Yazar "Deniz, B" seçeneğine göre listele

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    The effect of pyridoxine supplementation on plasma lipoproteins and its relationship with atherogenic risk
    (Faculty Press, 1999) Sermet, A; Atmaca, M; Diken, H; Kelle, M; Deniz, B
    The effect of pyridoxine-HCl on cholesterol in plasma lipoprotein fractions and its relationship with atherogenic risk were investigated in mate Sprague-Dawley rats and healthy human volunteers. Plasma cholesterol, very low and low density lipoprotein cholesterol (VLDL-C and LDL-C) decreased, and high density lipoprotein cholesterol (HDL-C) increased, in rats treated with pyridoxine. Although the cholesterol content of the liver did not change, it decreased significantly in the aorta. Atherogenic risk decreased in rats treated with pyridoxine because of a decrease in the plasma/HDL or LDL/HDL cholesterol ratio and the aorta cholesterol. Plasma cholesterol and cholesterol in the lipoprotein fractions of healthy volunteers given a placebo did not change significantly at the end of the experimental period. Pyridoxine affected the plasma cholesterol and cholesterol in lipoproteins in healthy persons as well as in the rats. Plasma cholesterol, VLDL-C and LDL-C decreased while HDL-C increased. Thus, the atherogenic risk decreased significantly. These findings; indicate that pyridoxine may be an antiatherogenic agent.
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    Öğe
    Time-dependent changes in superoxide dismutase, catalase, xanthine dehydrogenase and oxidase activities in focal cerebral ischaemia
    (Faculty Press, 2000) Sermet, A; Tasdemir, N; Deniz, B; Atmaca, M
    Time-dependent changes in the activities of antioxidant enzymes and an oxidant enzyme, xanthine oxidase (XO), were detected in primary and peri-ischaemic brain regions during permanent occlusion of the middle cerebral artery (MCAO) in rats. There were no changes in superoxide dismutase (SOD) and catalase (CAT) activities after 3 h of MCAO, whereas antioxidant enzyme activities decreased significantly in ischaemic brain areas following 24 h of ischaemia. After 48 h, the enzyme activities returned to the baseline but then a further increase was observed in ischaemic brain areas by 72 h post-ischaemia. Normally, XO exists as a dehydrogenase (XD), but it is converted to XO which contributes to injury in some ischaemic tissues. The XO activity increased slightly at 3 h after ischaemia, but after 24 h of ischaemia it returned to the baseline and then remained relatively unchanged in ischaemic areas. Pretreatment with allopurinol before ischaemia prevented changes in SOD and CAT activities and attenuated brain oedema during 24 h of ischaemia. Neither XO nor XD activity changed in allopurinol-treated rats at the times of ischaemia. These results indicated that ischaemic brain tissue remained vulnerable to free radical damage for as long as 48 h after ischaemia, and XO was probably not an important source of free radicals in cerebral ischaemia.