Plasma homocysteine levels in children and adolescents with type 1 diabetes.

OBJECTIVE: Hyperhomocysteinemia has been established as a risk factor for cardiovascular disease. The objective was to investigate total plasma homocysteine concentrations in children and adolescents with type 1 diabetes and a control group. METHOD: Twenty-seven children with type 1 diabetes and 27 subjects of an age- and sex-matched control group were recruited. Fasting samples were collected for plasma total homocysteine, serum vitamin B12, folate, and creatinine. RESULTS: Fasting total homocysteine concentrations showed no difference between patients and controls (5.6 +/- 2.9 micromol/L vs 5.7 +/- 2.2 micromol/L; p greater than 0.05). The diabetic patients had significantly higher serum folate than the healthy controls (11.4 +/- 3.3 ng/mL vs 9.4 +/- 4.1 ng/mL; P = 0.02 and higher serum B12 than the control group (282.8 +/- 119 pg/mL vs 228.5 +/- 50.9 pg/mL; P = 0.03). Total plasma homocysteine concentration correlated with age (r = 0.44, P = 0.02), weight (r = 0.56, P = 0.002), body mass index (r = 0.57, P = 0.002), folate (r = -0.48, P = 0.01), and creatinine (r = 0.41, P = 0.03) in diabetic patients. In stepwise multivariate regression model for diabetics, the independent correlates for total plasma homocysteine concentration was folate (P = 0.002). CONCLUSION: We concluded that fasting plasma total homocysteine concentrations were within normal limits in children and adolescents with type 1 diabetes who were without any clinical evidence of microvascular and macrovascular complications.

Superoxide dismutase and glutathione peroxidase enzyme activities in larynx carcinoma.

CONCLUSIONS: It can be concluded that these changes are related to damage at the DNA level or to the inhibitory effects of tumor promoters. Increases in GSH-Px activities may be related to the independence of this enzyme from the suppressive effects of tumor promoters. This study and others in the literature show that it is not possible to generalize the activities of SOD and GSH-Px in cancer. OBJECTIVE: There has been growing interest in the role of free radicals as a cause of cancer. It has been suggested that an increase in activated forms of oxygen in cells due to overproduction and/or the inability to destroy them may lead to severe damage of cell structures. As a result of these changes, some chromosomal aberrations and carcinogenesis may develop. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) are two important antioxidant enzymes involved in enzymatic antioxidant defense mechanisms. To our knowledge there have been no previous studies in the literature investigating the activities of SOD and GSH-Px in laryngeal cancer. MATERIAL AND METHODS: The study subjects comprised 10 male patients (age range 43-76 years) with laryngeal carcinoma and 10 healthy controls (4 males, 6 females; age range 40-69 years) with intraoral hyperplastic fibrous tissue. Homogenate SOD and GSH-Px activities were measured using commercially available kits. RESULTS: GSH-Px levels were significantly increased in the cancerous tissues compared with cancer-free adjacent tissues and fibrous hyperplasia tissues (p < 0.05), whereas there was no significant difference between SOD activities (p > 0.05). There was also no significant difference between GSH-Px activity in cancer-free adjacent tissues and fibrous hyperplasia tissues (p > 0.05).

Effects of hypertonic saline, HAES and dimethylsulphoxide on free oxygen radicals in haemorrhagic shock oxygen radicals in haemorrhagic shock.

BACKGROUND: The aim of this study was to investigate the effects of antioxidant and resuscitation fluids which were used during haemorrhagic shock on tissue ischemia. METHODS: Forty New Zealand type rabbits were divided into four groups as C (control), I (hypertonic saline), H (HAES) and D (Dimethylsulphoxide-DMSO). Haemorrhagic shock was induced by bleeding from carotid artery. Thirty minutes after shock, Group C was not resuscitated while Group I was resuscitated with Hypertonic saline 7.2, Group H with 10 % HAES and Group D with HAES 10 % and DMSO. Thiobarbituric acid reactive substances (TBARS) and lactate levels in blood, liver and small bowel samples were measured. RESULTS: There were no significant differences among the groups tissue and plasma TBARS and lactate levels. CONCLUSION: Resuscitation fluids and addition of antioxidants to the resuscitation fluids do not have any superiorities over each other to prevent tissue ischemic insult in haemorrhagic shock.

Enteral glutamine supplementation and dexamethasone attenuate the local intestinal damage in rats with experimental necrotizing enterocolitis.

The pathogenesis of necrotizing enterocolitis (NEC) presumptively is due to an inappropriate intestinal epithelial immunologic response of immature gut to luminal stimuli. Glutamine is essential for intestinal crypt cell proliferation and enhances the cellular response to growth factors. We aimed to test the hypothesis that the supplementation of enteral feedings with glutamine may stimulate an immature intestine and decrease the intestinal inflammatory change in NEC. Immediately after birth, the neonatal rats were weighed and randomized into one of four treatment groups. Group 1 consisted of rats whom were breast-fed. Group 2 (NEC group) consisted of neonates whom were fed with a special rodent formula. Rats in groups 3 and 4 were fed in a similar fashion to those in group 2, and glutamine 0.3 mg/kg per day and dexamethasone 0.5 mg/kg per day were added to their formula, respectively. The neonatal rats were weighed and killed on day 4: the last 4 cm of terminal ileum was harvested for morphological studies and detection of nitrite and nitrate levels in tissue. The animals in the NEC group showed various degrees of inflammatory changes similar to clinical NEC. The inflammatory changes of the intestine appeared to be attenuated in both glutamine- and steroid-treated animals compared to those in the NEC group. Only steroid treatment decreased the tissue levels of these nitrogen oxides that were increased in rats in the NEC group. We herein provide evidence that maturational agents such as glutamine and dexametasone can attenuate the local intestinal inflammatory damage in experimental NEC. These findings support the hypothesis that the gut immaturity in premature infants represents a risk factor for NEC.