Effect of cow's milk with different PUFA n-6: n-3 ratios on performance, serum lipid profile, and blood parameters of grower gilts.

The concern with human health has increased the interest in producing foods enriched with polyunsaturated fatty acids (PUFA), directly or naturally, by inclusion in the animals' diet. The positive effects such as antithrombotic, anti-inflammatory, and hypolipidemic have been observed in pigs and rats, used as human models for study. The present study evaluated the effect of cow's milk with different lipid profiles on performance, serum fatty acid profile, biochemical analysis, and a complete blood count of gilts used as a human model. At 34 days, thirty gilts were equally distributed in three treatments. Experimental treatments were milk from cows without the oil supplementation (C), milk from cows fed an enriched diet with linseed oil (n-3), and milk from cows fed an enriched diet with soybean oil (n-6). Milk supplementation was performed until 190 days old, provided once in the morning. The n-3 and n-6 milk reduced the concentration of myristic acid in the blood and increased the leukocytes. Milk enriched with n-3 compared to n-6 reduced the stearic acid. In conclusion, milk with a better PUFA profile can reduce saturated fatty acids in the blood and alter the concentration of cells in the defense system.

Folic acid-deficient diet during gestation and post-weaning alters Pomc gene and protein expression in rat offspring / La dieta deficiente en ácido fólico durante la gestación y el destete altera la expresión del gen Pomc y de proteínas en la descendencia de ratas

Background: folic acid participates in one-carbon metabolism, which supplies methyl groups to numerous reactions in the body. Impaired delivery of these methyl groups affects gene expression. We hypothesize that offspring exposed to less folic acid will express higher levels of Pomc (proopiomelanocortin) gene mRNA. Aim: to investigate the Pomc gene and protein expression pattern in the female offspring of female rats receiving a folic acid-deficient diet during gestation, lactation, and post-weaning. Methods: the study involved female rat offspring (n = 10) born from mothers subjected to a control (2.0 mg of folic acid/kg of food) or folic acid-deficient (0.5 mg of folic acid/kg of food) diet, and fed the same diet during post-weaning. Samples were collected from the arcuate nucleus of the hypothalamus of the female offspring for real-time PCR and Western blotting analyses. Results: the female offspring in the folic acid-deficient diet group had significantly higher Pomc gene and protein expression than the female offspring in the control diet group (p = 0.03, p = 0.01, respectively). Conclusion: a folic acid-deficient diet during gestation, lactation, and post-weaning increases Pomc gene and protein expression, but does not modify food intake or body weight of female rat offspring

Antecedentes: el ácido fólico participa en el metabolismo de un solo carbono, que suministra grupos metilo a numerosas reacciones del cuerpo. La aportación alterada de estos grupos metilo afecta a la expresión génica. Nuestra hipótesis es que la descendencia expuesta a menos ácido fólico expresará niveles más altos de ARNm del gen Pomc (proopiomelanocortina). Objetivo: investigar el patrón de expresión del gen Pomc y de sus proteínas en crías de ratas hembras que recibieron una dieta deficiente en ácido fólico durante la gestación, la lactancia y el destete. Métodos: el estudio incluyó crías hembras (n = 10) nacidas de madres sometidas a una dieta control (2,0 mg de ácido fólico/kg de alimento) o deficiente en ácido fólico (0,5 mg de ácido fólico/kg de alimento) durante la gestación y la lactancia, y alimentadas con la misma dieta durante el destete. Se recolectaron muestras del núcleo arqueado del hipotálamo de las hembras para el análisis de la expresión génica (PCR en tiempo real) y de proteínas (inmunomanchado Western). Resultados: las hembras pertenecientes al grupo de dieta deficiente en ácido fólico tuvieron una expresión del gen Pomc y sus proteínas significativamente mayor que la de las hembras pertenecientes al grupo con dieta de control (p = 0,03, p = 0,01, respectivamente). Conclusión: la dieta deficiente en ácido fólico durante la gestación, la lactancia y el destete modifica la expresión del gen Pomc y sus proteínas pero no modifica la ingesta de alimentos ni el peso corporal de las ratas hembra

Folic acid-deficient diet during gestation and post-weaning alters Pomc gene and protein expression in rat offspring.

INTRODUCTION: Background: folic acid participates in one-carbon metabolism, which supplies methyl groups to numerous reactions in the body. Impaired delivery of these methyl groups affects gene expression. We hypothesize that offspring exposed to less folic acid will express higher levels of Pomc (proopiomelanocortin) gene mRNA. Aim: to investigate the Pomc gene and protein expression pattern in the female offspring of female rats receiving a folic acid-deficient diet during gestation, lactation, and post-weaning. Methods: the study involved female rat offspring (n = 10) born from mothers subjected to a control (2.0 mg of folic acid/kg of food) or folic acid-deficient (0.5 mg of folic acid/kg of food) diet, and fed the same diet during post-weaning. Samples were collected from the arcuate nucleus of the hypothalamus of the female offspring for real-time PCR and Western blotting analyses. Results: the female offspring in the folic acid-deficient diet group had significantly higher Pomc gene and protein expression than the female offspring in the control diet group (p = 0.03, p = 0.01, respectively). Conclusion: a folic acid-deficient diet during gestation, lactation, and post-weaning increases Pomc gene and protein expression, but does not modify food intake or body weight of female rat offspring.

INTRODUCCIÓN: Antecedentes: el ácido fólico participa en el metabolismo de un solo carbono, que suministra grupos metilo a numerosas reacciones del cuerpo. La aportación alterada de estos grupos metilo afecta a la expresión génica. Nuestra hipótesis es que la descendencia expuesta a menos ácido fólico expresará niveles más altos de ARNm del gen Pomc (proopiomelanocortina). Objetivo: investigar el patrón de expresión del gen Pomc y de sus proteínas en crías de ratas hembras que recibieron una dieta deficiente en ácido fólico durante la gestación, la lactancia y el destete. Métodos: el estudio incluyó crías hembras (n = 10) nacidas de madres sometidas a una dieta control (2,0 mg de ácido fólico/kg de alimento) o deficiente en ácido fólico (0,5 mg de ácido fólico/kg de alimento) durante la gestación y la lactancia, y alimentadas con la misma dieta durante el destete. Se recolectaron muestras del núcleo arqueado del hipotálamo de las hembras para el análisis de la expresión génica (PCR en tiempo real) y de proteínas (inmunomanchado Western). Resultados: las hembras pertenecientes al grupo de dieta deficiente en ácido fólico tuvieron una expresión del gen Pomc y sus proteínas significativamente mayor que la de las hembras pertenecientes al grupo con dieta de control (p = 0,03, p = 0,01, respectivamente). Conclusión: la dieta deficiente en ácido fólico durante la gestación, la lactancia y el destete modifica la expresión del gen Pomc y sus proteínas pero no modifica la ingesta de alimentos ni el peso corporal de las ratas hembra.

Effects of the Consumption of Milk Biofortified with Selenium, Vitamin E, and Different Fatty Acid Profile on Immune Response in the Elderly.

SCOPE: Nutrition is a major contributing factor for immunocompetence. The aim was to assess the immune status of older people after consuming milk produced by lactating cows fed with one of the following diets: control diet (C), C + vitamin E + selenium (C + A), C + sunflower oil (C + O), and C + sunflower oil + vitamin E + selenium (A + O). METHODS AND RESULTS: Sixty elderly people received one of these biofortified milks for 12 weeks. Immune response was assessed by measurement of the expression of COX-1, COX-2, MCP-1, PPAR (δ, α, and ß/δ) genes, neutrophil production of oxygen reactive species induced by immune complexes, neutrophil phagocytosis and lytic activity of the alternative pathway of the complement system, and cytokine levels. Variables were assessed before and after treatment. Our findings showed stability of some inflammatory mediators (complement activity and neutrophils burst) in treatment groups, except complement activity in C + A, and an increase of these markers in C, especially reactive oxygen species production and phagocytic activity. TNF-α was significantly increased in all groups. In C + A, IL-4 and IL-2 increased after treatment, and in the group that received the milk produced by cows fed with "O" diet, CCL20 and IL-27 increased. CONCLUSION: Overall, as compared to C, milk biofortification was associated with stabilization of the activity of alternative complement pathway and the neutrophils burst, and modulated different cytokines levels.

Modulation of doxorubicin-induced clastogenesis in Wistar rat bone marrow cells by vitamin B(6).

Vitamin B(6) has shown to be a potentially effective antioxidant agent, and dietary antioxidants are also frequently valuable inhibitors of clastogenesis and carcinogenesis. The purpose of the present work was to study the clastogenicity of different doses of vitamin B(6) and to examine the possible modulating effect of this vitamin on chromosomal damage induced by the antitumor agent doxorubicin in Wistar rats. Experimental groups were set up for pre- and simultaneous treatment with vitamin B(6) alone or in combination with DXR. The data obtained from administering different doses of vitamin B(6) (12.5-100 mg/kg b.w.) showed no significant increase in total chromosomal aberrations when compared with the negative control. The administration of two doses of 25 mg/kg b.w. or one dose of 50 mg/kg b.w. of vitamin B(6) before doxorubicin injection seemed equally effective in protecting cells against doxorubicin clastogenicity. The anticlastogenic effect of vitamin B(6) on DXR-induced chromosomal damage could be ascribed to its antioxidant properties. Vitamin B(6) was not clastogenic or cytotoxic in rat bone marrow cells and it plays a role in inhibiting the clastogenicity induced by DXR.

Evaluation of the clastogenicity and anticlastogenicity of vitamin B6 in human lymphocyte cultures.

Insufficient intakes of many micronutrients found in fruits and vegetables, such as folic acid, vitamins C and B6 may lead to DNA damage, cancer, and degenerative disease. The investigation of dietary antioxidants is a field of great interest for elucidating mechanisms of mutagenesis/carcinogenesis. The present study was undertaken to investigate the effects of vitamin B6 on the induction of chromosomal aberrations in cultured human lymphocytes and to examine the possible anticlastogenic effect of this vitamin on chromosomal damage induced by the antitumor drug doxorubicin. The results showed that when the cultures treated with vitamin B6 were compared with the untreated control in terms of total chromosomal damage and abnormal metaphases, pre- and simultaneous treatment with this vitamin showed no significant differences. In the post-treatment, average and above average concentrations of vitamin B6 alone showed a clastogenic effect. In the simultaneous protocol, this vitamin (15, 90 and 120 microg/mL) was effective in inhibiting chromosomal aberrations induced by doxorubicin (p<0.05), with a reduction of 33.1% with the highest concentration tested. However, in the post-treatment, the associations of vitamin B6 and doxorubicin exerted a more evident clastogenic effect than that observed in the cultures exposed only to the antitumor drug. In the present investigation, the inability of vitamin B6 to decrease chromosomal damage induced by doxorubicin in the pre- and post-treatments could be justified by the instability of this vitamin as a free radical scavenger. In conclusion, the results from this study confirmed that vitamin B6 is protective against chromosomal damage induced by doxorubicin in cultured human lymphocytes, but that the effects depend on concentration and form of treatment.

Use of the TSPY gene for sexing cattle

The Y-encoded, testis-specific protein (TSPY) is a Y-specific gene. The copy numbers of TSPY range from 20 to 60 in men and up to 200 in bulls. In this study, we examined the possibility of using the TSPY gene to sex cattle. DNA from blood samples of 100 Nelore cattle (50 males and 50 females) from the Nelore Cattle Breeding Program (PMGRN) was screened for TSPY by PCR using TSPY-specific primers. The assay was highly specific since all male samples were TSPY-positive and all female samples were negative. Positive results were also obtained at low DNA concentrations (less than 1 rhog/muL). These results showed that TSPY was a good male-specific marker, the usefulness of which was enhanced by the high copy number of the gene. This is the first report to demonstrate the applicability of TSPY for sexing cattle.