Novel oxidising feed additives reduce in vitro methane emissions using the rumen simulation technique.

Enteric methane (CH) produced by ruminant livestock is a potent greenhouse gas and represents significant energy loss for the animal. The novel application of oxidising compounds as antimethanogenic agents with future potential to be included in ruminant feeds, was assessed across two separate experiments in this study. Low concentrations of oxidising agents, namely urea hydrogen peroxide (UHP) with and without potassium iodide (KI), and magnesium peroxide (MgO), were investigated for their effects on CH production, total gas production (TGP), volatile fatty acid (VFA) profiles, and nutrient disappearance in vitro using the rumen simulation technique. In both experiments, the in vitro diet consisted of 50:50 grass silage:concentrate on a dry matter basis. Treatment concentrations were based on the amount of oxygen delivered and expressed in terms of fold concentration. In Experiment 1, four treatments were tested (Control, 1× UHP + KI, 1× UHP, and 0.5× UHP + KI), and six treatments were assessed in Experiment 2 (Control, 0.5× UHP + KI, 0.5× UHP, 0.25× UHP + KI, 0.25× UHP, and 0.12× MgO). All treatments in this study had a reducing effect on CH parameters. A dose-dependent reduction of TGP and CH parameters was observed, where treatments delivering higher levels of oxygen resulted in greater CH suppression. 1× UHP + KI reduced TGP by 28 % (p = 0.611), CH% by 64 % (p = 0.075) and CH mmol/g digestible organic matter by 71 % (p = 0.037). 0.12× MgO reduced CH volume by 25 % (p > 0.05) without affecting any other parameters. Acetate-to-propionate ratios were reduced by treatments in both experiments (p < 0.01). Molar proportions of acetate and butyrate were reduced, while propionate and valerate were increased in UHP treatments. High concentrations of UHP affected the degradation of neutral detergent fibre in the forage substrate. Future in vitro work should investigate alternative slow-release oxygen sources aimed at prolonging CH suppression.