Possible radioprotective effect of folic acid supplementation on low dose ionizing radiation-induced genomic instability in vitro.

Ionizing radiation (IR) induces DNA damage through production of single and double-strand breaks and reactive oxygen species (ROS). Folic acid (FA) prevents radiation-induced DNA damage by modification of DNA synthesis and/or repair and as a radical scavenger. We hypothesized that in vitro supplementation with FA will decrease the sensitivity of cells to genetic damage induced by low dose of ionizing radiation. Annexin V, comet and micronucleus assays were performed in cultured CHO cells. After 7 days of pre-treatment with 0, 100, 200 or 300 nM FA, cultures were exposed to radiation (100 mSv). Two un-irradiated controls were executed (0 and 100 nM FA). Data were statistically analyzed with X2-test and linear regression analysis (P 0.05). We observed a significantly decreased frequency of apoptotic cells with the increasing FA concentration (P <0.05). The same trend was observed when analyzing DNA damage and chromosomal instability (P <0.05 for 300 nM). Only micronuclei frequencies showed significant differences for linear regression analysis (R2=94.04; P <0.01). Our results have demonstrated the radioprotective effect of folic acid supplementation on low dose ionizing radiation-induced genomic instability in vitro; folate status should be taken into account when studying the effect of low dose radiation in environmental or occupational exposure.

Alteraciones cromosómicas en niños con malnutrición proteico-energética: resultados preliminares / Chromosomic alterations in child by malnutrition energetics-proteine: results preliminary

Objetivos: algunos autores encontraron una relación entre la Malnutrición Proteico Energética (MPE) y elaumento de la frecuencia de Aberraciones Cromosómicas Estructurales (ACE) en niños menores de 5 años.El objetivo del siguiente trabajo es analizar la incidencia de ACE en una población de niños del partido de La Plata que presentan MPE. Material y Métodos: se tomó una muestra de 30 niños de 1 a 60 meses de edad cronológica, 15 controles sanos y 15 diagnosticados como MPE primarios a través de una evaluación antropométrica y clínica. Se aplicó una encuesta semiestructurada en la que se tuvieron en cuenta peso al nacimiento, variables antropométricas, alimentación, enfermedades virales, y/o infecciosas y exposición a agentes potencialmente genotóxicos. Se realizaron cultivos de sangre periférica y se analizó la frecuencia de ACE en 100 células por individuo. Los resultados obtenidos fueron sometidos a evaluación estadística utilizando el programa Epi Info 6.0. Resultados: la diferencia en la frecuencia global de ACE entre ambas muestras resultó significativa. Al tratar cada tipo de aberración en forma independiente se encontraron diferencias significativas para gaps y fracturas de mono e isocromátidas, cromosomas dicéntricos, fragmentos y asociaciones telométricas. No se encontraron diferencias significativas respecto a la exposición de los niños a agentes potencialmente genotóxicos tales como medicamentos, radiaciones, pesticidas y desechos industriales. Conclusiones: la MPE es capaz de inducir daño genotóxico, este efecto podria explicarse por la distorsión del ambiente químico interno o bien por la disminución de la acción de los mecanismos de reparación del ADN como consecuencia del déficit proteico

Protective effect of butylated hydroxytoluene (BHT) against the clastogenic acitivity of cadmium chloride and potassium dichromate in hamster ovary cells

The effect of butylated hydroxytoluene (BHT), a widely used food additive, on chromosomal alterations induced by cadmium chloride (CC) and potassium dichromate (PD) in Chinese hamster ovary (CHO) cells was studied both at metaphase and anaphase-telophase. CHO cells were cultured for 15-16 h in the presence of PD (6.0, 9.0 or 12.0 mM), BHT (1.0 mg/ml), or PD plus BHT as well as CC (0.5, 1.0 and 2.0 mM), BHT or CC plus BHT for the analysis of chromosomal aberrations. To perform the anaphase-telophase test, cells were cultured in cover glasses and treated 8 h before fixation with the same chemicals. An extra dose of CC (4 mM) was used in this test. Both metal salts significantly increased chromosomal aberration frequencies in relation to untreated controls, and to DMSO- and BHT-treated cells. Post-treatment with BHT decreased the yield of chromosomal damage in relation to treatments performed with CC and PD. However, chromosomal aberration frequencies were significantly higher than those of the controls. In the anaphase-telophase test, CC significantly increased the yield of lagging chromosomes with the four doses employed and the frequency of lagging fragments with the highest dose. In combined treatments of CC and BHT, frequencies of the two types of alterations decreased significantly in relation to the cells treated with CC alone. No significant variation was found in the frequencies of chromatin bridges. Significant increases of numbers of chromatin bridges, lagging chromosomes and lagging fragments were found in cells treated with PD. The protective effect of BHT in combined treatments was evidenced by the significant decrease of chromatid bridges and lagging chromosomes in relation to PD-treated cells. Whereas BHT is able to induce chromosomal damage, it can also protect against oxidative damage induced by other genotoxicants.