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

Citation
J. Koska et al., Insulin, catecholamines, glucose and antioxidant enzymes in oxidative damage during different loads in healthy humans, PHYSL RES, 49, 2000, pp. S95-S100
Citations number
25
Categorie Soggetti
Physiology
Journal title
PHYSIOLOGICAL RESEARCH
ISSN journal
08628408 → ACNP
Volume
49
Year of publication
2000
Supplement
1
Pages
S95 - S100
Database
ISI
SICI code
0862-8408(2000)49:<S95:ICGAAE>2.0.ZU;2-3
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 partici pated 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 plas ma glucose. The activity of superoxide dismutase (SOD) was determined in re d blood cells, whereas glutathione peroxidase (GSH-Px) activity was measure d in whole blood. The concentration of malondialdehyde (MDA) was determined by HPLC, catecholamines were assessed radioenzymatically and glucose was m easured by the glucose-oxidase method. Exercise increased MDA concentration s, GSH-Px and SOD activities as well as plasma noradrenaline and adrenaline levels. Insulin hypoglycemia increased plasma adrenaline levels, but the c oncentrations of MDR and the activities of GSH-Px and SOD were decreased. H yperglycemia 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 trans ient increase of plasma catecholamine and insulin concentrations did not in duce oxidative damage, while glucose already in the low dose was an importa nt triggering factor for oxidative stress.