The aim of this study was to examine the effect of allopurinol, a xanthine oxidase inhibitor, on oxidative stress and physical performance after swimming until exhaustion in rats. Blood and gastrocnemius muscle samples were collected before, immediately after, and 5 h after exercise and the respective timepoints after allopurinol administration. Xanthine oxidase and total antioxidant capacity (TAC) were determined in plasma and muscle, whereas catalase activity and reduced (GSH) and oxidized (GSSG) glutathione were measured in erythrocytes and muscle. Thiobarbituric acid-reactive substances (TBARS) and protein carbonyls (PC) were determined in plasma, erythrocytes, and muscle. As expected, allopurinol inhibited xanthine oxidase activity. Compared with their nonallopurinol-treated counterparts, rats treated with allopurinol showed a 35% decrease in physical performance, as indicated by the shorter swimming time to exhaustion. Exercise alone increased PC and TBARS concentration in plasma, erythrocytes, and gastrocnemius muscle. Similarly, allopurinol alone increased PC and TBARS concentration in erythrocytes and gastrocnemius muscle, decreased TAC in plasma and gastrocnemius muscle, and decreased the GSH:GSSG ratio in erythrocytes. Our data illustrate that, in general, exercise and allopurinol alone increased the levels of most of the oxidative stress markers measured in plasma, erythrocytes, and gastrocnemius muscle. Xanthine oxidase inhibition provoked a marked reduction in physical performance.

Osteoarthritis (OA) and osteoporosis (OP) are associated skeletal pathologies and have as a distinct feature the abnormal reconstruction of the subchondral bone. OA and OP have been characterized as age-related diseases and have been associated with telomere shortening and altered telomerase activity (TA). This review discusses the role of telomeres and telomerase in OA and OP pathologies and focuses on the usability of telomere length (TL) and the rate of telomere shortening as potential disease biomarkers. A number of studies have demonstrated that telomere shortening may contribute to OA and OP as an epigenetic factor. Therefore, it has been claimed that the measurement of TL of chondrocytes and/or peripheral blood cells may be an appropriate marker for the evaluation of the progression of these diseases. However, there is a need to be perform further studies with larger cohorts, with the aim of obtaining objective results and a better understanding of the association between TL, inflammation and aging, in order to provide further insight into the pathophysiology of degenerative joint diseases.

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Among the various side effects of supra-physiological dose of anabolic androgenic steroids that are described, renal toxicity remains the least evaluated. The present study provides evidence that long-term administration of nandrolone decanoate could lead to alterations of renal function and structure in the experimental rabbit model. A pronounced increase in serum urea, creatinine, SGOT and SGPT is observed in the treated animals, with intramuscular administration being more detrimental. Histopathological evaluation of kidneys indicated hyperaemia, fibrosis and focal inflammation. Furthermore, the significantly increased telomerase activity found in the kidneys of the intramuscularly treated animals could possibly represent a counteracting survival mechanism. Oxidative stress markers that were influenced the most were TBARS, indicating lipid peroxidation, and GSH. An interesting finding in our study though, was that while intramuscular administration showed the highest biochemical derangement, oxidative stress markers provided mixed results between intramuscularly and subcutaneously treated rabbits. In conclusion, nephrotoxicity of nandrolone decanoate remains a multi-factorial, partly irreversible effect that involves augmented tissue oxidative status.