Expression of the antioxidant stress protein heme oxygenase-1 (HO-1) in human leukocytes - Acute and adaptational responses to endurance exercise

Citation
Am. Niess et al., Expression of the antioxidant stress protein heme oxygenase-1 (HO-1) in human leukocytes - Acute and adaptational responses to endurance exercise, FREE RAD B, 26(1-2), 1999, pp. 184-192
Citations number
47
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
26
Issue
1-2
Year of publication
1999
Pages
184 - 192
Database
ISI
SICI code
0891-5849(199901)26:1-2<184:EOTASP>2.0.ZU;2-#
Abstract
Inducible heme oxygenase (HO-1) is an antioxidant stress protein, that is m ainly induced by reactive oxygen species (ROS), cytokines and hyperthermia. By using flow cytometry the present investigation demonstrated a rise in t he cytoplasmic expression of HO-1 in lympho- (L), mono- (M) and granulocyte s (G) of 9 endurance-trained male subjects after a half marathon run. The e xpression was more pronounced in M (median: 98.3% HO-1 positive cells/4.31 mfc) and G (94.8%/1.93 mfc) than in L (80.1%/ 1.51 mfc) when measured 3 h p ost-exercise. Additionally the exercise protocol caused a rise in the plasm a levels of myeloperoxidase, TNF alpha and interleukin-8 (IL-8), indicating an inflammatory response. We could detect a correlation between IL-8 and H O-1, directly after exercise, that was apparent in G (r = 0.67, p <.05) and L (r = 0.80, p < .05), but did nor reach significance in M (r = 0.65, p = 0.06). An additional detection of HO-1 at rest in 12 untrained subjects sho wed a higher baseline expression of HO-1 compared to the athletes. The regu latory pathways leading to an increased expression of HO-1 after endurance exercise are not completely clear, but a causal involvement of a cytokine-m ediated generation of ROS must be discussed. We supposed that the down-regu lation of the baseline expression of HO-1 in athletes reflects an adaptiona l mechanism to regular exercise training. (C) 1998 Elsevier Science Inc.