An inventory of grassland use on horse farms.

Horses can contribute to the maintenance of grassland. To determine the potential contribution of grassland to horse nutrition, we investigated the seasonal variation of herbage on offer and its nutritional quality in an inventory on six practical horse farms in Central Germany during 2019. On all horse-grazed pastures compressed sward height (CSH) was measured monthly and converted into aboveground herbage (AGH) to allocated short and tall grass sward areas (area-specific) via calibration cuts. In addition, four focus pastures were selected for monthly obtained area-specific herbage quality samples. The farm-specific management was monitored using questionnaires and grazing diaries to determine underlying factors influencing herbage biomass and quality. The proportion of short grass sward areas increased during the grazing season (p=0.0010), which was related to high stocking intensity in terms of livestock unit grazing days (LUGD, p <.0001). On most farms, LUGD were constant throughout the growing season and not adjusted to changing grass growth. Herbage crude protein (CP, p=0.0038), metabolizable energy (ME, p <.0001) concentrations and acid detergent fibre in the organic matter (ADF, p <.0001) differed among the grass sward areas. The results suggest that sufficient ME (4.2 ± 0.32 - 8.4 ± 0.15 MJ ME kg-1 DM) for maintenance and pre-caecal digestible CP (pcdCP) (37.0 ± 3.86 - 77.4 ± 4.44 g kg-1 DM) could be provided during the grazing season. The study highlights the need to incentivise grassland management for herbage provision among horse owners to exploit the potential of grassland during the grazing season.

Protective effects of organoselenium compounds against methylmercury-induced oxidative stress in mouse brain mitochondrial-enriched fractions

We evaluated the potential neuroprotective effect of 1-100 µM of four organoselenium compounds: diphenyl diselenide, 3’3-ditri-fluoromethyldiphenyl diselenide, p-methoxy-diphenyl diselenide, and p-chloro-diphenyl diselenide, against methylmercury-induced mitochondrial dysfunction and oxidative stress in mitochondrial-enriched fractions from adult Swiss mouse brain. Methylmercury (10-100 µM) significantly decreased mitochondrial activity, assessed by MTT reduction assay, in a dose-dependent manner, which occurred in parallel with increased glutathione oxidation, hydroperoxide formation (xylenol orange assay) and lipid peroxidation end-products (thiobarbituric acid reactive substances, TBARS). The co-incubation with diphenyl diselenide (100 µM) completely prevented the disruption of mitochondrial activity as well as the increase in TBARS levels caused by methylmercury. The compound 3’3-ditrifluoromethyldiphenyl diselenide provided a partial but significant protection against methylmercury-induced mitochondrial dysfunction (45.4 ± 5.8 percent inhibition of the methylmercury effect). Diphenyl diselenide showed a higher thiol peroxidase activity compared to the other three compounds. Catalase blocked methylmercury-induced TBARS, pointing to hydrogen peroxide as a vector during methylmercury toxicity in this model. This result also suggests that thiol peroxidase activity of organoselenium compounds accounts for their protective actions against methylmercury-induced oxidative stress. Our results show that diphenyl diselenide and potentially other organoselenium compounds may represent important molecules in the search for an improved therapy against the deleterious effects of methylmercury as well as other mercury compounds.