The aim of this experimental study was to evaluate the effects of light-emitting diode-mediated-photobiomodulation therapy (LPT), on the rate of orthodontic tooth movement (TM) and orthodontically induced root resorption, in rats. Twenty male 12-week-old Wistar rats were separated into two groups (control and LPT) and 50 cN of force was applied between maxillary left molar and incisor with a coil spring. In the treatment group, LPT was applied with an energy density of 20 mW/cm(2) over a period of 10 consecutive days directly over the movement of the first molar teeth area. The distance between the teeth was measured with a digital caliper on days 0 (T0), 10 (T1), and 21 (T2) on dental cast models. The surface area of root resorption lacunae was measured histomorphometrically using digital photomicrographs. Mann-Whitney U and Wilcoxon tests were used for statistical evaluation at p< 0.05 level. TM during two different time intervals (T1-T0 and T2-T1) were compared for both groups and a statistically significant difference was found in the LPT group (p = 0.016). The TM amount at the first time period (1.31 ± 0.36 mm) was significantly higher than the second time period (0.24 ± 0.23 mm) in the LPT group. Statistical analysis showed significant differences between two groups after treatment/observation period (p = 0.017). The magnitude of movement in the treatment group was higher (1.55 ± 0.33 mm) compared to the control group (1.06 ± 0.35 mm). Histomorphometric analysis of root resorption, expressed as a percentage, showed that the average relative root resorption affecting the maxillary molars on the TM side was 0.098 ± 0.066 in the LPT group and 0.494 ± 0.224 in the control group. Statistically significant inhibition of root resorption with LPT was determined (p < 0.001) on the TM side. The LPT method has the potential of accelerating orthodontic tooth movement and inhibitory effects on orthodontically induced resorptive activity.
Objectives: The aim of this study was to investigate the preventive effects of melatonin and vitamin C as antioxidants on renal injury in chronic alcohol consumption. Materials and methods: A total of 24 adult male Wistar rats weighing 200-250 g were used in the study. Rats were divided into four equal groups. Group I (control): rats were not fed on alcohol; Group II: rats were fed on alcohol; Group III: rats were fed on alcohol and 40 mg/kg vitamin C; and Group IV: rats were fed on alcohol and 4 mg/kg melatonin. Results: Light microscopic examination revealed atrophic renal corpuscles, dilatation and congestion of the peritubular vessels, and renal corpuscles with obscure Bowman's space and a few foamy-appearing tubules due to alcohol consumption were observed. Expression of endothelial nitric oxide synthase (eNOS) was localized to glomerulus, distal, and collector tubules. eNOS staining decreased in alcohol treatment group and melatonin and vitamin C encore increased expression pattern of eNOS. Alcohol consumption increased malondialdehyde (MDA) level and superoxide dismutase (SOD) and catalase (CAT) activities significantly in the alcohol consumption groups compared with that in the control group, while in melatonin give group just MDA level was decreased statistically significant and SOD and CAT activities were also decreased numerically compared with the alcohol consumption groups. Conclusions: These results indicated that chronic alcohol consumption caused renal damage by increased lipid peroxidation and melatonin and vitamin C administration produced in some degree protection against alcohol-induced damage.
The aim of this study was to investigate the effects of melatonin and vitamin C on expression of endothelial nitric oxide synthase (NOS) in heart tissue of chronic alcoholic rats. Twenty-four adult male Wistar rats weighing 200-250 g were used in this study. Rats were divided into four groups. The first group served as control (n = 6). The second group was treated with ethanol (%7.2) for 28 days (n = 6), which was administered in artificial isocaloric diets. The third group was given ethanol and supplemented with 40 mg/kg vitamin C [intraperitoneally (i.p.)] (n = 6). The fourth group was given ethanol and supplemented with 4 mg/kg melatonin (i.p.) (n = 6). At the end of the experiment, rats were sacrificed and heart tissues were processed for immunohistochemistry analysis to endothelial NOS (eNOS). eNOS immunoreactivity showed heterogeneous distribution in control group. eNOS immunoreactivity was (+) in some myocytes and (++) in some others. Expression of eNOS in alcohol group was heterogeneous like control group but also stronger than that. Immunoreactivity was (+++) in myocytes near the epicardial zone and (++) in myocytes near the endocardium border. In melatonin and vitamin C-treated groups, eNOS immunoreactivity was diffuse and the intensity of reaction was (+++) in subepicardial region. However, eNOS immunoreactivity scores were weaker in these groups when compared with the alcohol group. Our results indicate that alleviation of oxidative stress by antioxidant therapy reduces reactive oxygen species-mediated nitric oxide inactivation.
Nitric oxide (NO) plays a significant role in the development of diabetic nephropathy. We investigated the effects of an antioxidant, carnosine, on streptozotocin (STZ)-induced renal injury in diabetic rats. We used four groups of eight rats: group 1, control; group 2, carnosine treated; group 3, untreated diabetic; group 4, carnosine treated diabetic. Kidneys were removed and processed, and sections were stained with periodic acid-Schiff (PAS) and subjected to eNOS immunohistochemistry. Examination by light microscopy revealed degenerated glomeruli, thickened basement membrane and glycogen accumulation in the tubules of diabetic kidneys. Carnosine treatment prevented the renal morphological damage caused by diabetes. Moreover, administration of carnosine decreased somewhat the oxidative damage of diabetic nephropathy. Appropriate doses of carnosine might be a useful therapeutic option to reduce oxidative stress and associated renal injury in diabetes mellitus.
In rats 2-APB reduced the oxidative stress and apoptosis caused by testicular ischemia-reperfusion injury. The testicular protective effect of 2-APB appears to be mediated through its antiapoptotic and antioxidative effects.