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Our objective was to estimate the energy and protein requirements of Holstein young calves up to 87 days old. Forty-two Holstein calves aged 4 days were used. From these, ten were randomly selected and slaughtered to compose the baseline slaughter (BS) group. The remaining calves were randomly assigned to eight treatments in a 4 × 2 factorial using a completely randomized design. The treatments were 2, 4, 6, and 8 kg/day of milk (297 g/kg CP; 319 g/kg of fat) fed twice daily, and then harvested at 59 or 87 days of age. Calves were fed a starter (193 g/kg CP; 133 g/kg NDF) ad libitum in all treatments. The calves slaughtered at 87 days of age had milk replaced by Coast-cross (Cynodoon sp.) hay (125 g/kg CP; 728 g/kg NDF). The net requirement of energy for maintenance (NEm) was 0.36 MJ/kg EBWG, with efficiency of utilization of energy for maintenance (k m) of 59.4 %. The equation obtained to estimate the net requirement of energy for gain (NEg; MJ/d) was 4.40 × EBW(0.099), with the efficiency of utilization of energy for gain (k g) equal to 46.5 %. The observed requirements of net and metabolizable protein for maintenance (NPm and MPm) were 3.67 and 3.88 g/kg BW(0.75), respectively. The efficiency of use of metabolizable protein for maintenance (k pm ) was 94.6 %. The predicted requirements were higher than those observed in the literature, and this study demonstrated that the requirements of newborn calves are higher than the recommended.

The objective of this study was to compare the intake, digestibility, and performance of dairy cows fed corn silage, fresh sugarcane, and sugarcane ensiled in three different forms. Twenty-five Holstein cows at 114 ± 12.6 days in milk (DIM) were used. A randomized block design was adopted, using an arrangement of repeated measures over time. The following treatments were tested: corn silage (CS); fresh sugarcane (FS); sugarcane silage without additives (SCS); sugarcane silage enriched with calcium oxide at 5 g/kg of forage (SCSc); and sugarcane silage enriched with Lactobacillus buchneri at 5 × 10(4) cfu/kg of forage (SCSb). The roughage to concentrate ratio was 60:40 for the CS diet and 40:60 for the sugarcane-based diets. The dry matter intake (DMI) as a function of body weight had a downward trend for the cows fed sugarcane silage, compared with those fed FS. The sugarcane silages had higher digestibilities of dry matter (DM), organic matter (OM), and neutral detergent fiber (NDFap), compared with FS. The use of L. buchneri or calcium oxide improved the diet's digestibility. The use of FS, sugarcane silage, or sugarcane silage with additives had no effects on milk and fat-corrected milk yield, compared to corn silage. Cows fed FS presented lower milk total solids content and had a downward trend for milk fat, compared with cows fed sugarcane-silage diets. Cows fed sugarcane silages produced milk with higher casein stability in the alcohol test than cows fed fresh-sugarcane diet. Sugarcane silage, with or without additives, did not reduce the intake of dairy cows, and the use of additives improved the fiber's digestibility.

The epidemiological impact of SOD2 imbalance on prostate cancer (PC) risk associated with genetic variations has previously been studied. However, we found no previous studies clarifying the nature of SOD2 effects on prostate cancer. Here, we performed integrated in vivo and in vitro protocols that analyzed the association between Ala16Val-SOD2 polymorphism and prostate cancer aggressiveness at the time of diagnosis and evaluated the effect of the imbalance on PC proliferation using the DU-145 PC cell line treated with paraquat and porphyrin. In the pharmacological model, paraquat was used to increase superoxide anion levels and porphyrin was the SOD2 analog. The results confirmed the impact of superoxide-hydrogen peroxide imbalance on PC cell biology since porphyrin decreased cell proliferation and both treatments modulated antioxidant genes. Therefore, our results corroborate previous suggestions that alteration of redox status could be exploited therapeutically in the treatment of PC.

Hypercholesterolemia and oxidative stress have been implicated in the pathophysiology of atherosclerosis and coronary artery disease. We investigated whether the carotenoid bixin (BIX) may reduce oxidative damage, inflammatory response, and the atherosclerotic lesion induced by hypercholesterolemia in rabbits. Rabbits received regular chow (control) or a hypercholesterolemic diet (0.5% cholesterol) alone or supplemented with BIX (10, 30 or 100 mg/kg body weight, b.w.) or simvastatin (15 mg/kg b.w.) for 60 days. Treatment with BIX or simvastatin reduced the atherosclerotic lesions in cholesterol-fed rabbits (up to 55 and 96% reduction, respectively). This protective effect of BIX was accompanied by decrease in the levels of tumor necrosis factor alpha by 15%, interleukin 6 by 19%, lipid peroxidation by 60%, non-high-density lipoprotein cholesterol (non-HDL-C) by 37%, and triglycerides by 41%. BIX increased by 160% the HDL-C levels and decreased by 67% the atherogenic index of hypercholesterolemic rabbits. In atherosclerotic rabbits, the non-protein thiol groups content and the activity of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase, and thioredoxin reductase were increased in the aortic tissue, whereas paraoxonase activity was reduced in the serum. All these changes were completely prevented by BIX or simvastatin treatment. These results demonstrate that BIX reduces the extent of atherosclerotic lesions and this effect was associated with the decrease in oxidative stress, inflammatory response, and improvement of dyslipidemia, which were most effectively controlled after treatment with 10-30 mg BIX/kg b.w. BIX consumption may, therefore, be an adjuvant to prevent atherosclerosis reducing risk factors for coronary diseases.

Perinatal hypoxic-ischemic (HI) brain injury is a common problem with severe neurologic sequelae. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of HI insult and may extend for days or weeks. In this context, the inflammatory response and the formation of reactive oxygen species seem to play a key role during evolution of brain damage after injury. Thus, the aim of this study was to describe the chronological sequence of acetylcholinesterase (AChE) activity and the lipid peroxidation changes in the cerebral cortex using the classic model of neonatal HI. Furthermore, the erythrocyte AChE and adenosine deaminase (ADA) activities as well as the serum levels of proinflammatory cytokines were assessed. We observed that neonatal HI caused an increase of lipid peroxidation immediately after HI insult, which remained for several days afterward. There was a time-related change in the AChE activity in the cerebral cortex and the same was observed in erythrocyte AChE and ADA activities. In addition, immediately after HI, ADA activity showed a strong positive correlation with all proinflammatory cytokines assessed. Together, these findings may help the understanding of some mechanism related to the pathophysiology of neonatal HI, therefore highlighting the putative therapeutic targets to minimize brain injury and enhance recovery.