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健康人在不同负荷下氧化损伤过程中的胰岛素、儿茶酚胺、葡萄糖和抗氧化酶。

Insulin, catecholamines, glucose and antioxidant enzymes in oxidative damage during different loads in healthy humans.

作者信息

Koska J, Blazícek P, Marko M, Grna J D, Kvetnanský R, Vigas M

机构信息

Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic.

出版信息

Physiol Res. 2000;49 Suppl 1:S95-100.

Abstract

Exercise, insulin-induced hypoglycemia and oral glucose loads (50 g and 100 g) were used to compare the production of malondialdehyde and the activity of antioxidant enzymes in healthy subjects. Twenty male volunteers participated in the study. Exercise consisted of three consecutive work loads on a bicycle ergometer of graded intensity (1.5, 2.0, and 2.5 W/kg, 6 min each). Hypoglycemia was induced by insulin (Actrapid MC Novo, 0.1 IU/kg, i.v.). Oral administration of 50 g and 100 g of glucose was given to elevate plasma glucose. The activity of superoxide dismutase (SOD) was determined in red blood cells, whereas glutathione peroxidase (GSH-Px) activity was measured in whole blood. The concentration of malondialdehyde (MDA) was determined by HPLC, catecholamines were assessed radioenzymatically and glucose was measured by the glucose-oxidase method. Exercise increased MDA concentrations, GSH-Px and SOD activities as well as plasma noradrenaline and adrenaline levels. Insulin hypoglycemia increased plasma adrenaline levels, but the concentrations of MDA and the activities of GSH-Px and SOD were decreased. Hyperglycemia increased plasma MDA concentrations, but the activities of GSH-Px and SOD were significantly higher after a larger dose of glucose only. Plasma catecholamines were unchanged. These results indicate that the transient increase of plasma catecholamine and insulin concentrations did not induce oxidative damage, while glucose already in the low dose was an important triggering factor for oxidative stress.

摘要

通过运动、胰岛素诱导的低血糖以及口服葡萄糖负荷(50克和100克)来比较健康受试者体内丙二醛的生成以及抗氧化酶的活性。20名男性志愿者参与了该研究。运动包括在自行车测力计上连续进行三个强度递增的工作负荷(1.5、2.0和2.5瓦/千克,各6分钟)。低血糖由胰岛素(诺和灵MC诺和诺德,0.1国际单位/千克,静脉注射)诱导。口服50克和100克葡萄糖以升高血浆葡萄糖水平。超氧化物歧化酶(SOD)的活性在红细胞中测定,而谷胱甘肽过氧化物酶(GSH-Px)的活性在全血中测量。丙二醛(MDA)的浓度通过高效液相色谱法测定,儿茶酚胺通过放射酶法评估,葡萄糖通过葡萄糖氧化酶法测量。运动增加了MDA浓度、GSH-Px和SOD活性以及血浆去甲肾上腺素和肾上腺素水平。胰岛素低血糖增加了血浆肾上腺素水平,但MDA浓度以及GSH-Px和SOD的活性降低。高血糖增加了血浆MDA浓度,但仅在较大剂量葡萄糖后GSH-Px和SOD的活性显著更高。血浆儿茶酚胺未发生变化。这些结果表明,血浆儿茶酚胺和胰岛素浓度的短暂升高并未诱导氧化损伤,而低剂量的葡萄糖已然是氧化应激的一个重要触发因素。

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