title: Effect of the proline-rich polypeptide complex/colostrinin™ on the enzymatic antioxidant system.
abstract: Proline-rich polypeptide complex (PRP) and its constituent nonapeptide (NP) possess immunoregulatory and procognitive properties. PRP in the form of sublingually administered tablets called Colostrinin™ improves the outcome of patients with Alzheimer's disease (AD). Free radical-induced oxidative stress has been implicated in the pathogenesis of AD. It has been previously shown that PRP and NP inhibit overproduction of reactive oxygen species, nitric oxide and proinflammatory cytokines induced by lipopolysaccharide or PMA. Antioxidant defense includes both low molecular weight components and enzymatic systems including dismutases, catalase, glutathione reductase (GSSGR) and glutathione peroxidase (GSHPx). An early event during the development of AD is lipid and protein peroxidation. PRP and NP showed no modulatory effect on lipid peroxidation. A protective effect on protein oxidation was found only when high doses of NP were used. We have previously shown, in a model of human peripheral blood mononuclear cells, that PRP/NP affects activities of superoxide dismutase and NF-κB. In the present study with the use of the same cell model and whole blood cells we observed an activatory effect of PRP/NP on GSHPx and GSSGR activity but not catalase. The observed effect suggests that PRP/NP can act as a modulatory agent of the "first line" of antioxidant defense. It can be assumed therefore that PRP/Colostrinin by regulation of the early phase of the redox system does not reduce but rather prevents oxidative damage. This effect may shed some light on the beneficial effect of PRP/Colostrinin in AD patients.
authors.affiliation: Department of Immunochemistry, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Weigla 12, 53-114, Wrocław, Poland. zablocka@iitd.pan.wroc.pl
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Zabłocka
authors.forename: Maria
authors.initials: M
authors.lastname: Janusz
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism; D000975:Antioxidants / Q000737:chemistry*; D002374:Catalase / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000737:chemistry; D036341:Intercellular Signaling Peptides and Proteins; D007963:Leukocytes, Mononuclear / Q000166:cytology; D015227:Lipid Peroxidation; D008055:Lipids / Q000737:chemistry; D008070:Lipopolysaccharides / Q000737:chemistry; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress; D010100:Oxygen / Q000737:chemistry; D010455:Peptides / Q000494:pharmacology*; D055232:Proline-Rich Protein Domains; D011506:Proteins / Q000737:chemistry; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D008055:Lipids; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010455:Peptides; D011506:Proteins; C105874:colostrinine; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D010100:Oxygen