IGEVET   21075
INSTITUTO DE GENETICA VETERINARIA "ING. FERNANDO NOEL DULOUT"
Unidad Ejecutora - UE
artículos
Título:
Protein-energy malnutrition contributes to increased structural
Autor/es:
PADULA, GISEL; SALCEDA, SUSANA; SEOANE, ANALIA
Revista:
NUTRITION RESEARCH
Editorial:
Elsevier
Referencias:
Lugar: Amsterdam, Holanda; Año: 2009 vol. 29 p. 35 - 40
ISSN:
0271-5317
Resumen:
The relationship between protein-energy malnutrition and genetic damage has been studied in 12 human beings and laboratory animals, but results are still conflicting. The aim of the present studyhuman beings and laboratory animals, but results are still conflicting. The aim of the present study 13 was to assess the induction of structural chromosomal aberrations in peripheral blood lymphocyteswas to assess the induction of structural chromosomal aberrations in peripheral blood lymphocytes 14 of children with primary protein-energy malnutrition. A case-control study was performed.of children with primary protein-energy malnutrition. A case-control study was performed. 15 Samples were obtained from 25 primary malnourished infants (mean age, 22 months; range, 1-66Samples were obtained from 25 primary malnourished infants (mean age, 22 months; range, 1-66 16 months). The control group consisted of 35 eutrophic Q1 children from the same population who weremonths). The control group consisted of 35 eutrophic Q1 children from the same population who were 17 matched 1:1 by age and sex. Anthropometric and clinic evaluations were performed to assessmatched 1:1 by age and sex. Anthropometric and clinic evaluations were performed to assess 18 nutritional condition. Before blood collection, we interviewed each individual´s parent to completenutritional condition. Before blood collection, we interviewed each individual´s parent to complete 19 a semistructural survey specifying age, dietary habits, viral or bacterial diseases; previous exposurea semistructural survey specifying age, dietary habits, viral or bacterial diseases; previous exposure 20 to diagnostic x-rays; and use of therapeutic drugs. After 48 hours, 100 cultured lymphocytes wereto diagnostic x-rays; and use of therapeutic drugs. After 48 hours, 100 cultured lymphocytes were 21 analyzed per patient. Statistical analysis was performed using the Epi Dat 3.0 program (P ¡Ü .05).analyzed per patient. Statistical analysis was performed using the Epi Dat 3.0 program (P ¡Ü .05). 22 The chromosomal aberration frequency was nearly 7 times higher in malnourished infants than inThe chromosomal aberration frequency was nearly 7 times higher in malnourished infants than in 23 controls (14.61% vs 2.2%, respectively). This difference was statistically significant (P b .001) andcontrols (14.61% vs 2.2%, respectively). This difference was statistically significant (P b .001) and 24 may be explained by the occurrence of achromatic lesions, breaks, and telomeric associations.may be explained by the occurrence of achromatic lesions, breaks, and telomeric associations. 25 DNA damage could be attributed to several factors: severe deficiency of essential nutrients (ieDNA damage could be attributed to several factors: severe deficiency of essential nutrients (ie 26 zinc, iron, and vitamin A) required in the synthesis of DNA maintenances factors; deterioration ofzinc, iron, and vitamin A) required in the synthesis of DNA maintenances factors; deterioration of 27 repair mechanisms allowing the persistence of an unusually high number of structuralrepair mechanisms allowing the persistence of an unusually high number of structural 28 chromosomal aberrations; and/or the absence of specific factors needed to protect the cell againstchromosomal aberrations; and/or the absence of specific factors needed to protect the cell against 29 oxidative DNA damageoxidative DNA damage