Nandrolone decanoate and resistance exercise affect body composition and energy metabolism.

Our aim was to evaluate the independent and associated effects of nandrolone decanoate (DECA) and resistance exercise (REx) on central and peripheral hormones and neuropeptides related to energy balance in male rats. The experimental protocol was performed for eight weeks and comprised four groups: control (C) - exposed to vehicle 3x/wk; trained (T) - REx 5x/wk and vehicle 3x/wk; decanoate (D) - exposed to DECA (5 mg/kg) 3x/wk, and REx with DECA (TD) - submitted to REx 5x/wk and DECA (5 mg/kg) 3x/wk. Cross-sectional area analysis of the gastrocnemius muscle was higher in the T and TD groups compared to the C group. Biometrical analyses showed a decrease in body weight only in the TD compared to the C group, however, a reduction in total fat mass was observed in both the T and TD when compared to the C group. In respect of hypothalamic mRNA expression, there was an increase in prepro-orexin in the T compared to the C group. In mesenteric fat there was a decrease in leptin expression in the T and TD compared to the C group. Plasma evaluations showed reduced leptin concentrations in D, T and TD compared to C, and an increase in orexin-A in the D group compared to the C and T groups. Our data showed that REx was related to central and peripheral changes in energy metabolism, while DECA changed only peripheral components. REx associated with DECA promoted peripheral changes in energy metabolism and decreased body and fat weights.

Helium-neon laser improves bone repair in rabbits: comparison at two anatomic sites.

The purpose of this study was to evaluate the influence of helium-neon laser on bone repair of femur and tibia in rabbits. For this purpose, 15 New Zealand rabbits underwent bilateral bone damage (tibia and femur) using a spherical bur. Helium-neon laser light, at a fluency of 6 J∕cm(2) and wavelength of 632.8 nm was applied on the left legs (laser group). The right tibia or femur lesions (control group) served as negative control. All sections were histopathologically analyzed using HE sections and the morphometric data from bone tissue and hyaline cartilage were achieved. Histopathological analysis showed regular bone trabeculae covered by osteoblastic cells after 1 week in the group exposed to laser therapy from femur and tibia indistinctly. After 3 weeks, the laser group showed new bone formation coming from the bony walls in the femur and tibia as well. On the 5th week, well-defined trabecula undergoing remodeling process was detected for the most intense pattern in tibia only. Morphometric analysis revealed significant statistical differences (p < 0.05) in the bone tissue for the laser-exposed group on 1st and 3rd weeks. After 5th week, bone formation was increased to tibia only. Taken together, such findings suggest that helium-neon laser is able to improve bone repair in rabbits being the most pronounced effect in tibia.

Nandrolone decanoate induces genetic damage in multiple organs of rats.

To evaluate the impact potential of nandrolone decanoate on DNA damage in multiple organs of Wistar rats by means of single-cell gel (comet) assay and micronucleus test. A total of 15 animals were distributed into three groups of five animals each as follows: control group = animal not exposed to nandrolone decanoate; experimental group = animals exposed to nandrolone decanoate for 24 h at 5 mg/kg subcutaneously; and experimental group = animals exposed to nandrolone decanoate for 24 h at 15 mg/kg subcutaneously. Significant statistical differences (p < 0.05) were noted in peripheral blood, liver, and heart cells exposed to nandrolone decanoate at the two doses evaluated. A clear dose-response relationship was observed between groups. Kidney cells showed genetic damage at only the highest dose (15 mg/kg) used. However, micronucleus data did not show remarkable differences among groups. In conclusion, the present study indicates that nandrolone decanoate induces genetic damage in rat blood, liver, heart, and kidney cells as shown by single-cell gel (comet) assay results.

DNA damage, p53, Ki-67 and COX-2 expression in rat tongue cells exposed to nandrolone decanoate.

The objective of this article was to evaluate the impact potential of nandrolone decanoate on DNA damage, cellular regulatory proteins and cyclooxygenase (COX)-2 in oral mucosa cells of Wistar rats. A total of 40 rats were distributed into four groups. Two experimental groups were treated with nandrolone decanoate, at 5 mg/kg doses, subcutaneously, three times a week in two periods: 15 and 30 days. The remaining groups received only 0.9% saline subcutaneously, three times a week. To evaluate genetic damage, nandrolone decanoate at 15 mg/kg dose was exposed to 24 h. In the histopathological analysis, no remarkable morphological changes were observed in tongue tissue in all groups. Significant increase in immunoexpression of Ki-67, p53, COX-2 proteins was detected in the groups treated with nandrolone decanoate during 15 and 30 days, when compared to their respective controls. A positive correlation between immunoexpression of p53 and COX-2 protein was detected following nandrolone decanoate exposure. DNA damage was induced by nandrolone decanoate in oral mucosa cells at 15 mg/kg dose. Our results suggest that nandrolone decanoate was able to alter the expression of cell cycle-related proteins, as well as to induce genetic damage and COX-2 immunoexpression in tongue cells of Wistar rats.

Acute spinal cord injury induces genetic damage in multiple organs of rats.

Spinal cord injury (SCI) is a devastating condition with important functional and psychological consequences. However, the underlying mechanisms by which these alterations occur are still not fully understood. The aim of this study was to analyze genomic instability in multiple organs in the acute phase of SCI by means of single cell gel (comet) assay. Rats were randomly distributed into two groups (n = 5): a SHAM and a SCI group killed 24 h after cord transection surgery. The results pointed out genetic damage in blood cells as depicted by the tail moment results. DNA breakage was also detected in liver and kidney cells after SCI. Taken together, our results suggest that SCI induces genomic damage in multiple organs of Wistar rats.

Cellular death but not genetic damage in oral mucosa cells after exposure to digital lateral radiography.

The aim of the present study was to evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis, and karyorrhexis) in exfoliated buccal mucosa cells from individuals following digital lateral radiography. A total of 30 healthy patients (15 men and 15 women) indicated to the orthodontic therapy were submitted to digital lateral X-ray. Exfoliated oral mucosa cells were collected immediately before the X-ray exposure and after 10 days. The results pointed out no significant statistically differences (p > 0.05) of micronucleated oral mucosa cells. On the other hand, X-ray was able to increase other nuclear alterations closely related to cytotoxicity such as karyorrhexis, pyknosis, and karyolysis. In summary, these data indicate that exposure to digital lateral radiography may not be a factor that induced chromosomal damage, but it is able to promote cytotoxicity.

Genetic damage in multiple organs of acutely exercised rats.

The aim of this study was to investigate the effects of acute exercise on genomic damage in an animal model. Male adult Wistar rats were divided into the following groups: control and acute exercised (experimental). For this purpose, 15 animals were accustomed to running on a rodent treadmill for 15 min per day for 5 days (10-20 m min(-1); 08 grade). After 4 days at rest, active animals ran on the treadmill (22 m min(-1), 58 grade) till exhaustion. Cells from peripheral blood, liver, heart, and brain were collected after 0, 2, and 6 h after exercise. The results showed that acute exercise was able to induce genetic damage in peripheral blood cells after 2 and 6 h of exercise, whereas liver pointed out genetic damage for all periods evaluated. No genetic damage was induced either in brain or in heart cells. In conclusion, our results suggest that acute exercise could contribute to the genetic damage in peripheral blood and liver cells. It seems that liver is a sensitive organ to the genotoxic insult after acute exercise.