Bone Mineral Density in Hemifacial Microsomia / Oral Science International

We aimed to assess whether patients with hemifacial microsomia can be quantitatively identified using bone mineral density information. Mandibular bone mineral density was studied using computer assisted analysis between the nonaffected (r) and the affected (l) sides with an orthopantomograph in a patient with hemifacial microsomia with median mandibular cleft, and four patients who suffered from hemifacial microsomia in the left side. Fifty controls without bone diseases were randomly selected. Bone mineral density r/l ratios in the controls ranged from 0.479 to 2.064, and those in two patients that were associated with and without median mandibular cleft were higher than those in the controls, with a maximum of 8.622 in a particular male with median mandibular cleft after bone graft, whereas the r/l ratios in the other three cases were similar to the controls. Our findings indicate that the quantitative character in the case with median mandibular cleft reveals a large discrepancy of bone mineral density between the nonaffected and the affected sides. This may suggest a compensatory mechanism for bone hypertrophy from regulated bone mineral density with underdevelopment in hemifacial microsomia.

Inhibitory effect of α-tocopherol on methylmercury-induced oxidative steress

<p><b>OBJECTIVES</b>The present study investigated the involvement of oxidative stress in the degeneration of the cerebellum during methylmercury (MeHg) intoxication and the protective effect of α-tocopherol (Vit E) against MeHg toxicity.</p><p><b>METHODS</b>After 5 mg/kg of MeHg was administered to Wistar rats for 12 consecutive days, the cerebellum were examined histopathologically. In addition, the same amount of MeHg was administered to 3 different groups of Wistar rats: rats with a Vit E-deficient diet, rats fed 150 mg/kg of Vit E for 20 consecutive days after initial MeHg administration, and rats with an ordinary diet.</p><p><b>RESULTS</b>Positive immunoreactivity against anti-hydroxynonenal (HNE), a marker of lipid peroxidation, was observed in the cerebellum after MeHg administration. Levels of thiobarbituric acid reactive substance (TBARS), another marker of lipid peroxidation, and those of protein carbonyl, a biomarker for protein oxidation, increased after MeHg administration. In the rats with MeHg and a Vit E-deficient diet, mortality and prevalence of piloerection significantly increased, and in the rats with MeHg and Vit E, mortality, piloerection, retracted and crossed hind leg, and ataxic gait significantly decreased, compared with the rats with MeHg alone. The levels of NO(2) (-) and NO(3) (-) in the serum significantly increased in the rats with MeHg alone 14 days after the initial MeHg administration, but were significantly suppressed by Vit E administration.</p><p><b>CONCLUSIONS</b>Oxidative stress, especially lipid peroxidation, may play an important role in the cerebellar degeneration process during MeHg intoxication and Vit E may play a protective role against MeHg toxicity as an effective antioxidant.</p>

Inhibitory Effect of $\alpha$-Tocopherol on Methylmercury-Induced Oxidative Steress

Objectives: The present study investigated the involvement of oxidative stress in the degeneration of the cerebellum during methylmercury (MeHg) intoxication and the protective effect of α-tocopherol (Vit E) against MeHg toxicity. Methods: After 5 mg/kg of MeHg was administered to Wistar rats for 12 consecutive days, the cerebellum were examined histopathologically. In addition, the same amount of MeHg was administered to 3 different groups of Wistar rats: rats with a Vit E-deficient diet, rats fed 150 mg/kg of Vit E for 20 consecutive days after initial MeHg administration, and rats with an ordinary diet. Results: Positive immunoreactivity against anti-hydroxynonenal (HNE), a marker of lipid peroxidation, was observed in the cerebellum after MeHg administration. Levels of thiobarbituric acid reactive substance (TBARS), another marker of lipid peroxidation, and those of protein carbonyl, a biomarker for protein oxidation, increased after MeHg administration. In the rats with MeHg and a Vit E-deficient diet, mortality and prevalence of piloerection significantly increased, and in the rats with MeHg and Vit E, mortality, piloerection, retracted and crossed hind leg, and ataxic gait significantly decreased, compared with the rats with MeHg alone. The levels of NO2− and NO3− in the serum significantly increased in the rats with MeHg alone 14 days after the initial MeHg administration, but were significantly suppressed by Vit E administration. Conclusions: Oxidative stress, especially lipid peroxidation, may play an important role in the cerebellar degeneration process during MeHg intoxication and Vit E may play a protective role against MeHg toxicity as an effective antioxidant.