IGEVET   21075
INSTITUTO DE GENETICA VETERINARIA "ING. FERNANDO NOEL DULOUT"
Unidad Ejecutora - UE
artículos
Título:
Protein-energy malnutrition contributes to increase structural chromosomal alterations frequencies in Argentinean children: a case-control study.
Autor/es:
PADULA G, SALCEDA SA Y SEOANE AI
Revista:
NUTRITION RESEARCH
Editorial:
Heldref Publications, Helen Dwight Reid Educational Foundation
Referencias:
Lugar: Washington; Año: 2009 vol. 29 p. 35 - 40
ISSN:
0271-5317
Resumen:
The relationship between PEM and genetic damage has been studied in human beings and laboratory animals, but results are still conflicting. The aim of the present study was to assess the induction of Structural Chromosomal Aberrations (SCA) in peripheral blood lymphocytes of children suffering from primary protein-energy malnutrition (pPEM). A case-control study was performed. Samples were obtained from twenty-five primary malnourished infants (mean age 22 month, range 1 and 66). The control group consisted of twenty-five euthrophic children from the same population, whom were matched 1:1 by age and sex. Anthropometric and clinic evaluation were performed to assess nutritional condition. Prior to blood collection, we interviewed each individual¡¯s parent to complete a semi-structural survey specifying age, dietary habits, viral or bacterial diseases, previous exposure to diagnostic x-rays and use of therapeutic drugs. After 48 hours, 100 cultured lymphocytes were analyzed per patient. Statistical analysis was performed by the Epi Dat 3.0 program (P ¡Ü .05). The chromosomal aberration frequency was nearly seven times higher in malnourished infants than controls (14.61% versus 2.2%, respectively). This difference was statistically significant (P < 0.001) and may be explained by the occurrence of achromatic lesions, breaks and telomeric associations. DNA damage could be attributed to several factors: Severe deficiency of essential nutrients (e.i. zinc, iron, and vitamin A) required in the synthesis of DNA maintenances factors, deterioration of repair mechanisms allowing the persistence of an unusually high number of SCAs, and/or the absence of specific factors needed to protect the cell against oxidative DNA damage.