The influence of low-level laser therapy on parameters of oxidative stress and DNA damage on muscle and plasma in rats with heart failure.

In heart failure (HF), there is an imbalance between the production of reactive oxygen species and the synthesis of antioxidant enzymes, causing damage to the cardiovascular function and increased susceptibility to DNA damage. The aim of this study was to evaluate the influence of low-level laser therapy (LLLT) on parameters of oxidative stress and DNA damage in skeletal muscle and plasma of rats with HF. Wistar rats were allocated into six groups: "placebo" HF rats (P-HF, n = 9), "placebo" Sham rats (P-sham, n = 8), HF rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-HF, n = 8), sham rats at a dose 3 J/cm(2) of LLLT (3 J/cm(2)-sham, n = 8), HF rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-HF, n = 8) and sham rats at a dose 21 J/cm(2) of LLLT (21 J/cm(2)-sham, n = 8). Animals were submitted to a LLLT protocol for 10 days at the right gastrocnemius muscle. Comparison between groups showed a significant reduction in superoxide dismutase (SOD) activity in the 3 J/cm(2)-HF group (p = 0.03) and the 21 J/cm(2)-HF group (p = 0.01) compared to the P-HF group. 2',7'-Dihydrodichlorofluorescein (DCFH) oxidation levels showed a decrease when comparing 3 J/cm(2)-sham to P-sham (p = 0.02). The DNA damage index had a significant increase either in 21 J/cm(2)-HF or 21 J/cm(2)-sham in comparison to P-HF (p = 0.004) and P-sham (p = 0.001) and to 3 J/cm(2)-HF (p = 0.007) and 3 J/cm(2)-sham (p = 0.037), respectively. Based on this, laser therapy appears to reduce SOD activity and DCFH oxidation levels, changing the oxidative balance in the skeletal muscle of HF rats. Otherwise, high doses of LLLT seem to increase DNA damage.

Antioxidant effect of cysteamine in brain cortex of young rats.

Cysteamine is a cystine-depleting drug used in the treatment of cystinosis, a metabolic disorder caused by deficiency of the lysosomal cystine carrier. As a result, cystine accumulates within lysosomes in many tissues and organs, including the nervous system. Studies with cystine dimethyl ester loaded cells suggest that cystine might induce apoptosis through oxidative stress. Our objective was to investigate the effects of co-administration of cysteamine with the oxidant cystine dimethyl ester on several parameters of oxidative stress in the brain cortex of rats. Animals were injected with 1.6 micromol/g cystine dimethyl ester and/or 0.26 micromol/g body weight cysteamine. Cystine dimethyl ester induced lipoperoxidation, protein carbonylation, and stimulated superoxide dismutase, glutathione peroxidase and catalase activities, probably through the formation of free radicals. Cysteamine prevented those effects, possibly increasing cellular thiol pool and acting as a scavenger of free radicals. These results suggest that the antioxidant effect of cysteamine may be important in the treatment of cystinosis.

Effects of cysteamine on oxidative status in cerebral cortex of rats.

Cystinosis is a systemic genetic disease caused by a lysosomal transport deficiency accumulating cystine in most tissues. Tissue damage depends on cystine accumulation, but the mechanisms of this damage are still obscure. Cysteamine administration depletes cystine accumulated, increasing survive of affected patients. Studies performed in fibroblasts of cystinotic patients suggest that apoptosis is enhanced in this disease. Considering that oxidative stress is a known apoptosis inducer, our main objective was to investigate a possible antioxidant effect of cysteamine on several parameters of oxidative stress in the brain of young rats. Animals received three subcutaneous injections at 3-h intervals of a buffered solution (pH 7.4) of 10 mg/kg body weight cysteamine and were sacrificed 1 h after the last injection. Cysteamine decreased lipoperoxidation and glutathione peroxidase activity, and increased the carbonyl content of proteins and catalase activity. In vitro studies showed that cysteamine reduced lipoperoxidation, 2',7'-dihydrodichlorofluorescein oxidation, carbonyl content of proteins and catalase activity, and increased glutathione peroxidase activity. These results suggest that cysteamine may act as a scavenger of superoxide free radicals and hydrogen peroxide. Therefore, it is possible that cysteamine may extend life of cystinotic patients acting not only as a cystine depleting drug, but also as a free radical scavenger, reducing cell damage by apoptosis.