Melatonin promotes fracture healing in the rat model.

OBJECTIVES: In this study, we investigated the effect of melatonin on fracture healing in the rat tibia model by using biochemical and histopathologic methods. MATERIALS AND METHODS: In this study 80 male Sprague-Dawley rats were randomized into two groups, a control group (Group 1) and melatonin group (Group 2) with eight rats per group according to the day of sacrifice (Days 1, 3, 7, 14 and 28). The fractures were produced by the manual breakage using plate-bending devices, placed at the distal 3(rd) of the right tibia. Group 2 received 30 mg/kg/day melatonin and group 1 1% alcohol in saline 5 ml/kg/day intraperitoneally during the experiment. Plasma Malondialdehyde (MDA) levels, activity of superoxide dismutase (SOD) and myeloperoxidase (MPO) were measured biochemically. The fracture healing was evaluated using a five-point scale defined by Allen et al. RESULTS: Malondialdehyde levels in group 2 decreased at days 3, 7, 14, and 28 compared to control values (p<0.05). Superoxide dismutase activity in group 2 decreased at days 3, 7 and 14, and returned to the 1(st) day value after 28 days. Myeloperoxidase values in group 2 decreased at days 1, 3, and 7 (p<0.001). Histopathological specimens of healed tibias showed two animals with complete cartilaginous union, five with incomplete bony union and one with complete bony union in the group 2. In contrast, in the group 1, six rats showed complete cartilaginous union and two showed incomplete cartilaginous union (p<0.05). CONCLUSION: The administration of melatonin maybe beneficial in suppressing the effects of free oxygen radicals and regulating antioxidant enzyme activity in the fracture healing process.

Plasma homocysteine and retinal artery occlusive disease: a case-control study.

BACKGROUND: Previous studies have documented that elevated plasma homocysteine is a risk factor for cardiovascular, cerebrovascular and peripheral vascular disease. In a case-control study, we sought to determine whether elevated homocysteine (HCY) is a risk factor for retinal artery occlusive disease PATIENTS AND METHODS. Study subjects consisted of 20 patients (12 male, 8 female) (mean age, 55.8; range 42-70 years) with clinical and objective evidence of retinal vascular occlusive disease and 20 age-matched control subjects (9 males, 11 females) (mean age, 55.3 years; range 50-68 years). Hyperhomocysteinemia was defined as a plasma HCY level >15 micromol/L by HPLC. We also measured concentrations of triglycerides, and total cholesterol, LDL cholesterol, and HDL cholesterol. RESULTS: The mean plasma HCY level in the patient group was 21.23+/-9.53 micromol/L (range, 8.00-43.99 micromol/L) compared with 12.59+/-4.97 micromol/L (range, 6.38 to 22.88 micromol/L) in the control group (P<0.008). There was no correlation between HCY and serum triglycerides or cholesterol levels within each group. We conclude that high plasma HCY level may be a risk factor for retinal artery occlusive disease.

Nitric oxide metabolities in acute rheumatic fever.

Acute rheumatic fever (ARF), is a systemic inflammatory disease etiologically related to infection with group A beta hemolytic streptococcus, characterized by a broad spectrum of disorders in cellular immunity. To estimate the activity of the immunopathological process in patients with ARF, plasma nitric oxide metabolities (NOx) concentrations, IL-1alpha and IL-2 levels were investigated in 22 patients with ARF at the time on admission, and after 3 months, in children with chronic rheumatic heart disease (CRHD). Plasma NOx concentrations, IL-1alpha and IL/2 levels in patients with ARF on admission were significantly higher than in the same patients 3 months later, and higher than in CRHD, or controls. Increased plasma NO may be a useful index for the quantitative assessment of the activity during immunological challenge. This information may be useful for the prognosis and monitoring of ARF.

The effect of folic acid, vitamin B6 and vitamin B12 on the homocysteine levels in rabbits fed by methionine-enriched diets.

Atherosclerosis is an important cause of cardiovascular morbidity and mortality in recent years. Hyperhomocysteinemia is recognized as an independent risk factor for premature atherosclerosis and venous thrombosis. It is suggested that administration of folic acid, vitamin B6 and vitamin B12 may decrease homocysteine levels. In our study, we induced hyperhomocysteinemia in rabbits by giving methionine and studied the effects of folic acid, vitamin B6 and vitamin B12 on homocysteine levels. A total of 40 (20 female, 20 male New Zealand rabbits) were divided into four groups, each consisting of 10 rabbits. Methionine (100 mg/kg/day), methionine (100 mg/kg/day) plus vitamin B6 (30 mg/kg/day), methionine (100 mg/kg/day) plus vitamin B12 (80 mg/kg/day) and methionine (100 mg/kg/day) plus folic acid (20 mg/kg/day) were given to the first, second, third and forth groups respectively. These rabbits were followed up for two months. We studied homocysteine levels on the 0, 20th, 40th and 60th days in all groups. In rabbits we induced hyperhomocysteinemia by giving methionine for 2 months. The decreases of homocysteine levels in the forth group were significant with respect to the second and third groups. Folic acid supplementation clearly resulted in a reduction of plasma homocysteine levels, whereas vitamin B12 was little effective and vitamin B6 failed to show an effect. We conclude that even folic acid treatment alone may be sufficient for decreasing negative effects of homocysteine.