A review on protein–phenolic interactions and associated changes

Interactions of polyphenols with carbohydrates, lipids and proteins

While many epidemiological studies have associated the consumption of polyphenols within fruits and vegetables with a decreased risk of developing several chronic diseases, intervention studies have generally not confirmed these beneficial effects. The reasons for this discrepancy are not fully understood but include potential differences in dosing, interaction with the food matrix, and differences in polyphenol bioavailability. In addition to endogenous factors such as microbiota and digestive enzymes, the food matrix can also considerably affect bioaccessibility, uptake, and further metabolism of polyphenols. While dietary fiber (such as hemicellulose), divalent minerals, and viscous and protein-rich meals are likely to cause detrimental effects on polyphenol bioaccessibility, digestible carbohydrates, dietary lipids (especially for hydrophobic polyphenols, e.g., curcumin), and additional antioxidants may enhance polyphenol availability. Following epithelial uptake, polyphenols such as flavonoids may reduce phase II metabolism and excretion, enhancing polyphenol bioavailability. Furthermore, polyphenols may act synergistically due to their influence on efflux transporters such as p-glycoprotein. In order to understand polyphenol bioactivity, increased knowledge of the factors affecting polyphenol bioavailability, including dietary factors, is paramount.

Dietary factors affecting polyphenol bioavailability

https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1214&context=foodsciefacpub

Food processing and allergenicity

proceedings, in not being up-to-date. There are almost no references to papers later than 1990, except for some self-citations which extend to 1991. In addition to well known major contributors to the field of metastasis, research participants were also drawn from laboratories in Continental Europe, which are not frequently represented at Symposia of this type. Some of the papers are general overviews, while others report the Authors own studies in detail. On the whole the various contributions are rather disparate, but occasionally authors compare and contrast a related phenomenon. An example is the role of the CD-44, a transmembrane protein involved in lymphocyte transport, for which the group of Herrlich (Karlsruhe, Germany) have obtained convincing evidence of a role in metastasis. On the other hand, I.R. Hart (London, UK) described studies involving a panel of melanoma cells in which no evidence for a direct involvement of CD-44 in metastasis was found. The subject matter is divided into the following sections: The first section has papers dealing with the role of ras oncogenes and bladder carcinoma and the initial steps in cancer dissemination of rat bladder carcinoma. These raise questions without providing any answers. The second section is concerned principally with cell adhesion and highlights complexity and conflicting results. In the third section the discussion of angiogenesis is disappointing and work is reported from investigators who are not prominent in the area. There is, however, a very valuable chapter from L. Weiss (Buffalo, New York). He analyses, in detail, a mechanism for the destruction of cancer cells in the microvasculature based on deformation. Weiss' data for the destruction of cancer cells when trapped in capillaries has long been a key observation in the field of blood-borne metastatic spread. It leads to the concept of metastatic inefficiency which is so evident when the relative infrequency of metastasis is compared with the number of cancer cells shed into the circulation. Weiss' suggestion as to how this destruction occurs is compelling and he provides most interesting new data which indicates that treatment of cells with doxorubicin increases biomechanical destruction. In the section on melanoma there are two rather unconvincing contributions on metastasis-associated surface molecules, in addition to the critical analysis of the role of CD-44 to which reference has already been made. The last two sections contain a mixture of topics and on the whole are of little interest. Immunotherapy with autologous tumour 'vaccines' …

Protein Kinase C

Warfarin (4-hydroxy coumarin) is Vitamin K (VK) antagonist that inhibits
 Vitamin K-dependent (VKD) processes, such as blood coagulation. It exerts
 influence on some non-VKD-related activities as well. In this study, the
 effect of subacute (30-day) oral warfarin (2 mg L-1 and 1 mg L-1) intake on
 hematological parameters was examined in two rat strains, Albino Oxford (AO)
 and Dark Agouti (DA), that differ in their sensitivity to certain chemicals.
 Greater susceptibility to anticoagulant effect of 2 mg L-1 of warfarin was
 observed in AO rats and was associated with an increase in relevant
 hematological parameters in this strain. Although both strains responded to 2
 mg L-1 of warfarin with quantitative changes in peripheral blood leukocytes
 differential bone marrow and lung responses were observed. Strain-related
 differences in proinflammatory activity of peripheral blood granulocytes and
 in mononuclear cell IFN-γ production were observed. Recognition of
 differences in quantitative and qualitative effects of oral warfarin on
 processes other than hemostasis might be of relevance for those humans who
 are on warfarin therapy. [Projekat Ministarstva nauke Republike Srbije, br.
 173039]

/pdf/strain-differences-in-the-toxicity-of-the-vitamin-k-4t30gukp34.pdf

Strain differences in the toxicity of the vitamin K antagonist warfarin in rats

Comparative digestion of thermally treated vertebrates and invertebrates allergen pairs in real food matrix.

Modified allergens are a safer and more efficient alternative to natural allergens for specific immunotherapy. As the modification of an allergen can diminish its immunogenicity due to the alteration of T-cell epitopes, in this paper we study the effects of a reversible chemical modification of Art v 1, the main allergen of mugwort pollen, on its allergenicity and immunogenicity. Modification of Art v 1 by cis-aconitylation into a polyanionic derivative (CAA) did not result in any significant structural alteration. However, IgE-binding epitopes on CAA were blocked, resulting in a reduced IgE-binding and basophil activation. Both proteins induced proliferation of CD3+CD4+ T-cells in mugwort-allergic patients, but only unmodified allergens increased IL-4, IL-5 and IL-10 production. Rabbit and mouse anti-CAA antibodies exhibited cross-reactivity with native allergens and blocked human IgE-binding to Art v 1. Degradation of CAA by lysosomal fraction enzymes resulted in a similar set of peptides, harboring MHC class II-binding peptides, as unmodified proteins. Thus, cis-aconitylation modified Art v 1 had a significantly reduced allergenicity, whereas its immunogenicity was completely preserved. Acid-environment-responsive modification, which releases a full repertoire of native allergen epitopes within a particular site, can be considered a smart drug delivery system, which is able to deliver a therapeutically-effective dose in a controlled manner, and minimizes adverse side effects.

/pdf/hypoallergenic-acid-sensitive-modification-preserves-major-bb9115qhh1.pdf

Hypoallergenic acid-sensitive modification preserves major mugwort allergen fold and delivers full repertoire of MHC class II-binding peptides during endolysosomal degradation

Marija Stojadinovic

Papers

Strain differences in the toxicity of the vitamin K antagonist warfarin in rats

Comparative digestion of thermally treated vertebrates and invertebrates allergen pairs in real food matrix.

Hypoallergenic acid-sensitive modification preserves major mugwort allergen fold and delivers full repertoire of MHC class II-binding peptides during endolysosomal degradation