Effect of a high-altitude expedition to a Himalayan peak (Pumori, 7,161�m) on plasma and erythrocyte antioxidant profile

Abstract

The effects of a high-altitude exposure were studied in six mountaineers who spent 3 weeks at an altitude range between 5,250 and 7,161 m after 1 week in an acclimatization trek (2,800-5,250 m). Blood drawn from the antecubital vein was collected at sea level 1 day before and 1 day after the expedition to analyse some haematological variables [haemoglobin (Hb), haematocrit (Htc) and red blood cell (RBC) count], erythrocyte antioxidant enzyme activity [superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (Gr)] and membrane fatty acid profile [mono-unsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), saturated fatty acids (SFA), trans fatty acids (TRANS)]. Moreover, total antioxidant status (TAS), thiobarbituric acid reactive substances (TBARS), thiol protein groups (SH), SOD, GPx and Gr were measured in plasma. High-altitude exposure induced polycythaemia, with significant increases in RBC count (5.26%), Hb concentration (4.83%) and Htc (6.26%). Furthermore, a significant increase in plasma TBARS, SOD and Gr was observed after the expedition, whereas SH, TAS and GPx decreased. Erythrocyte glutathione-cycle-related antioxidant enzyme activity was upregulated, whereas SOD activity was maintained after the expedition. In addition, despite the unchanged (MUFA+PUFA)/SFA ratio, the membrane erythrocyte fatty acid content showed a significant increase in PUFAs and a decrease in TRANS, suggesting enhanced membrane fluidity. In conclusion, it seems that high-altitude exposure, besides quantitative variations in RBC expression, induced plasma oxidative stress and damage, and significant changes in erythrocyte components, namely in antioxidant enzyme activity and membrane fatty acid profile that might modify RBC functionality.

Caleidoscópio do ano olímpico

“…Attempting to emphasize the role of hypoxia, a number of acute, chronic and intermittent hypoxia studies with rats (22,97,106) and humans (7,9,54) have been conducted in both hypobaric and normobaric conditions confirming high-altitude hypoxia per se as an independent modulator of cell and tissue redox status. Data from Magalhães and co-workers in humans and rats, both in plasma (69,73) and skeletal muscle (70)(71)(72) , are consistent with others reporting increased oxidative damage and an inability of the antioxidant system to cope with the increased production of RONS under hypoxia (7,23,52,54,66,77,89,98,106) . Increased lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS) or malondialdehyde (MDA), and enhanced protein oxidation estimated by carbonyl derivatives groups or sulfhydryl groups (SH) were found at distinct levels of cell organization (69)(70)(71)(72)(73) .…”

“…Data from Magalhães and co-workers in humans and rats, both in plasma (69,73) and skeletal muscle (70)(71)(72) , are consistent with others reporting increased oxidative damage and an inability of the antioxidant system to cope with the increased production of RONS under hypoxia (7,23,52,54,66,77,89,98,106) . Increased lipid peroxidation measured by thiobarbituric acid reactive substances (TBARS) or malondialdehyde (MDA), and enhanced protein oxidation estimated by carbonyl derivatives groups or sulfhydryl groups (SH) were found at distinct levels of cell organization (69)(70)(71)(72)(73) . Moreover, DNA damage expressed as increased strand breaks and endonuclease III-sensitive sites was described in human skeletal muscle after 2 weeks of hypoxia (107) .…”

Moderate altitude but not additional endurance training increases markers of oxidative stress in exhaled breath condensate

“…Earlier we described a rapid increase in mouse erythrocytes GSH levels on 0.5% O 2 hypoxic exposure in vitro (Bogdanova et al 2003), and others showed an increase in mouse muscle reduced GSH with acute hypoxia equivalent to an altitude of 7000 m (Magalhaes et al 2004), a result that correlates with the observation of suppressed ROS production in hepatocytes primary cultures in response to acute hypoxia (Bogdanova et al 2005). Chronic hypoxic exposure reduces erythrocytes GSH content (Singh et al 2001) and triggers activation of glutathione cycle related enzyme activity (Magalhaes et al 2005) leading to improved antioxidant capacity of blood.…”

Low 8-oxo-7,8-dihydro-2′-deoxyguanosine levels and influence of genetic background in an Andean population exposed to high levels of arsenic

“…Populations living in the Andes have been exposed to As through drinking water for thousands of years and live at a high altitude, which is associated with increased oxidative stress [46,47]. However, this rural environment is also lacking a number of factors associated with oxidative stress; e.g.…”