between different species. To test these hypotheses, we have introduced specific modifications into the endogenous mouse Prnp gene by gene targeting. The mutated PrP gene is in the correct location under the control of the endogenous Prnp regulatory sequences and thus expressed in the same tissues and amounts as the wild type Prnp gene. By altering the murine PrP coding region to that of another species we have established that increasing overall identity between host and donor PrP can lead to either an increase or a decrease in incubation time of disease in a strain dependent manner. We have introduced a point mutation (101L) into the N-terminus of the host PrP and shown that it dramatically changes the susceptibility of the host to infection from different species. We have in addition demonstrated that polymorphisms in the N terminus (L108T) and C-terminus (F189V) of host PrP both alter the incubation time of disease. We have in addition introduced mutations into the Prnp gene which prevent glycosylation at each or both of the two N-linked glycosylation sites of PrP. Inoculation of these mice with infectivity has established that glycosylation of host PrP can influence incubation time of disease, vacuolar pathology and strain determination.
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    The transmissible spongiform encephalopathies: emerging and declining epidemics
    (Portland Press, 2006-10-25) Manson, Jean C.; Cancellotti, Enrico; Bishop, Matthew T.; Hart, Patricia; Barron, Rona
    TSEs (transmissible spongiform encephalopathies) are neurodegenerative diseases of various mammalian species, the best known of which include BSE (bovine spongiform encephalopathies) in cattle, CJD (Creutzfeldt–Jakob disease) in humans, scrapie in sheep and CWD (chronic wasting disease) in deer. This review examines the emergence of various TSE strains and their transmission, and discusses disease surveillance and control.
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    The nature of the prion
    (2009) Barron, Rona