RESUMO
Vitamin E is important because of its antioxidant activity in situations of oxidative stress, especially postnatally. Hence, the objective was to verify whether maternal alpha-tocopherol level is associated with the alpha-tocopherol levels of the newborn and colostrum. This is a cross-sectional study of 58 women and their term newborns from a public hospital. Blood and colostrum were collected to measure alpha-tocopherol levels by high-performance liquid chromatography. Mothers with serum alpha-tocopherol levels <16.2 mmol L(-1) and newborns <11.6 mmol L(-1) were indicative of deficiency or low levels. Mothers were divided into two groups: <16.2 mmol L(-1) and those with levels ≥16.2 mmol L(-1) . The mean (95% confidence interval) serum alpha-tocopherol levels of mothers, umbilical cords and colostrum were 28 (24-32), 6 (5-8) and 39 mmol L(-1) (32-45), respectively (P < 0.001); 19% of the women and 90% of the newborns had low alpha-tocopherol levels. Maternal alpha-tocopherol level was associated with that of the umbilical cord. Newborns from mothers at risk of deficiency had low alpha-tocopherol levels (P < 0.001). Colostrum levels of vitamin E were not influenced by maternal serum. Maternal deficiency influenced the vitamin E level of the umbilical cord but does not in the colostrum, evidencing distinct transfer mechanisms via the mammary gland.
Assuntos
Colostro/química , Fenômenos Fisiológicos da Nutrição Materna , Vitamina E/sangue , alfa-Tocoferol/sangue , Adolescente , Adulto , Estudos Transversais , Feminino , Humanos , Recém-Nascido , Lactação , Mães , Estado Nutricional , Gravidez , Cordão Umbilical/química , Deficiência de Vitamina E/sangue , Deficiência de Vitamina E/diagnóstico , Adulto JovemRESUMO
In order to investigate the pathogenic mechanism responsible for liver injury associated with chronic alcoholism, we studied the effects of different dietary vitamin E levels in chronically ethanol (EtOH)-fed rats on the activity and mRNA regulation of the manganese superoxide dismutase (MnSOD) enzyme. Evidence is accumulating that intermediates of oxygen reduction may in fact be associated with the development of alcoholic liver disease. Since low vitamin E liver content seems to potentiate EtOH-linked oxidative stress, we studied the effect of EtOH treatment in livers from rats fed a diet deficient or supplemented with vitamin E. Chronic EtOH feeding enhanced hepatic consumption of vitamin E in both groups of EtOH-treated animals, irrespectively of the vitamin E level of the basal diet and the effect was observed in both the microsomal and mitochondrial fractions. Both EtOH-fed groups exhibited increased MnSOD gene expression, while the enzyme activity was enhanced only in the vitamin E-deprived group of EtOH-treated animals. The significant increase in manganese liver content found only in this last group could explain the rise of enzyme activity. In fact, in the absence of a parallel increase of the prosthetic ion manganese, MnSOD mRNA induction was not accompanied by a higher enzymatic activity. These findings support the role of oxidative alteration in the EtOH-induced chronic hepatotoxicity in which MnSOD response might represent a primary defence mechanism against the damaging effect of oxygen radical species.
Assuntos
Alcoolismo , Modelos Animais de Doenças , Etanol/farmacologia , Alimentos Formulados , Superóxido Dismutase/efeitos dos fármacos , Deficiência de Vitamina E/diagnóstico , Vitamina E/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Doença Crônica , Masculino , RNA Mensageiro/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
OBJECTIVE: To prospectively evaluate the biochemical status of vitamins A, D, and E in children with cystic fibrosis (CF). SUBJECTS: A total of 127 infants identified by the Colorado CF newborn screening program. DESIGN: Vitamin status (serum retinol, 25-hydroxy vitamin D, ratio of alpha-tocopherol/total lipids) and serum albumin were assessed at diagnosis (4 to 8 weeks), ages 6 months, 12 months, and yearly thereafter, to age 10 years. RESULTS: Deficiency of 1 or more vitamins was present in 44 (45.8%) of 96 patients at age 4 to 8 weeks as follows: vitamin A 29.0%, vitamin D 22.5%, and vitamin E 22.8%. Of these patients with initial deficiency, the percent that was deficient at 1 or more subsequent time points, despite supplementation, was vitamin A 11.1%, vitamin D 12.5%, and vitamin E 57.1%. Of the initial patients with vitamin sufficiency, the percent who became deficient at any time during the 10-year period was as follows: vitamin A 4.5%, vitamin D 14.4%, and vitamin E 11.8%. The percent of patients deficient for 1 or more vitamins ranged from 4% to 45% for any given year. CONCLUSIONS: Despite supplementation with standard multivitamins and pancreatic enzymes, the sporadic occurrence of fat-soluble vitamin deficiency and persistent deficiency is relatively common. Frequent and serial monitoring of the serum concentrations of these vitamins is therefore essential in children with CF.
Assuntos
Fibrose Cística/metabolismo , Deficiência de Vitamina A/epidemiologia , Deficiência de Vitamina D/epidemiologia , Deficiência de Vitamina E/epidemiologia , Criança , Pré-Escolar , Fibrose Cística/diagnóstico , Fibrose Cística/tratamento farmacológico , Seguimentos , Fármacos Gastrointestinais/uso terapêutico , Humanos , Lactente , Recém-Nascido , Triagem Neonatal , Pancrelipase/uso terapêutico , Estudos Prospectivos , Fatores de Tempo , Vitamina A/sangue , Deficiência de Vitamina A/diagnóstico , Vitamina D/sangue , Deficiência de Vitamina D/diagnóstico , Vitamina E/sangue , Deficiência de Vitamina E/diagnóstico , Vitaminas/uso terapêuticoRESUMO
OBJECTIVE: To determine the oral supplement doses of dl-alpha-tocopheryl-acetate to maintain normal serum alpha-tocopherol concentrations in children with chronic cholestasis and vitamin-E deficient. BACKGROUND: Malabsorption and deficiency of vitamin E in children with chronic cholestasis causes a progressive, neuromuscular degeneration at approximately 18-24 months of life, if left untreated. Using prompt treatment, it can be completely prevented and reversed to normal. METHOD: Longitudinal, prospective and comparative study was performed on consecutive sixty vitamin E deficient children with chronic cholestasis divided in three groups. After initial evaluation, therapy was started for 15 days in each group with 100 IU, 200 IU and 400 IU/day of oral dl-alpha-tocopheryl-acetate, respectively; alpha-tocopherol-status, neurological function and biochemical parameters were monitored during therapy. RESULTS: Any oral supplement does administrated for 15 days of dl-alpha-tocopheryl-acetate were enough to maintain the normalization of alpha-tocopherol status (p > 0.06). Neurological function, which had not deteriorated before entry in the trial, stabilized in all after 15 days of therapy. No adverse effects were observed. CONCLUSIONS: Oral supplement of dl-alpha-tocopheryl-acetate for 15 days with 100 IU, 200 IU, and 400 IU, in spite of safety, weren't enough to maintain the alpha-tocopherol serum concentration in children with chronic cholestasis and vitamin-E deficient.
Assuntos
Antioxidantes/administração & dosagem , Colestase/tratamento farmacológico , Deficiência de Vitamina E/tratamento farmacológico , Vitamina E/análogos & derivados , alfa-Tocoferol/análogos & derivados , Adolescente , Fatores Etários , Criança , Pré-Escolar , Colestase/diagnóstico , Doença Crônica , Feminino , Humanos , Lactente , Estudos Longitudinais , Masculino , Estudos Prospectivos , Fatores de Tempo , Tocoferóis , Vitamina E/administração & dosagem , Deficiência de Vitamina E/diagnósticoRESUMO
Vitamin E malabsorption and deficiency during chronic childhood cholestasis has been associated with a progressive ataxic neurologic syndrome. Hyporeflexia, the first sign of neurologic dysfunction, may begin prior to age 2 years, but severe symptoms do not develop until age 5 to 10 years. To establish the age of onset of neuropathologic lesions, we prospectively evaluated four young children with severe cholestasis. Malabsorption and deficiency of vitamin E were documented by low serum vitamin E concentrations, low serum vitamin E to total serum lipids ratios, elevated hydrogen peroxide hemolysis, and impaired absorption of a pharmacologic dose of alpha-tocopherol. Abnormal neurologic findings in two patients were limited to areflexia, ptosis, mild truncal ataxia, and hypotonia; two patients had minimal signs of neurologic dysfunction. Sural nerve histology at age 6 to 25 months revealed a degenerative axonopathy involving large-caliber myelinated fibers, but without quantitative axonal loss. Muscle histology and histochemistry tests yielded normal results. Our study suggests that neurologic injury may occur during the first two years of life in vitamin E-deficient children with cholestatic hepatobiliary disease, obligating aggressive attempts at correcting this deficiency state at a very young age.