Our study confirms that oxidative stress is involved in the pathophysiology of vitiligo, as indicated by the high levels of erythrocyte superoxide dismutase activity and plasma nitrite/nitrate.
Spinal cord injury (SCI) results in the loss of function below the lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death. Methylprednisolone (MP), by reducing edema and protecting the cell membrane against peroxidation, is the only pharmacological agent with a proven clinically beneficial effect on SCI. Melatonin, known as a free radical scavenger, has been shown to have an effect on lipid peroxidation following experimental SCI. The purpose of this study was to examine the effect of MP and melatonin on neurological, ultrastructural, and electrophysiological recovery. Female albino rats weighing 200-250 g were randomized into five groups of 18 rats each and six rats for the control group. Weight-drop trauma was performed for each group and a 30-mg/kg single dose of MP for rats in group 1, a 10-mg/kg single dose of melatonin for rats in group 2, and MP and melatonin in the same doses for rats in group 3 were administered immediately after trauma. The rats in group 4 were the vehicle group (treated with ethanol) and group 5 was the trauma group. The motor and somatosensory evoked potentials were recorded at the 4th hour, the 24th hour, and on the 10th day of the study for six rats in each group. Posttraumatic neurological recovery was recorded for 10 days using "motor function score" and inclined plane test. After electrophysiological study the rats were terminated for an analysis of lipid peroxidation level of the injured site of the spinal cord. Electron microscopic studies were performed to determine the effects of melatonin, MP, and the combined treatment with MP and melatonin on axons, neurons, myelin, nucleus, and intracytoplasmic edema. The groups treated with MP, melatonin, and a combination of both had significantly enhanced electrophysiological, biochemical, and neurological recovery and also showed better ultrastructural findings than the trauma and vehicle groups. Although combined treatment was significantly more effective on lipid peroxidation than melatonin or MP treatments alone, at the 10th day, neurobehavioral, electrophysiological, and ultrastructural recovery were at the same level. In conclusion, MP, melatonin, and MP and melatonin combined treatment modalities improved functional recovery at the same level. Future studies involving different doses of melatonin and different dose combinations with MP could promise better results since each drug has a different antioxidative mechanism of action.
Although the relationship between hearing loss and hyperlipoproteinemia (HLP) or diabetes mellitus (DM) has been shown in many clinical investigations, this concept is still controversial. A prospective study was designed to search for the existence of subclinical auditory dysfunction related to HLP and DM by transient-evoked (TEOAEs) and distortion-product otoacoustic emissions (DPOAEs) in patients with hearing levels better than 30 dB. Evoked otoacoustic emissions were utilized to investigate subclinical auditory dysfunction. Fifteen hypercholesterolemic patients (28 ears), 21 hypertriglyceridemic patients (42 ears) and 21 DM patients (40 ears) were eligible for investigation. The results of the DPOAEs and TEOAEs of the study groups were compared with the control group composed of individuals with similar ages and with normal blood lipids and glycemia. This group consisted of 22 people (44 ears). There was no difference in the existence of TEOAEs at all frequencies among the groups (P>0.05). No differences were found in the amplitudes of the DPOAES between the groups except at 4 kHz (P>0.05). The difference was caused by the hypertriglyceridemia group (P=0.014) and the non-insulin-dependent diabetes mellitus (NIDDM) group (P=0.012) when compared with the control group. The mean DPOAE amplitudes of the hypertriglyceridemic and NIDDM groups at 4 kHz were higher than those of the control group. The decreased DPOAE amplitudes at 4 kHz in hypertriglyceridemic and diabetic patients without clinical findings are compatible with the sensorineural hearing loss observed with hyperviscosity and increased noise susceptibility, as was shown before in these patients. Longitudinal investigations should be performed with otoacoustic emissions to help with the early prediction of the prospective effects of HLP and DM on the auditory system.
In this study, the relationship between selenium (Se) and glutathione peroxidase (GSHPx) levels was investigated in 7,12-dimethylbenz(a)anthracene (7,12-DMBA)-treated mouse liver. The potential mammary carcinogen 7,12-DMBA, was injected intraperitoneally (20 mg kg(-1) day(-1)) into 10-12 month old female mice. After 21 days of application the mice were sacrificed and GSHPx and Se levels of liver homogenates were measured. Se and GSHPx levels in 7,12-DMBA-treated mice were significantly lower than those of controls (p < 0.05). The control group exhibited 0.9 +/- 0.066 U mg(-1) protein and 0.86 +/- 0.058 p.p.m. levels of GSHPx and Se respectively. The 7,12-DMBA-treated group had significantly (p < 0.05) decreased GSHPx and Se levels (0.42 +/- 0.062 U mg(-1) protein and 0.69 +/- 0.034 p.p.m. respectively). The results show a direct relationship between Se and GSHPx activity and a negative correlation between antioxidant capacity and existence of a carcinogen in metabolism.
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