doi: 10.1096/fj.201601156R 50 FuruyaS.MitomaJ.MakinoA.HirabayashiY
342 However, its side effects, such as transient thrombocytopenia and neutropenia, remain obstacles to clinical translation

Moreover, albumin interferes with hemostasis inhibiting platelet aggregation and promoting vasodilation,17 for example through NO-albumin complexes.18 It may also play a role in acid-base homeostasis: on one hand, it behaves as a weak acid and, on the other hand, it can buffer non-volatile acids.19 Lastly, studies in animal models of liver cirrhosis, also found that albumin exerts a positive cardiac inotropic effect counteracting the oxidative stress and TNF- effect in NFB-NOS pathway and b-receptor signalling.55 Forms of Albumin in Liver Cirrhosis Albumin can undergo several posttranslational modifications (PTM) under physiological or pathological conditions, such as oxidation,56,57 glycosylation,5860 truncation at the C- or N-terminus,61,62 dimerization63 and carboxylation.64,65 These PTM result in important structural and functional heterogeneity of circulating albumin.66 Oxidation of cysteine-34 residue is the most frequent PTM in albumin, and is a result of oxidative-stress induced protein damage.62 In healthy subjects, 7080% of albumin circulates in its reduced form, dubbed mercaptoalbumin (HMA), which has a free sulfidril group at cysteine-34.1115 Up to 25% of circulating albumin suffers reversible oxidative modifications through reversible binding via mixed disulfide bridges between cysteine-34 and compounds containing sulfidril groups such as cysteine, homocysteine and glutathione

Improved spatial learning strategy and memory in aged Alzheimer AbetaPPswe/PS1dE9 mice on a multi-nutrient diet