Important sources for superoxide (O2 x -) include
the itochondrial respiratory  chain and cytosolic xanthine oxidase (XO).nThese free radicals may  induce damage to DNA, RNAproteins, or induce free  radical chain reactions inlipid membranes.
  Free radicals may alsoinduce reversible oxidation of
 thiols, resulting in modifi-cation of receptor/protein function

Clinical Chemistry 50: 1668-1670, 2004;10.1373/clinchem.2004.034553(Clinical Chemistry. 2004;50:1668-1670.) © 2004 American Association for Clinical Chemistry, Inc.

Increased Concentrations of Cell-Free Plasma DNA after Exhaustive Exercise 
Johanna Atamaniuk1,a, Claudia Vidotto1, Harald Tschan2, Norbert Bachl2, Karl M. Stuhlmeier3 and Mathias M. Müller1 


1 Institute of Laboratory Diagnostics, Kaiser Franz Josef Hospital, Vienna, Austria;2 Institute of Sports Science, Department of Sports and Exercise Physiology, University of Vienna, Vienna, Austria;3 Ludwig Boltzmann Institute for Rheumatology, Vienna, Austria; 

aaddress correspondence to this author at: Institute of Laboratory Diagnostics, Kaiser Franz Josef Hospital, Kundratstrasse 3, A-1100 Vienna, Austria; fax 43-60191-3309, e-mail johanna.atamaniuk@wienkav.at

n Increased oxidant production in mitochondria of muscles during acute exercise, followed by reoxygenation, has been shown to cause cellular damage, which may be reflected by increased serum myoglobin concentrations

n In this study the significant increase in cell-free plasma DNA immediately after exhaustive exercise and its disappearance within 2 h after the race suggests that cell-free plasma DNA could possibly be an important tool for monitoring and quantification of cellular damage.

NEURO-SIGNALS Vol. 10, No. 1-2, 2001 

Oxidative Stress in Mitochondria Disorders of Aging
Mitochondria Control Cell Death
Guest Editor: M. Ebadi, Grand Forks, N. Dak., USA

The mitochondrial respiratory chain could also be a potential source of ROS in tissues, such as liver, kidney and nonworking muscles, that during exercise undergo partial ischemia because of reduced blood supply. Sufficient oxygen is available to interact with the increasingly reduced respiratory chain and enhance the ROS generation. At the cessation of exercise, blood flow to hypoxic tissues resumes leading to their reoxygenation. This mimics the ischemia-reperfusion phenomenon, which is known to cause excessive production of free radicals.

Sports as a cause of oxidative stress and hemolysis

Colombia Medica Vol. 36 Nº 4, 2005 (Octubre-Diciembre)

Javier F. Bonilla, M.D.1, Raúl Narváez, M.D., M.Sc.2, Lilian Chuaire, M.Sc.

Sportsmen pseudoanemia is related with a plasma expansion. In individuals who practice frequent aerobic sport activity it could coexist associated events such hematuria, gastrointestinal blood loss, as well as an increase in the intravascular hemolysis. These factors link exercise with the deterioration of corporal iron reserve and the erythrocyte number and morphology. Likewise there are foreseen much more etiological possibilities not only of entities like anemia, but of a great number of other diseases related to exhaustive and competitive exercise with damaging responses to the organism. It is necessary to deeply study the reasons why some sportsmen present higher grades of hemolysis than others, even when they are submitted to similar conditions of intensity  and work terms. For this, it must be considered that hemolysis in exercise could result not only from running long distances where erythrocytes are stroke, but also from other mechanisms such as the oxidative stress.

Ascorbic acid doesn't seem to help physical exercise performance
Medical Research News 
Published: Thursday, 6-Jan-200

Orange juice or other sources of vitamin C (ascorbic acid), may (or may not) benefit you in terms of health and exercise, but contrary to what many people thought previously, ascorbic acid doesn't seem to help physical exercise performance. And in terms of such endurance exercise as running, walking or cycling, whereas vitamin C reduces physiological "oxidative stress," that reduction didn't help performance for either men or women, whether they were in their 20s or 60s.

LE Magazine June 2001

Why CoQ10 is needed by those who take vitamin E

There are additional pieces to the vitamin E puzzle. A series of groundbreaking studies by Roland Stocker and his colleagues at The Heart Research Institute in Sydney, Australia demonstrates that vitamin E (alpha-tocopherol) systematically promotes LDL oxidation. Stocker calls this pro-oxidant action of vitamin E “tocopherol-mediated peroxidation,” or TMP. Through the TMP process, vitamin E amplifies mild oxidative stresses so that they do much more damage to LDL.(9-11)

The good news is that Stocker’s group discovered that CoQ10 naturally present in the body protects against TMP. They showed that one molecule of CoQ10 can prevent two TMP chain reactions involving as many as 40 to 80 free radicals. In pilot studies they tested LDL from the blood of human subjects given vitamin E and/or CoQ10 supplements. CoQ10 supplements reduced TMP, while vitamin E supplements increased it. When given together, the CoQ10 supplement significantly counteracted the TMP side-effect of the vitamin E supplement.(12-14) Here is a conclusion from one of several studies that show that adequate levels of CoQ10 are required for vitamin E to function as an efficient antioxidant in the body:

“These results demonstrate that oral supplementation with alpha-tocopherol alone results in LDL that is more prone to oxidation initiation, whereas co-supplementation with coenzyme Q not only prevents this prooxidant activity of vitamin E but also provides the lipoprotein with increased resistance to oxidation.” 

The work of Stocker and his colleagues agrees with other lines of recent research suggesting that CoQ10 cooperates with vitamin E in a complex partnership that we are only beginning to understand. Indeed these “co-antioxidants” are always found together in cell membranes and LDL. CoQ10 regenerates vitamin E, which would otherwise be quickly exhausted fighting oxidative stress. Vitamin E breaks off the chain reaction of lipid peroxidation, while CoQ10 helps to prevent it from starting.

The many studies of vitamin E supplementation published over the years did not take into account the CoQ10 naturally present in the body, but we can now see that this was a crucial factor. In these studies of vitamin E, CoQ10 served as the “silent partner,” amplifying the effect of vitamin E, regenerating vitamin E as it was exhausted, and preventing TMP.

  Free Radicals: nature's way of saying NO or Molecular murder 
from the 1993 Gray Laboratory Annual Repor

Oxidative damage from cellular free radicals, as with radiation damage, can be repaired by natural antioxidants. The most important are vitamin C (ascorbate), vitamin E (ŕ-tocopherol), and glutathione (a thiol, GSH). These can donate either an electron or a hydrogen atom to cellular molecules oxidized by free radicals, including those generated by ionizing radiation. They can thus influence damage to all cellular constituents, including DNA, proteins and lipids (membranes). Lipid peroxidation can be effectively inhibited. In 1979, Robin Willson and colleagues at Brunel University (working with CRC support) showed using pulse radiolysis that after vitamin E (vit-E(OH)) has repaired oxidative damage by donating its hydrogen atom, it can itself be restored to carry out more radical repair reactions by reaction with vitamin C (ascorbate, AH- ):

damage + vit-E(OH) ® repaired damage + vit-E(O· ) (22) 
vit-E(O· ) + AH- ® vit-E(OH) + A·- + H+ (23)

Sports Injury Bulletin -2006

...remember that exercise generates increased quantities of 'oxygen free radicals' and increases lipid peroxidation (the oxidative attack on key fats found in cell membranes, including muscle-fibre membranes). Strenuous exercise can induce oxidative damage in muscles and result in serious muscle injury.
The human body is well aware of this disastrous possibility, of course, and as a defence it produces a potent anti-oxidant called superoxide dismutase; superoxide-dismutase production speeds up when individuals embark on regular and at least moderately strenuous training programmes. Evidence suggests, however, that the superoxide-dismutase system is prone to being overwhelmed. Prolonged submaximal exercise has been shown to result in elevated amounts of skeletal-muscle lipid-peroxidation byproducts, indicating significant damage to the muscles (Free Radicals and Tissue Damage Produced by Exercise, Biochem Biophys Res Commun, Vol. 107, pp. 1198-1205, 1982).
Before we continue, let's recap. Exercise can greatly increase the production of cell-damaging free radicals. The magnified rates of lipid peroxidation resulting from this oxygen-radical production may cause skeletal damage. The human body has its own anti-radical defence system, but it doesn't always work effectively. In addition, the damage produced in the muscles as a result of exercise can snowball over relatively short periods of time. For example, in one study researchers found more muscle damage three days after a strenuous workout than they had found one hour after exercise ceased ('Adaptive response in human skeletal muscle subjected to prolonged eccentric training', Int J Sports Med, Volume 4, pp. 177-183, 1983). This was a bit surprising, since researchers believed significant muscle repair would have occurred during the three-day interim.

Delayed-onset muscle soreness
In another investigation, exercise scientists found that intense exercise produced immediate muscle damage, but the damage actually became much worse 24 and 48 hours after the workout was over, even though no follow-up exercise had taken place ('Ultrastructural changes after concentric and eccentric contractions of human muscle', J Neurol Sci Vol. 61, pp. 109-122, 1983). In other words, in a muscle traumatised by exertion, there is a post-exercise period lasting for up to three days or more in which muscle damage is actually accelerated, rather than minimised, even when no further exercise occurs.