ABSTRACT
The purpose of this study was to determine the relationship between the pollution levels recorded in Madrid and the number of hospital admissions made on the grounds of respiratory disorders.
Subject(s)
Air Pollution/adverse effects , Respiratory Tract Diseases/etiology , Air Pollution/analysis , Hospitalization , Humans , Respiratory Tract Diseases/epidemiology , Spain/epidemiology , Urban HealthABSTRACT
We have investigated the effects of iodine (I) intake on urinary I excretion in preterm (PT) babies up to 2 months after birth and its effect on serum T4, free T4 (FT4), T3, TSH, and thyroglobulin (Tg) levels compared to those in term (T) newborns. Very premature and very sick infants were in negative I balance for the first weeks after birth. Later, these same infants, as well as the other PT and T newborns, were in positive balance; 75- 80% of the ingested I was not accounted for in the urine. The urinary I levels of PT and T neonates cannot be equated to their I intakes. T4, FT4, and T3 levels in PT and T neonates increased with postmenstrual age, whereas Tg decreased and TSH did not change. Serum FT4, T3, Tg, and TSH levels in PT neonates were affected negatively, independently from age, by a low I intake. PT birth also affected T4, FT4, and Tg negatively, independently from I intake and postmenstrual age, for at least 6-8 weeks after birth. Care should be taken to avoid I deficiency in PT neonates. However, even when I intake is adequate, PT newborns are hypothyroxinemic compared to T babies during an important period of brain development. This suggests the possible convenience of interventions that might mimic the intrauterine hormone environment and accelerate maturation.
Subject(s)
Diet , Infant, Newborn/blood , Infant, Premature/blood , Iodine/administration & dosage , Thyroxine/blood , Creatinine/urine , Fetal Blood , Humans , Infant , Iodine/metabolism , Iodine/pharmacology , Thyroid Function Tests , Thyroid Gland/physiology , Urine/chemistryABSTRACT
As part of a study of thyroid function in premature babies, the iodine content of their mothers' breast milk, that of 32 formulas from different brands used in Spain, and that of 127 formulas used in other countries was determined. Breast milk contained more iodine--mean (SEM) 10 (1) microgram/dl--than most of the formulas, especially those for premature babies. Iodine intakes were therefore below the recommended daily amount (RDA) for newborns: babies of 27-30 weeks' gestational age took 3.1 (1.1) micrograms/day at 5 days of age and 29.8 (2.7) micrograms by 2 months of age. This problem is not exclusive to Spanish premature babies as the iodine content of many of the formulas on sale in other countries was also inadequate. It is concluded that preterm infants who are formula fed are at high risk of iodine deficiency.
Subject(s)
Infant Food/analysis , Infant, Premature/metabolism , Iodine/deficiency , Bottle Feeding , Female , Humans , Infant, Newborn , Iodine/administration & dosage , Iodine/analysis , Iodine/metabolism , Milk, Human/chemistry , Nutrition Policy , Pregnancy , SpainABSTRACT
Liver, kidney, and lung microsomes prepared from nonpretreated female Sprague-Dawley rats catalyze the NADPH- and oxygen-dependent S-oxygenation of para-methoxyphenyl-1,3-dithiolane. Studies on the biochemical mechanism of dithiolane S-oxygenation in liver, kidney, and lung microsomes suggest that this reaction is catalyzed in a diastereoselective and enantioselective fashion by the flavin-containing monooxygenase and, to a lesser extent, the cytochromes P-450. This conclusion is based on results examining the effects of selective cytochrome P-450 inhibitors and positive effectors, microsome heat-inactivation treatment, and alternate substrates for the flavin-containing monooxygenase. Liver and kidney microsomes prepared from ovarectomized female rats tended to have decreased S-oxygenase activity, compared with nonpretreated female rats, whereas ovarectomized rats pretreated with estradiol had markedly lower S-oxygenase activity. In contrast, lung microsomal S-oxygenase activity, which is low in pulmonary microsomes from nonpretreated female rats, increases 2-4-fold after ovariectomization and estradiol pretreatment. In female Sprague-Dawley rats, estradiol pretreatment is mainly responsible for the large decrease (or increase) in S-oxygenase activity observed in the tissues examined, although it is unlikely that estradiol alone controls flavin-containing monooxygenase S-oxygenase activity.
