Physical exercise prevents the exacerbation of oxidative stress parameters in chronic kidney disease.

OBJECTIVE: Reactive oxygen species play an important role in the pathogenesis of chronic kidney disease (CKD). Physical exercise was suggested as a useful approach to diminish impaired oxidative defense mechanisms. This study sought to observe the effects of physical training before the induction of renal lesions on oxidative stress parameters in animals induced for CKD. METHODS: Twenty-four male Wistar rats were divided into four groups (n = 6): sham, sham plus exercise, CKD, and CKD plus exercise. Exercise groups performed physical training on a treadmill for 8 weeks (up to 1 km/h for 50 min/day, 5 days/week). Forty-eight hours after the final exercise session, a surgical reduction of renal mass was performed (5/6 nephrectomized). Thirty days later, blood samples were collected to determine serum creatinine and urea concentrations, and the right kidney was surgically removed and stored at -70 degrees C for later analysis of superoxide production, antioxidant enzymes (superoxide dismutase and catalase), and oxidative damage of lipids (thiobarbituric acid reactive susbstances level) and proteins (carbonyl groups and sulfhydryl content). RESULTS: A significant increase occurred in creatinine and urea levels, superoxide production, antioxidant enzymes, and oxidative damage in the CKD group, compared with sham-treated animals (P < .05). Physical training prevented superoxide production, and decreased the oxidative damage in the CKD group (P < .05), but did not increase the effect of antioxidants. CONCLUSION: Physical training before induction of a renal lesion is capable of improving oxidative damage parameters and oxidant production, without altering renal function and the antioxidant defense system.

Effect of different models of physical exercise on oxidative stress markers in mouse liver.

The aim of this study was to investigate the effect of different protocols of physical exercise on oxidative stress markers in mouse liver. Twenty-eight male CF1 mice (30-35 g) were distributed into 4 groups (n = 7) - untrained (UT), continuous running (CR), downhill running (D-HR), and intermittent running (IR) - and underwent an 8-week training program. Forty-eight hours after the last training session, the animals were killed, and their livers were removed. Blood lactate, creatine kinase, citrate synthase, thiobarbituric acid reactive species, carbonyl, superoxide dismutase (SOD), and catalase (CAT) activities were assayed. Results show a decrease in the level of lipoperoxidation and protein carbonylation in the CR and D-HR groups. SOD activity was significantly increased and CAT activity was reduced in the CR and D-HR groups. Our findings indicate that CR and D-HR may be important for decreasing oxidative damage and in the regulation of antioxidant enzymes (SOD and CAT) in the livers of trained mice.

Effects of Mikania glomerata Spreng. and Mikania laevigata Schultz Bip. ex Baker (Asteraceae) extracts on pulmonary inflammation and oxidative stress caused by acute coal dust exposure.

Several studies have reported biological effects of Mikania glomerata and Mikania laevigata, used in Brazilian folk medicine for respiratory diseases. Pneumoconiosis is characterized by pulmonary inflammation caused by coal dust exposure. In this work, we evaluated the effect of pretreatment with M. glomerata and M. laevigata extracts (MGE and MLE, respectively) (100 mg/kg, s.c.) on inflammatory and oxidative stress parameters in lung of rats subjected to a single coal dust intratracheal instillation. Rats were pretreated for 2 weeks with saline solution, MGE, or MLE. On day 15, the animals were anesthetized, and gross mineral coal dust or saline solutions were administered directly in the lung by intratracheal instillation. Fifteen days after coal dust instillation, the animals were killed. Bronchoalveolar lavage (BAL) was obtained; total cell count and lactate dehydrogenase (LDH) activity were determined. In the lung, myeloperoxidase activity, thiobarbituric acid-reactive substances (TBARS) level, and protein carbonyl and sulfhydryl contents were evaluated. In BAL of treated animals, we verified an increased total cell count and LDH activity. MGE and MLE prevented the increase in cell count, but only MLE prevented the increase in LDH. Myeloperoxidase and TBARS levels were not affected, protein carbonylation was increased, and the protein thiol levels were decreased by acute coal dust intratracheal administration. The findings also suggest that both extracts present an important protective effect on the oxidation of thiol groups. Moreover, pretreatment with MGE and MLE also diminished lung inflammatory infiltration induced by coal dust, as assessed by histopathologic analyses. The present study indicates that M. glomerata and M. laevigata might become good candidates for the prevention of lung oxidative injury caused by coal dust exposure.

Attenuation of bleomycin-induced lung injury and oxidative stress by N-acetylcysteine plus deferoxamine.

Reactive oxygen species (ROS) play an important role in the pathogenesis of pulmonary injury and antioxidant therapy may be useful with impaired oxidative defense mechanism. This study examines the effect of N-acetylcysteine (NAC) and deferoxamine (DFX) on inflammatory indicators and oxidative stress in the lungs of mice exposed to bleomycin (BLM). The animals received endotracheally a single dose of BLM (2.5 U/kg body weight dissolved in 0.25 ml of 0.9% NaCl) or saline (0.9% NaCl) and were divided into eight groups (n=8): saline; BLM; saline+NAC; BLM+NAC; saline+DFX; BLM+DFX; saline+NAC+DFX; BLM+NAC+DFX. Treatments with NAC (20mg/kg) or DFX (30 mg/kg) were administered for 60 days after BLM exposure. Lactate dehydrogenase (LDH) activity and total cell count, neutrophil and protein concentration were determined in the bronchoalveolar lavage fluid (BALF). Lipid peroxidation thiobarbituric acid-reactive species (TBARS), oxidative protein damage (carbonyl contents), and catalase and superoxide dismutase activities were determined in the lung tissue. BLM administration resulted in lung lesion as determinated lung histology, which is almost completely prevented by NAC plus DFX. The results of total cell counts and neutrophils and LDH increased after BLM exposure and were reduced with NAC. DFX and NAC plus DFX also caused a significant decrease of LDH activity. The increased malondialdehyde equivalents and carbonyl contents in lung tissue produced by BLM were also prevented by NAC plus DFX. However, the isolated use of NAC increased lipid peroxidation. SOD activity increased after BLM exposure only in the group treated with DFX and catalase activity not was altered in the presence of BLM. Data presented here indicates that the isolated use of NAC had limited effects on BLM-induced pulmonary oxidative stress in mice. The use of DFX improves the defense response and in association with NAC may be a good alternative in the treatment or prevention of diseases that have ROS and iron involved in their pathogenesis.

Effect of therapeutic pulsed ultrasound on parameters of oxidative stress in skeletal muscle after injury.

Contusion injuries are a very common form of both athletic and non-athletic injury, that effect muscle function. Treatments to augment the normal repair and regeneration processes are important for a wide variety of patients. Therapeutic ultrasound has been claimed to promote tissue repair, especially by enhancing cell proliferation and protein synthesis. The present study aimed to investigate the effect of therapeutic pulsed ultrasound (TPU) on parameters of oxidative stress, namely thiobarbituric acid-reactive substances (TBARS), protein carbonyl content and the activities of antioxidant enzymes, catalase and superoxide dismutase (SOD), in skeletal muscle after injury. Wistar rats were submitted to an animal model of muscle (gastrocnemius) laceration. TPU was used once a day. One, three or five days after muscle laceration, the animals were killed by decapitation and oxidative stress parameters were evaluated. Serum CK levels were increased in muscle-injured animals, indicating that the laceration animal model was successful. TBARS were not altered after muscle injury, when compared to the sham group. Protein carbonyl content was increased after muscle laceration. Catalase and SOD activities were increased 1 day after muscle injury and not altered at days 3 and 5. TPU decreased TBARS levels after muscle laceration when compared to injured muscle animals without treatment. Protein carbonyl content evaluation presented similar results. It is tempting to speculate that TPU seems to protect the tissue from oxidative injury. TPU diminished catalase and SOD activities, especially on the first day following muscle laceration.