Feeding 3-nitrooxypropanol reduces methane emissions by feedlot cattle on tropical conditions.

Our objective was to evaluate the effects of feeding 3-nitrooxypropanol (3-NOP; Bovaer, DSM Nutritional Products) at two levels on methane emissions, nitrogen balance, and performance by feedlot cattle. In experiment 1, a total of 138 Nellore bulls (initial body weight, 360 ± 37.3 kg) were housed in pens (27 pens with either 4 or 5 bulls per pen) and fed a high-concentrate diet for 96 d, containing 1) no addition of 3-NOP (control), 2) inclusion of 3-NOP at 100 mg/kg dry matter (DM), and 3) inclusion of 3-NOP at 150 mg/kg DM.

3-Nitrooxypropanol decreases methane emissions and increases hydrogen emissions of early lactation dairy cows, with associated changes in nutrient digestibility and energy metabolism.

The aim of this study was to determine the methane (CH) mitigation potential of 3-nitrooxypropanol and the persistency of its effect when fed to dairy cows in early lactation. Sixteen Holstein-Friesian cows (all multiparous; 11 cows in their second parity and 5 cows in their third parity) were blocked in pairs, based on actual calving date, parity, and previous lactation milk yield, and randomly allocated to 1 of 2 dietary treatments: a diet including 51 mg of 3-nitrooxypropanol/kg of dry matter (3-NOP) and a diet including a placebo at the same concentration (CON). Cows were fed a 35% grass silage, 25% corn silage, and 40% concentrate (on dry matter basis) diet from 3 d after calving up to 115 d in milk (DIM).

The combined effects of supplementing monensin and 3-nitrooxypropanol on methane emissions, growth rate, and feed conversion efficiency in beef cattle fed high-forage and high-grain diets.

The study objective was to evaluate the combined effects of supplementing monensin (MON) and the methane (CH4) inhibitor 3-nitrooxypropanol (NOP) on enteric CH4 emissions, growth rate, and feed conversion efficiency of backgrounding and finishing beef cattle. Two hundred and forty crossbred steers were used in a 238-d feeding study and fed a backgrounding diet for the first 105 d (backgrounding phase), transition diets for 28 d, followed by a finishing diet for 105 d (finishing phase). Treatments were as follows: 1) control (no additive); 2) MON (monensin supplemented at 33 mg/kg DM; 3) NOP (3-nitrooxypropanol supplemented at 200 mg/kg DM for backgrounding or 125 mg/kg DM for finishing phase); and 4) MONOP (33 mg/kg DM MON supplemented with either 200 mg/kg DM or 125 mg/kg DM NOP).

Nutritional strategies in ruminants: A lifetime approach.

This review examines the role of nutritional strategies to improve lifetime performance in ruminants. Strategies to increase ruminants' productive longevity by means of nutritional interventions provide the opportunity not only to increase their lifetime performances and their welfare, but also to decrease their environmental impact. This paper will also address how such nutritional interventions can increase herd efficiency and farm profitability.

Ruminal methane inhibition potential of various pure compounds in comparison with garlic oil as determined with a rumen simulation technique (Rusitec).

Ruminants represent an important source of methane (CH(4)) emissions; therefore, CH(4) mitigation by diet supplementation is a major goal in the current ruminant research. The objective of the present study was to use a rumen simulation technique to evaluate the CH(4)-mitigating potential of pure compounds in comparison with that achieved with garlic oil, a known anti-methanogenic supplement. A basal diet (15 g DM/d) consisting of ryegrass hay, barley and soyabean meal (1:0·7:0·3) was incubated with the following additives: none (negative control); garlic oil (300 mg/l incubation liquid; positive control); allyl isothiocyanate (75 mg/l); lovastatin (150 mg/l); chenodeoxycholic acid (150 mg/l); 3-azido-propionic acid ethyl ester (APEE, 150 mg/l); levulinic acid (300 mg/l); 4-[(pyridin-2-ylmethyl)-amino]-benzoic acid (PABA, 300 mg/l).

An NAD(+)-dependent glutamate dehydrogenase cloned from the ruminal ciliate protozoan, Entodinium caudatum.

An NAD(+)-dependent glutamate dehydrogenase (GDH; EC 1.4.1.