RESUMO
The present study investigated production responses and ruminal fermentation characteristics of lactating dairy cows when supplemented with N-acetyl-l-Met (NALM) as a source of rumen-protected Met in metabolizable protein (MP)-deficient (MPD) or MP-adequate diet (MPA). Eight lactating dairy cows (53 ± 10.4 d in milk, average ± standard deviation) were blocked by parity and days in milk, and the experiment was performed in a replicated 4 × 4 Latin square design. Within each square, cows were randomly assigned to a sequence of 4 diets during each of the four 21-d periods (14 d of treatment adaptation and 7 d of data collection and sampling). A 2 × 2 factorial arrangement was used; MPD or MPA was combined without or with NALM: MPD without NALM, MPD with NALM (MPD+NALM), MPA without NALM, and MPA with NALM (MPA+NALM). A NALM product was supplemented in the MPD+NALM and the MPA+NALM at 30 g/cow per d. Supplementation of NALM did not affect dry matter intake (DMI) and milk yield regardless of MP concentration. In addition, supplementing NALM resulted in a similar milk true protein concentration and yield. In contrast, NALM supplementation increased milk fat concentration and yield and 3.5% fat-corrected milk yield and tended to increase energy-corrected milk yield regardless of MP difference. Additionally, trends were observed for increased 3.5% fat-corrected milk yield/DMI and energy-corrected milk yield/DMI, and the positive effects were greater under the MPA than the MPD diet, resulting in trends toward interactions between MP and NALM. Dietary treatments had similar effects on ruminal fermentation characteristics and microbial protein yield. Plasma concentration of Met increased under the MPD but not the MPA diet, leading to an MP × NALM interaction. Overall results in the current study suggest that NALM exerted a minor influence on ruminal metabolism, but increased milk fat concentration, resulting in increases in milk fat yield and feed efficiency. Yet, potential effects of NALM on intermediary metabolism between the gastrointestinal tract, the liver, and the mammary gland need to be explored to understand utilization efficiency for production of dairy cows.
Assuntos
Ração Animal , Dieta , Lactação/fisiologia , Metionina/administração & dosagem , Rúmen/metabolismo , Fenômenos Fisiológicos da Nutrição Animal , Animais , Bovinos , Digestão , Feminino , Fermentação , LeiteRESUMO
The extreme sensitivity of turkeys to aflatoxin B(1) (AFB(1)) is associated with efficient hepatic cytochrome P-450 (P450)-mediated bioactivation, and deficient glutathione S-transferase (GST) mediated detoxification. Butylated hydroxytoluene (BHT) protects against AFB(1) toxicity in turkeys through mechanisms that include competitive inhibition of P450-mediated AFB(1) bioactivation. To test whether dietary BHT alters hepatic AFB(1)-DNA adduct formation, excretion, and bioavailability of AFB(1)in vivo, turkeys were given diets with BHT (4000ppm) for 10 days, given a single oral dose of [(3)H]-AFB(1) (0.05microg/g; 0.02microCi/g), then sampled at intervals up to 24h. Radiolabel in serum, red blood cells, liver, and breast meat was frequently lower in BHT-treated compared to control. Hepatic AFB(1)-DNA adducts in BHT-treated turkeys were significantly lower at 12 and 24h. BHT-fed birds had significant higher bile efflux, though biliary radiolabel excretion was not different from control. The amount of aflatoxin M(1) (AFM(1)) excreted in the bile was lower than in control, but BHT had no effect on the biliary excretion of AFB(1), aflatoxin Q(1) or glucuronide and sulfate conjugates. Thus, the chemopreventive properties of BHT may also occur through a reduction in AFB(1) bioavailability in addition to inhibition of bioactivation.
Assuntos
Aflatoxina B1/farmacocinética , Aflatoxinas/toxicidade , Bile/metabolismo , Hidroxitolueno Butilado/uso terapêutico , Adutos de DNA/efeitos dos fármacos , Conservantes de Alimentos/uso terapêutico , Fígado/metabolismo , Perus/metabolismo , Aflatoxinas/antagonistas & inibidores , Animais , Disponibilidade Biológica , Peso Corporal/efeitos dos fármacos , Hidroxitolueno Butilado/farmacologia , Conservantes de Alimentos/farmacologia , Fígado/efeitos dos fármacos , Masculino , Tamanho do Órgão/efeitos dos fármacos , Distribuição TecidualRESUMO
These studies investigated the effects of retinoic acids on endothelial cell proliferation. Three human neoplastic cell lines, U-373 MG glioblastoma, DU-145 prostate carcinoma, and TCCSUP bladder transitional cell carcinoma, were treated with all-trans, 9-cis, or 13-cis retinoic acids at 0.0001 to 10 microM. Hypoxia was used to ensure the expression of the angiogenic phenotype. Conditioned media (CM) were prepared by hypoxic culturing of the tumor cells with retinoic acids for 24 hours. Then CM were transferred to bovine capillary endothelial cells for 48 hours of normoxic culturing, counted and compared to controls. CM from U-373 MG and DU-145 cells, but not TCCSUP cells, treated with all-trans or 9-cis retinoic acids at several concentrations below 1 microM, caused significant (P<0.05) increases in endothelial cell proliferation of between 13 to 18%. Both nonconditioned and conditioned media, for retinoic acid concentrations above 1 microM, inhibited endothelial cell proliferation. All CM for 13-cis retinoic acid decreased endothelial cell proliferation. These results show that the cytotoxicity of retinoic acids and the growth promoting/inhibiting ability of the conditioned media is retinoic acid isoform, time, concentration, and cell type dependent. Most importantly, the conditioned media from tumor cells treated with low concentrations of all-trans or 9-cis retinoic acids significantly increased endothelial cell proliferation.
Assuntos
Antineoplásicos/farmacologia , Endotélio Vascular/efeitos dos fármacos , Tretinoína/farmacologia , Animais , Bovinos , Contagem de Células , Divisão Celular/efeitos dos fármacos , Hipóxia Celular , Meios de Cultivo Condicionados/farmacologia , Relação Dose-Resposta a Droga , Endotélio Vascular/citologia , Humanos , Neoplasias , Neovascularização Patológica , Células Tumorais Cultivadas/efeitos dos fármacos , Células Tumorais Cultivadas/metabolismoRESUMO
For most patients with hallux valgus, the problem is caused by wearing shoes that are too tight, and conservative measures can help. We review how primary care physicians can evaluate and treat this problem, and when to refer to an orthopaedic surgeon.