Perfil de ácidos graxos do leite de vacas alimentadas com óleo de soja e monensina no início da lactação Milk fatty acid profile of cows fed monensin and soybean oil in early lactation

Avaliaram-se os efeitos da adição de monensina sódica combinada com óleo de soja na dieta de vacas lactantes sobre o perfil de ácidos graxos (AG) do leite na 5ª e 15ª semanas da lactação. Foram utilizadas 16 vacas multíparas cruzadas, dispostas em delineamento em blocos casualizados, em um arranjo fatorial 2 x 2 (presença ou não de monensina e presença ou não de óleo de soja). Os tratamentos consistiram das dietas: CT (controle) = sem monensina ou óleo; MN = 33 ppm de monensina; OL = 3,9% de óleo de soja; e OM = óleo e monensina. Os animais foram confinados e alimentados com 52% de silagem de milho e 48% de concentrado. Não foi verificada interação entre óleo de soja e monensina para os ácidos graxos avaliados. A monensina aumentou os AG insaturados, monoinsaturados e poliinsaturados em 9,0; 8,8; e 10,7%, respectivamente. O óleo apresentou maior impacto sobre os AG poliinsaturados, aumentando-os em 39,2; 39,3; e 24,2%, respectivamente. Também reduziu os AG de cadeias curta (43,7%) e média (49,1%) e aumentou os AG de cadeia longa (55,3%). Os isômeros trans-C18:1 foram aumentados tanto pelo óleo como pela monensina, indicando efeito aditivo para trans-10 C18:1, que foi negativamente correlacionado ao teor de gordura do leite. O isômero cis-9 trans-11 do ácido linoléico conjugado (CLA) não foi influenciado pelos tratamentos, observando-se que o óleo reduziu a atividade da delta9-desaturase. Houve interação entre tratamentos e semana da lactação sobre os AG de cadeias curta e média, C14:0, C16:0, cis-9 C18:1 e trans-10 C18:1. Os maiores efeitos sobre o perfil de AG do leite foram registrados quando monensina e óleo foram fornecidos em conjunto na dieta de vacas lactantes.<br>The objective of this trial was to evaluate the effects of dietary monensin and soybean oil on milk fatty acid (FA) profile in the 5th and 15th week of lactation of dairy cows. Sixteen multiparous crossbred dairy cows averaging 30 days in milk were assigned to a completely randomized block design in a 2 x 2 factorial arrangement (presence or absence of monensin and soybean oil). The following diets were used: control not supplemented with monensin or soybean oil (CT), 33 ppm of monensin (MN), 3.9% of soybean oil (OL) or a combination of soybean oil plus monensin (OM). Cows were confined and fed diets with 52% of corn silage and 48% of concentrate. No significant interaction between soybean oil and monensin was observed for any measured FA. Monensin increased unsaturated, monounsaturated, and polyunsaturated FA by 9.0, 8.8 and 10.7%, respectively, while supplementation with soybean oil resulted in greater responses: 39.2, 39.3, and 24.2% for the same FA. Soybean oil also reduced short chain FA (43.7%) and medium chain FA (49.1%) and increased long chain FA (55.3%) in this study. The isomers trans-C18:1 were increased by inclusion of oil and monensin in the diet indicating an additive effect for trans-10 C18:1 that was negatively correlated with milk fat content. The CLA isomer cis-9 trans-11 C18:2 was not affected by treatments but soybean oil reduced delta9-desaturase activity. There were interactions between treatment and week of lactation for short and medium chain FA, C14:0, C16:0, cis-9 C18:1 and trans-10. The combination of monensin and soybean oil in diet of lactating dairy cows was responsible for the most significant changes observed in the profile of milk FA

Type II Keratins Are Phosphorylated on a Unique Motif during Stress and Mitosis in Tissues and Cultured Cells

Epithelial cell keratins make up the type I (K9–K20) and type II (K1–K8) intermediate filament proteins. In glandular epithelia, K8 becomes phosphorylated on S73 ((71)LLpSPL) in human cultured cells and tissues during stress, apoptosis, and mitosis. Of all known proteins, the context of the K8 S73 motif (LLS/TPL) is unique to type II keratins and is conserved in epidermal K5/K6, esophageal K4, and type II hair keratins, except that serine is replaced by threonine. Because knowledge regarding epidermal and esophageal keratin regulation is limited, we tested whether K4–K6 are phosphorylated on the LLTPL motif. K5 and K6 become phosphorylated in vitro on threonine by the stress-activated kinase p38. Site-specific anti-phosphokeratin antibodies to LLpTPL were generated, which demonstrated negligible basal K4–K6 phosphorylation. In contrast, treatment of primary keratinocytes and other cultured cells, and ex vivo skin and esophagus cultures, with serine/threonine phosphatase inhibitors causes a dramatic increase in K4–K6 LLpTPL phosphorylation. This phosphorylation is accompanied by keratin solubilization, filament reorganization, and collapse. K5/K6 LLTPL phosphorylation occurs in vivo during mitosis and apoptosis induced by UV light or anisomycin, and in human psoriatic skin and squamous cell carcinoma. In conclusion, type II keratins of proliferating epithelia undergo phosphorylation at a unique and conserved motif as part of physiological mitotic and stress-related signals