Figure 6 Apoptotic and viable cells in DMA patients. Plasma protein carbonyls were significantly higher in patients compared to controls (Table ​(Table2,2, Fig. ​Fig.2).2). Post laser irradiation, the plasma protein carbonyls significantly decreased compared to their level before irradiation (Table ​(Table2,2, Fig. ​Fig.2).2). But still was significantly higher, when compared to controls (Table ​(Table2,2, Fig. ​Fig.22). Plasma Inhibitors,research,lifescience,medical nitric oxide was significant lower in DMD patients compared to controls (Table ​(Table3,3, Fig. ​Fig.8).8). Post laser

irradiation a significant increase was observed in plasma nitric oxide of DMD patients compared to their level before laser irradiation. Figure 8 Levels of inducible nitric oxide BIRB 796 nmr synthase among DMD patients compared to controls and compared to their levels post laser exposure. Table 3 Levels Inhibitors,research,lifescience,medical of inducible nitric oxide synthase among DMD patients compared to controls and compared to their levels post laser exposure. Inducible nitric Oxide

(iNOS) mRNA was expressed significantly lower in DMD neutrophils compared to controls. Post laser irradiation a significant increase was observed in iNOS mRNA of DMD patients compared to their level before laser irradiation, but still significantly lower than normal (Table ​(Table3,3, Figs. ​Figs.7,7, ​,88). Figure 7 Expression of iNOS mRNA Inhibitors,research,lifescience,medical pre and post laser irradiation, Lanes 1 and 3 for control pre and post laser respectively. Lanes 2 and 4 for DMD pre and post laser respectively. Inhibitors,research,lifescience,medical Discussion Replicative aging and oxidative stress are two plausible theories explaining muscular dystrophy. The first theory indicates that replicative aging of myogenic cells (satellite cells), owing to enhanced myofiber turnover, is a common explanation of the progression of DMD (6). The oxidative stress theory indicates that failure

Inhibitors,research,lifescience,medical of muscle regeneration to keep up with the ongoing apoptosis and necrosis following oxidative stress that normally associates muscular exercise leads to muscle atrophy in DMD (5). In the present study the two theories were tested to verify, which is fitter. Accordingly, markers of replicative aging were measured in terms of telomerase reverse transcriptase activity, RAGEs mRNA and Bax much mRNA, while markers of oxidative stress were measured in terms of lipid peroxidation, protein carbonyls and apoptosis percentage in circulating mononuclear cells of DMD patients. Markers of replicative aging were measured in peripheral blood mononuclear cells, which were previously shown to infiltrate degenerating muscles of DMD patients, where specific immune reaction at the site of tissue degeneration is suggested to play an important role in the pathogenesis of the disease (20). Accordingly, it is important to test for markers of ageing and replicative senescence in such cells. Results of the present study showed decreased telomerase activity, increased Bax mRNA and RAGEs mRNA expression in DMD blood mononuclear cells compared to controls.