Efectos de la suplementacion dietaria con soja en un modelo experimental de cáncer de colon / Effects of dietary supplementation with soya on a colon cancer experimental model

Objetivos: Estudiar la acción de la leche de soja en la aparición de focos de criptas displásicas (FCD) en un modelo experimental de cáncer de colon y su relación con el estrés oxidativo, la actividad apoptótica y la inestabilidad genómica. Metodología: La inducción de la carcinogénesis se produjo en ratas Wistar machos adultas por inoculación subcutánea de 1,2-dimetilhidrazina (DMH) (20 mg/kg) 2 dosis semanales de DMH durante 8 semanas. Se trabajó con 3 grupos (N=12 c/u): A) Control normal con dieta estándar B) Control de carcinogénesis, inoculados con DMH y dieta estándar C) Experimental: inoculados con DMH, con dieta con leche de soja. Los animales se estudiaron a los 4, 5 y 6 meses después de la última inoculación. El colon fue procesado con técnicas histológicas convencionales, se determinó proteína P53 (inmunohistoquímica) y actividad apoptó- tica (Test de Tunel). En suero se determinó (NO) Óxido Nítrico. En homogenatos de hígado se dosó malonildialdehído (MDA). Resultados: En el período estudiado los animales experimentales no desarrollaron cáncer, en tanto que en los controles de carcinogénesis, se detectaron tumores a partir del 5º mes. La detección de indicadores displásicos (FCD) se relacionó con la sobreexpresión de la proteína P53, el aumento de la actividad apoptótica y la disminución de NO y MDA. Conclusiones: La administración de leche de soja, como suplemento dietario por un tiempo prolongado podría retardar la aparición de FCD. La función anticancerígena se debería a la acción antioxidante de la soja que dismunuiría los daños acumulativos sobre el ADN (AU)

Objectives: to study the effects of soy milk consumption in the occurrence of dysplastic crypt foci (DCF) in an experimental model of colon cancer. To relate oxidative stress with apoptotic activity and genomic unsteadiness. Methods: experimental model of colon cancer was achieved by subcutaneous injections of 1,2-dimetilhidrazina (DMH, 20 mg/Kg) twice a week during eight weeks in adult male Wistar rats. Three groups were studied: A) Normal control: saline injections and standard diet (commercial formula and water ad libitum); B) Carcinogenesis control: DMH inoculation and standard diet; C) Experimental: DMH inoculation, soy diet (commercial formula and soy milk). Four rats of each group were study 4, 5 and 6 months after last inoculation: colon tissue was processed with conventional histological techniques; protein P53 was determined by inmunhistochemistry. Apoptotic activity was measured by Tunel test, Nitric Oxide in serum and malondialdehyde in liver homogenates were also determined. Results: Experimental rats did not develop cancer in the studied period, while we found tumors in carcinogenesis control groups in the 5th month. Dysplastic indicators (DCF) were related with P53 over expression, augmented apoptotic activity and decreases of nitric oxide and malondialdehyde. Conclusions: Soy milk intake as diet supplement for prolonged time could delay de DCF emergence. These anticancers effects may be due to the soy antioxidative action, that could decrease the accumulative ADN damage (AU)

Effects of soy milk as a dietary complement during the natural aging process.

INTRODUCTION: Oxidative stress is one mechanism that could contribute to the acceleration of aging and age-related diseases. On the other hand, because of their antioxidative qualities soybean derived foods could have beneficial effects on the aging process. OBJECTIVES: The aim of our work was to study the effects of a diet supplemented with soy milk on certain biological features of aging in rats. METHODS: Male Wistar rats of 3 to 18 months of age, were assigned to one of two diets: 1) Experimental Group, commercial rat formula and soy milk; 2) Control Group, commercial rat formula and water. Every three months both lipid profile and lipid peroxidation were determined and neuronal cells of hippocampus were counted in control and experimental rats. RESULTS: The soy milk diet significantly improved the plasmatic lipid profile, decreasing serum cholesterol (total as well as LDL) and serum triglycerides, HDL-cholesterol was significatively higher in experimental animals. The LDL/HDL ratio was thus significantly lowered. The soy diet also produced decreased values of lipid peroxidation in brain, liver and kidney. These effects were significant after 6 to 9 months. The experimental animals lost fewer hippocampal neurons than the controls. Finally at 18 months of age, a greater number of surviving animals in experimental group with respect to the control one was observed. CONCLUSIONS: 1) soy intake could have beneficial effects as a complement of normal diet, but not as a replacement for animal proteins and 2) these effects are the result of a very long period (almost lifelong) of consumption of this diet.

Recovery from experimental malnutrition with soymilk: immunological and genetic aspects.

Experimental malnutrition models have been useful to study the effects of malnutrition at early ages. Substantial evidence exists that malnutrition in critical stages of development could result in chromosomal damages. The effect of nutritional rehabilitation with soymilk as a complement of a restricted diet, on plasma and muscle proteins, chromosomal integrity, and unspecific and mucosa immune responses, was studied. Adult male and female Wistar rats (5 weeks old) were assigned to different nutritional conditions: (a) 14 days on protein restricted diet (corn flour and water), followed by 14 days in which water was replaced by soymilk, as nutritional rehabilitation; (b) the same conditions above but periods of 28 days of a protein restricted diet, and 28 days of nutritional rehabilitation and (c) age-matched malnourished (protein restricted diet without nutritional rehabilitation) and normally nourished controls. After both nutritional rehabilitation periods, the weights reached were significantly higher (p < 0.001) than the malnourished control values, but lower than the normal control ones. Plasma protein concentrations were similar in all groups. Muscle proteins that were diminished during the restricted diet, reached normal control values after both rehabilitation periods. The protein restricted diet, produced numeric and structural chromosomal abnormalities. Nutritional rehabilitation was only partially able to revert these abnormalities. The phagocytic activity and gut mucosa IgA-secreting cells were significantly reduced (p < 0.001) during the restricted diet; both nutritional rehabilitation periods induced a significant increase of both, phagocytic activity and IgA secreting cells. These values were similar to controls. Our results show that the supplementation of a protein-restricted diet with soymilk improved tissue protein content, as well as unspecific and gut mucosa immune responses, even though it was not able to reinstate fully normal body weight and a normal chromosome karyotype.