Acute incremental exercise to maximal performance does not cause alterations in serum oxidant levels of healthy young individuals.

AIM: This study was designed to analyze serum oxidative stress (OS) levels in healthy young individuals performing a routine maximal aerobic exercise and to evaluate the correlation between OS levels and physiological parameters. METHODS: Serum OS levels were studied by thermochemiluminescence (TCL) parameters at rest and following maximal aerobic exercise in 85 healthy young subjects. Levels were measured by a real time on line TCL assay (higher TCL-Ratio and TCL-H3 = lower OS level). RESULTS: Aerobic capacity had no effect on baseline OS levels. Post-exercise OS levels correlated with maximal oxygen uptake (V.O(2max)) (P<0.005), delta V.O(2) (V.O(2max)- V.O(2)rest) (P<0.005), anaerobic threshold (VTH) (P<0.01), and total oxygen uptake (especially O(2) after VTH), (P<0.005). TCL-Ratio was related to total running time (P<0.01), as well. Post-exercise OS levels for the whole study group did not vary from baseline values. However, individuals with higher fitness level (V.O(2max) >percentile 60) had significantly lower values of TCL-H3 (P=0.04) and tended to have lower TCL-Ratio, indicating they had elevated OS levels. In a multivariate analysis OS level was most affected by V.O(2) after VTH (anaerobic phase of the test) (P=0.003; adjusted odds ratio of 3.41, 95% confidence interval: 1.55-7.48). CONCLUSIONS: In conclusion, acute incremental exercise to maximal performance does not cause alterations in serum oxidant levels of healthy young individuals. In healthy individuals performing maximal aerobic exercise, OS levels correlate with maximal aerobic power.

Coenzyme Q10 can in some circumstances block apoptosis, and this effect is mediated through mitochondria.

The mitochondrial component coenzyme Q10 (CoQ10) has been used for many years as a dietary supplement intended to promote good health by trapping free radicals, thus preventing lipid peroxidation and DNA damage. We have tested its use as a generic anti-apoptotic compound and have found that its ability to protect against apoptosis varies depending on both cell type and mode of cell death induction. We have further established that this protection may be mediated by its effect on mitochondrial function and viability. We provide additional evidence that CoQ10's protective effect on mitochondrial membrane potential does not always result in altered mitochondrial enzyme activity and neither does it guarantee survival. These observations open the way for further investigations into the mechanisms involved in mitochondrial control of apoptosis.

Detection of apoptotic cells in the nervous system.

Over the course of an organism's life, cells divide, grow, differentiate, and die. For many years cell death has been recognized as significant in normal neuronal development. More recently, interest has grown in the mechanisms that regulate both cell death and cell survival in neurons during homeostasis and aging. Understanding these mechanisms depends largely on the ability to identify dead or dying cells. Several markers have been identified and developed for the detection of cell death in various tissues. In this chapter, we will present an overview of different approaches used to identify cell death in the nervous system while focusing on a few specific protocols.

[Study of the effect of an inhibitor of carnitine-dependent metabolism of mildronate on the oxidation of fatty acids in the liver mitochondria of intact rats]. / Izuchenie vliianiia ingibitora karnitinzavisimogo metabolizma mildronata na okislenie zhirnykh kislot mitokhondrii pecheni intaktnykh krys.

Effect af antiischemic drug mildronate 3-(2,2,2-trimethylhydrazinium) propionate on oxidation of sodium octanoate and L-palmitoyl carnitine was studied in liver mitochondria of intact rats using polarographic procedure. After 10 days of administration of mildronate at a dose of 200 mg/kg per os oxidation of sodium octanoate was stimulated in liver mitochondria while the rate of L-palmitoyl carnitine oxidation was unaltered. The data obtained suggest that mildronate stimulated the carnitine-independent fatty acid oxidation which appears to occur as a compensation for inhibition of the carnitine-dependent oxidation by the drug.