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Fig. 1 | BMC Neurology

Fig. 1

From: Albumin and multiple sclerosis

Fig. 1

Protective mechanisms by albumin in the CNS during active MS disease. a As a consequence of BBB damage, albumin (light blue dots) becomes extravasated and micro-hemorrhages (RBCs, rust color) can occur around vessels (royal blue) in MS CNS tissue. The RBCs breakdown (rust color with black spots) and heme/iron is released which can catalyze oxidation and nitration reactions. Albumin can bind heme and iron, which limits their ability to promote tissue damage. In addition, albumin is often the recipient of toxic species that are generated (pink dots – oxidized albumin; green dots – nitrated albumin), thereby protecting other CNS biomolecules. Albumin bound to heme may also detoxify ROS and RNS. b Inflammatory cells cross the BBB, and can be a source of ROS and RNS, particularly macrophages (e.g., M1 macrophages) (purple cells). The colocalization of albumin with macrophages positions albumin to be a target of ROS and RNS. c Besides macrophages, microglia that become activated during MS (yellow cell) can be a source of ROS and RNS. Extravasated albumin becomes a target for these toxic species and thereby limiting tissue damage to other important molecules in the CNS. d Myelin is a site of iron concentration, and during demyelination (black line fragments) iron is released. This iron can catalyze oxidation and nitration reactions together with inflammatory cells, e.g., macrophages. Albumin can be a recipient of reactive molecules and becomes modified. Note, the concentration of albumin would become diluted (top left to lower right) in relation to the distance from the site of the damaged (leaky) BBB, at least until an equilibrium is reached

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