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Protein-energy malnutrition contributes to increased structural chromosomal alteration frequencies in Argentinean
Gisel Padula1, Susana A Salceda, Analia I Seoane
1IGEVET, Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata-CONICET, Argentina; IDIP (MS/CIC-PBA) Hospital de Niños de La Plata, Ministerio de Salud de la Provincia de Buenos Aires, Argentina. giselpadula@yahoo.com.ar
Insights
Protein-energy malnutrition significantly increases genetic damage in children. Malnourished infants showed a nearly 7-fold higher frequency of chromosomal aberrations compared to healthy controls, highlighting critical nutrient and repair mechanism roles.
Area of Science:
- Biochemistry
- Genetics
- Pediatrics
Background:
- Conflicting results exist regarding the link between protein-energy malnutrition (PEM) and genetic damage.
- Previous studies in humans and animals have explored this relationship with inconclusive findings.
Purpose of the Study:
- To investigate the induction of structural chromosomal aberrations in peripheral blood lymphocytes of children suffering from primary protein-energy malnutrition.
- To compare the frequency of these aberrations in malnourished children versus a matched control group.
Main Methods:
- A case-control study involving 25 malnourished infants and 25 age- and sex-matched eutrophic children.
- Assessment of nutritional status via anthropometric and clinical evaluations.
- Analysis of 100 cultured lymphocytes per patient for chromosomal aberrations after a 48-hour culture period.
Main Results:
- The frequency of chromosomal aberrations was significantly higher (P < .001) in malnourished infants (14.61%) compared to controls (2.2%), representing a nearly 7-fold increase.
- Specific aberrations observed included achromatic lesions, breaks, and telomeric associations.
- Statistical analysis was performed using Epi Dat 3.0.
Conclusions:
- Primary protein-energy malnutrition is associated with a substantial increase in structural chromosomal aberrations in children.
- This DNA damage may stem from deficiencies in essential nutrients (e.g., zinc, iron, vitamin A), impaired DNA repair mechanisms, or reduced protection against oxidative stress.
Abstract:
The relationship between protein-energy malnutrition 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 in peripheral blood lymphocytes of children with primary protein-energy malnutrition. A case-control study was performed. Samples were obtained from 25 primary malnourished infants (mean age, 22 months; range, 1-66 months). The control group consisted of 25 eutrophic children from the same population who were matched 1:1 by age and sex. Anthropometric and clinic evaluations were performed to assess nutritional condition. Before 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 using the Epi Dat 3.0 program (P < or = .05). The chromosomal aberration frequency was nearly 7 times higher in malnourished infants than in controls (14.61% vs 2.2%, respectively). This difference was statistically significant (P < .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 (ie zinc, iron, and vitamin A) required in the synthesis of DNA maintenance factors; deterioration of repair mechanisms allowing the persistence of an unusually high number of structural chromosomal aberrations; and/or the absence of specific factors needed to protect the cell against oxidative DNA damage.
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