Hypoxia-induced free iron release in the red cells of newborn infants.

Heparinized blood samples were obtained at birth from 164 newborn infants (101 full term; 63 preterm). Intra-erythrocyte free iron concentration and hypoxanthine plasma levels were determined by high-pressure liquid chromatography. Intra-erythrocyte free iron concentration was higher in preterm than in full term babies (p < 0.0001) and adults (p < 0.0001). Statistically significant correlations were observed between intra-erythrocyte free iron concentration and hypoxanthine levels (r = 0.66; p = 0.0001), pH (r = -0.76; p = 0.0001), base excess (r = -0.79; p = 0.0001), and gestational age (r = -0.44; p = 0.0001) in both infant populations. Multiple regression analysis between intra-erythrocyte free iron concentration in cord blood, as an independent variable, and Apgar score at 1 min, pH, base excess, hypoxanthine values, FiO2 needed for resuscitation immediately after delivery, and gestational age, as dependent variables, identified hypoxanthine levels (p = 0.0003; partial F-test = 15.4) as the best single predictor of intra-erythrocyte free iron concentration. In conclusion, hypoxia induces intra-erythrocyte free iron release, and therefore enhances the risk of oxidative injury due to hydroxyl radical generation.

Effects of estradiol and medroxyprogesterone-acetate treatment on erythrocyte antioxidant enzyme activities and malondialdehyde plasma levels in amenorrhoic women.

Plasma levels of 17 beta-estradiol (E2) and malondialdehyde and erythrocyte antioxidant enzyme [superoxide dismutase, catalase, and glutathione-peroxidase (GSH-Px)] activities were evaluated in 20 healthy eumenorrhoic women (EW) on day 7 of the menstrual cycle and in 48 secondary hypothalamic amenorrhea patients (AP) (time 0). The AP were randomly divided into four subgroups of 12 subjects and treated with transdermal E2 for 30 days (subgroup A), oral medroxyprogesterone-acetate for 30 days (subgroup B), and transdermal E2 plus medroxyprogesterone-acetate for 30 days (subgroup C). The fourth subgroup acted as control. E2 and malondialdehyde plasma levels and superoxide dismutase, catalase, and GSH-Px activities were evaluated in subgroups A, B, and C on day 30 of therapy and in the control subgroup. GSH-Px activity was significantly higher in EW than in AP at time 0. A statistically significant increase in E2 plasma levels and GSH-Px activity was observed in subgroups A and C on day 30 of treatment, and there was a significant positive correlation between E2 plasma levels and GSH-Px activity in both subgroups. After a month of treatment, erythrocyte GSH-Px activity in subgroups A and C was not significantly different from that observed in EW. After a month of treatment, no significant variation was found in subgroup B nor in the control group. These results strongly suggest that when plasma E2 is restored to physiological levels in AP, it stimulates erythrocyte GSH-Px activity. Progesterone therapy did not induce significant modifications.

Changes in the erythrocyte antioxidant enzyme system during transdermal estradiol therapy for secondary amenorrhea.

Twenty-two hypothalamic amenorrheic patients, who were non-smokers and of normal weight, received replacement therapy for 1 month with transdermal patches containing 8 mg estradiol. No other drugs were prescribed or taken during the study. Before treatment (time 0) and 1 month after its start, blood samples were taken for assay of plasma estradiol levels, the erythrocyte antioxidant enzyme activities of superoxide dismutase, catalase, glutathione peroxidase (GSH-Px), and an age-dependent erythrocyte enzyme activity, pyruvate kinase. Plasma malondialdehyde levels, as an index of lipoperoxidation products, were also detected. The results showed no significant variations in superoxide dismutase, catalase, pyruvate kinase erythrocyte enzyme activities or plasma malondialdehyde levels. A significant increase in plasma estradiol levels (time 0, 17.33 +/- 4.12 pg/ml; 1 month, 81.25 +/- 10.45 pg/ml; means +/- SD; p < 0.0001) and in GSH-Px erythrocyte activity (time 0, 11.97 +/- 2.31 IU/g hemoglobin; 1 month, 16.88 +/- 4.38 IU/g hemoglobin; p < 0.004) was found. Plasma estradiol levels correlated significantly with GSH-Px erythrocyte activity 1 month after therapy was begun (r = 0.776, p < 0.003). We suggest that estrogens restored to physiological plasma levels, stimulate erythrocyte antioxidant GSH-Px activity, improving the antioxidant power of amenorrheic patients.

Determination of red blood cell superoxide dismutase and glutathione peroxidase in newborns in relation to neonatal hemolysis.

Superoxide dismutase and glutathione peroxidase activities have been determined in newborns. Their mean values are approximately the same as in normal adults. In some cases a low content of superoxide dismutase and/or a high (superoxide dismutase/glutathione peroxidase) ratio are associated with hematological symptoms. In addition, a low superoxide dismutase activity is associated with hyperbilirubinemia and is present in two of the three cases showing maximal acetylphenylhdrazine-induced hemoloysis.

Familial tyrosinaemia with eye and skin lesions. Presentation of two cases.

Two cases of tyrosinaemia with eye and skin lesions typical of the Richner-Hanhart syndrome are described. The patients are a 29- and 26-year-old brother and sister. They do not show neurological abnormalities or mental retardation. Parents are not consanguineous and family history is negative for similar conditions. The diagnosis of type II tyrosinaemia was based upon an increase of blood tyrosine (14-16mg/100 ml), tyrosinuria and absence of liver and kidney abnormalities. The treatment with a low tyrosine phenylalanine diet has resulted in a disappearence of the ocular manifestations while the cutaneous lesions are much improved.