Macroalgae and commercial macroalgal polysaccharides as potential functional ingredients in muscle foods

Ulva rigida (UR) and Palmaria palmata (PP) were included in farmed Atlantic salmon diets at levels of 0-15% for 19 and 16 weeks, respectively. Quality and shelf-life parameters of salmon fillets stored in modified atmosphere packs (MAP) (60% N2 : 40% CO2) at 4ºC were compared to controls fed astaxanthin. Salmon fillets were enhanced with a yellow/orange colour. Proximate composition, pH and lipid oxidation were unaffected by dietary UR and PP. Salmon fed 5% UR and 5-15% PP did not influence sensory descriptors (texture, odour, oxidation flavour and overall acceptability) of cooked salmon fillets. Pig diets were supplemented with commercial wet- and spray-dried macroalgal (Laminaria digitata) polysaccharide extracts containing laminarin (L, 500 mg/kg feed) and fucoidan (F, 420 mg/kg feed) (L/F-WS, L/F-SD) for 3 weeks and quality and shelf-life parameters of fresh pork steaks (longissimus thoracis et lumborum) stored in MAP (80% O2 : 20% CO2) were examined. Level (450 or 900 mg L and F/kg feed) and duration (3 or 6 weeks) of dietary L/F-WS and mechanisms of antioxidant activities in pork were investigated. L/F-WS reduced (p < 0.05) lipid oxidation and lowered levels of saturated fatty acids in fresh pork after 3 weeks feeding. L/F-SD was added directly to mince pork (0.01 - 0.5%) and quality and shelf-life parameters of fresh pork patties stored in MAP (80% O2 : 20% CO2) were assessed. Direct addition of the L/F-SD increased levels of lipid oxidation and decreased surface redness (a* values) of fresh pork patties. Lipid oxidation was reduced in cooked patties due to the formation of Maillard reaction products. Cooked pork patties containing L/F-SD were subjected to an in vitro digestion and a cellular transwell model to confirm bioaccessibility and uptake of antioxidant compounds. In mechanistic studies, fucoidan demonstrated antiand pro-oxidant activities on muscle lipids and oxymyoglobin, respectively.

A small molecule activator of p300/CBP histone acetyltransferase promotes survival and neurite growth in a cellular model of Parkinson’s disease

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterised by motor and non-motor symptoms, resulting from the degeneration of nigrostriatal dopaminergic neurons and peripheral autonomic neurons. Given the limited success of neurotrophic factors in clinical trials, there is a need to identify new small molecule drugs and drug targets to develop novel therapeutic strategies to protect all neurons that degenerate in PD. Epigenetic dysregulation has been implicated in neurodegenerative disorders, while targeting histone acetylation is a promising therapeutic avenue for PD. We and others have demonstrated that histone deacetylase inhibitors have neurotrophic effects in experimental models of PD. Activators of histone acetyltransferases (HAT) provide an alternative approach for the selective activation of gene expression, however little is known about the potential of HAT activators as drug therapies for PD. To explore this potential, the present study investigated the neurotrophic effects of CTPB (N-(4-chloro-3-trifluoromethyl-phenyl)-2-ethoxy-6-pentadecyl-benzamide), which is a potent small molecule activator of the histone acetyltransferase p300/CBP, in the SH-SY5Y neuronal cell line. We report that CTPB promoted the survival and neurite growth of the SH-SY5Y cells, and also protected these cells from cell death induced by the neurotoxin 6-hydroxydopamine. This study is the first to investigate the phenotypic effects of the HAT activator CTPB, and to demonstrate that p300/CBP HAT activation has neurotrophic effects in a cellular model of PD.