Anti-oxidant profiles and markers of oxidative stress in preterm neonates.

BACKGROUND: Preterm birth is associated with an increased oxidant burden which places these infants at a higher risk of injury. AIMS: This prospective study aimed to assess levels of antioxidants and a marker of oxidative stress in preterm neonates. OBJECTIVES: (i) To compare levels of anti-oxidants [vitamin A, vitamin E, catalase, total anti-oxidant status (TAS)] as well as malondialdehyde level (MDA) (a marker of lipid peroxidation) between preterm and full-term neonates; (ii) to determine changes in the values of measured vitamins at birth and at discharge among preterm neonates; and (iii) to compare levels of anti-oxidants with MDA levels in relation to complications of prematurity and outcome. METHODS: The study was undertaken in 100 preterm neonates and 100 full-term neonates as a control group. MDA was estimated by a thiobarbituric acid-reactive technique; TAS was determined using a Randox assay kit; catalase activity was measured spectrophotometrically and vitamin A and E levels were estimated by high performance liquid chromatography. RESULTS: The plasma levels of vitamin A, vitamin E, TAS and catalase were significantly lower in the preterm than in the full-term group (P < 0.01), and the plasma level of MDA was significantly higher in preterm than full-term neonates (P < 0.01). Vitamin A and E levels in preterm neonates were significantly higher at discharge than at birth (P < 0.01). Vitamin A, vitamin E and catalase levels at birth were significantly lower in patients who developed necrotizing enterocolitis or bronchopulmonary dysplasia than in those who did not. CONCLUSION: Preterm neonates are exposed to increased oxidant stress at birth and are susceptible to anti-oxidant deficiencies. A higher dose of enteral vitamin A supplementation in preterm neonates might reduce morbidity and improve outcome. Further studies are warranted to evaluate the appropriate dose of oral vitamin E supplementation for preterm neonates.

Effect of aspartame on oxidative stress and monoamine neurotransmitter levels in lipopolysaccharide-treated mice.

This study aimed at investigating the effect of the sweetener aspartame on oxidative stress and brain monoamines in normal circumstances and after intraperitoneal (i.p.) administration of lipopolysaccharide (LPS; 100 µg/kg) in mice. Aspartame (0.625-45 mg/kg) was given via subcutaneous route at the time of endotoxin administration. Mice were euthanized 4 h later. Reduced glutathione (GSH), lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), and nitrite concentrations were measured in brain and liver. Tumor necrosis factor-alpha (TNF-α) and glucose were determined in brain. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in liver. The administration of only aspartame (22.5 and 45 mg/kg) increased brain TBARS by 17.7-32.8%, decreased GSH by 25.6-31.6%, and increased TNF-α by 16.7-44%. Aspartame caused dose-dependent inhibition of brain serotonin, noradrenaline, and dopamine. Aspartame did not alter liver TBARS, nitrite, GSH, AST, ALT, or ALP. The administration of LPS increased nitrite in brain and liver by 26.8 and 37.1%, respectively; decreased GSH in brain and liver by 21.6 and 31.1%, respectively; increased brain TNF-α by 340.4%, and glucose by 39.9%, and caused marked increase in brain monoamines. LPS increased AST, ALT, and ALP in liver tissue by 84.4, 173.7, and 258.9%, respectively. Aspartame given to LPS-treated mice at 11.25 and 22.5 mg/kg increased brain TBARS by 15.5-16.9%, nitrite by 12.6-20.1%, and mitigated the increase in monoamines. Aspartame did not alter liver TBARS, nitrite, GSH, ALT, AST, or ALP. Thus, the administration of aspartame alone or in the presence of mild systemic inflammatory response increases oxidative stress and inflammation in the brain, but not in the liver.