Effect of Exercise Repetitions on Arylesterase Activity of PON1 in Plasma of Average-Trained Men-The Dissociation between Activity and Concentration.

Exercise may increase the antioxidant capacity of plasma by stimulating antioxidant enzymes. The study aimed to measure the effect of three repetitions of acute exercise on arylesterase (ARE) activity of the paraoxonase 1 (PON1) enzyme. Eleven average-trained men (age 34.0 ± 5.2 years) completed three treadmill runs. ARE activity in plasma was evaluated spectrophotometrically and compared with PON1 concentration (PON1c), paraoxonase (PON) activity, and high-density lipoprotein cholesterol (HDL-C) at rest and after exercise. In all repetitions of the exercise, ARE activity remained stable, and ARE activity standardized for PON1c (ARE/PON1c) was lower post- than pre-exercise. The ARE/PON1c ratio changes returned to baseline levels during rest after each exercise session. Pre-exercise ARE activity correlated negatively with post-exercise C-reactive protein (CRP) (ρ = -0.35, p = 0.049), white blood cell count (WBC) (ρ = -0.35, p = 0.048), polymorphonuclear leukocytes (PMN) (ρ = -0.37, p = 0.037), and creatine kinase (CK) (ρ = -0.37, p = 0.036). ARE activity may be depleted under conditions of oxidative stress, as increases in PON1c during acute exercise did not result in parallel increases in ARE activity. No adaptation of the response of ARE activity to exercise was detected in subsequent exercise sessions. Individuals with lower pre-exercise ARE activity may develop a higher inflammatory response to strenuous exercise.

Repetitions of Strenuous Exercise Consistently Increase Paraoxonase 1 Concentration and Activity in Plasma of Average-Trained Men.

OBJECTIVES: Oxidative stress, induced by physical activity, may stimulate the expression, release, and activity of certain antioxidant enzymes. We investigated the effect of three repeated bouts of strenuous exercise on paraoxonase 1 concentration (PON1c) and paraoxonase activity (PON). METHODS: Eleven average-trained healthy men (age 34.0 ± 5.2 years) performed three strenuous exercise tests on a treadmill separated by 72 hours periods of resting. PON1c, PON, ferric-reducing activity of plasma (FRAP), lipid profile, C-reactive protein concentration (CRP), and lactate concentration were determined in plasma. RESULTS: Each exercise bout resulted in similar PON1c, PON, FRAP, and high-density lipoprotein concentration (HDL-C) increments, while PON/HDL-C ratio remained stable in all repetitions. Percentage increments at the bout of each exercise were higher for PON1c (by 64.82% at the first, by 92.9% at the second, and by 77.02% at the third exercise) than for PON (by 6.49% at the first, 10.06% at the second, and by 12.32% at the third exercise). Association was found between preexercise PON and PON1c (r = 0.56, p = 0.029), pre- (r = 0.87, p = 0.00003) and postexercise HDL-C (r = 0.6, p = 0.0002), preexercise PON and cardiovascular fitness level of participants measured as VO2max (r = 0.39, p = 0.026), and postexercise PON and lactate concentration (r = 0.44, p = 0.01). CONCLUSIONS: PON1c and PON increase during strenuous exercise, yet the effect of exercise on PON1 concentration is more pronounced. PON1 does not show tolerance to physical activity. The enzyme may provide short-term protection from oxidative stress in each exercise bout. PON may depend on exercise load. Cardiovascular fitness levels may be associated with PON1 activity.

Aerobic training modulates the effects of exercise-induced oxidative stress on PON1 activity: a preliminary study.

The aim of the study was to compare the effect of maximal exercise (ME) on paraoxonase (PON) and arylesterase (ARE) activity depending on lifestyle in respect to physical activity. The study was performed on 46 young men divided into two groups: sedentary (S) and physically active (PA). All participants performed ME on a treadmill. PON1 activities, FRAP, uric acid, bilirubin, TBARS, and lipid profile were determined in their blood before, at the bout of, and after ME. No significant differences in PON1 activities were found between S and PA subjects at baseline. Nearly all biochemicals increased at ME in both groups. Both PON and ARE activity increased at the bout of ME in PA subjects and only ARE activity in S subjects. ARE/HDL-C ratio increased at the bout of ME in PA and S subjects. The difference in PON1 activity response to ME between study groups may be a result of adaptation of PA subjects to regular physical activity. We suggest that PON1 activity may be a marker of antioxidant protection at ME and an indicator of adaptation to exercise.

[Comparison of local and systemic inflammatory markers in patients with community-acquired pneumonia and pneumonia coexisting with lung cancer]. / Porównanie wybranych parametrów lokalnego i systemowego stanu zapalnego u chorych na pozaszpitalne zapalenie pluc i zapalenie pluc wspólistniejace z rakiem pluca.

BACKGROUND: The aim of the study was to compare the local and systemic markers of inflammatory processes in patients with community-acquired pneumonia (CAP) and in those with pneumonia coexisting with lung cancer. MATERIAL AND METHODS: Seventeen patients with community-acquired pneumonia (group I), 14 patients with pneumonia and lung cancer (group II), and 24 patients with lung cancer (group III) were enrolled into the study. Sixteen healthy smokers served as a control group (group IV). Concentration of hydrogen peroxide (H(2)O(2)), vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNF-α) were measured in exhaled breath condensate (EBC). The levels of VEGF and TNF-α were also measured in serum. RESULTS: The concentrations of VEGF (317.83 ± 77.78) and TNF-α (1.98 ± 0.13) in EBC were significantly higher in patients with pneumonia and lung cancer as compared to patients with community-acquired pneumonia (VEGF 30.20 ± 6.56; TNF-α 0.31 ± 0.05). Also the level of H(2)O(2) (0.96 ± 0.16) in EBC in patients with pneumonia and lung cancer was elevated in comparison to patients with CAP (0.66 ± 0.09), however the difference was not statistically significant (p 〉 0.05). The serum concentrations of both studied cytokines were significantly higher in patients with pneumonia (VEGF 1112.62 ± ± 244.38 and TNF-α 2.6 ± 0.48) than in those with pneumonia and lung cancer (VEGF 392.9 ± 78.2; TNF-α 1.6 ± 0.2). CONCLUSIONS: Patients with pneumonia and lung cancer exhibited higher levels of oxidative stress and local inflammatory reactions than those with pneumonia. However, inflammatory markers in serum were significantly lower in patients with pneumonia and lung cancer as compared to those with CAP.

Effect of inhaled N-acetylcysteine on hydrogen peroxide exhalation in healthy subjects.

N-acetylcysteine (NAC) has antioxidant properties and its oral administration decreased H(2)O(2) exhalation in patients with chronic obstructive pulmonary disease. In this study we tested whether inhaled NAC could suppress H(2)O(2) levels in exhaled breath condensate (EBC) of eight healthy subjects that have never smoked (never-smokers). Original NAC solution (ACC vial, 300 mg NAC in 3 ml solvent), NAC-placebo (vehicle), sterile 0.9% NaCl or distilled water were nebulized via the pneumatic De Vilbiss nebulizer once daily every 7 days and H(2)O(2) and thiols exhalation was measured just before, 30 min and 3 h after the end of drug administration. Additional in vitro experiments were performed to evaluate NAC stability during nebulization, reactivity with H(2)O(2) and possible H(2)O(2) generation in aqueous NAC solutions. NAC almost completely abolished H(2)O(2) exhalation 30 min after inhalation (0.02+/-0.04 vs. 0.21+/-0.09 microM, p<0.001). However, 3 h later the H(2)O(2) levels raised 1.8-fold from baseline (p<0.01). Other inhaled solutions did not affect H(2)O(2) levels. Mean thiol concentration in EBC rose (p<0.05) after treatment with NAC and reached 1.03+/-0.48 microM at 3 h. Although, 25 and 50 mM NAC completely inhibited H(2)O(2)-peroxidase-luminol-dependent chemiluminescence, detectable amounts of H(2)O(2) were generated in NAC solutions. It was accompanied by moderate loss of -SH groups. Catalase and ascorbic acid prevented H(2)O(2) formation in NAC solutions. In conclusion inhaled NAC revealed biphasic effect on H(2)O(2) exhalation in healthy subjects, which depends on direct H(2)O(2) scavenging and H(2)O(2) generation related to drug oxidation. The net result of these processes may determine anti- or pro-oxidant action of inhaled NAC.