Background/aims: We have previously shown that hydroxyethyl free radicals produced during cytochrome P4502E1-mediated oxidation of ethanol covalently bind to microsomal proteins. The present study examined whether alkylation of proteins by hydroxyethyl radicals induces an immunologic response in alcoholic patients.
Methods: A microplate enzyme-linked immunosorbent assay was developed using as antigen human serum albumin or bovine fibrinogen reacted with chemically produced hydroxyethyl radicals.
Results: This assay showed that the sera of alcoholic cirrhotics contained both immunoglobulin (Ig) Gs and IgAs that recognized proteins modified by hydroxyethyl radicals, whereas practically no reaction was observed in the sera of healthy controls or cirrhotics without evidence of alcohol abuse. The reactivity of the sera from alcoholic patients was not influenced by the protein to which hydroxyethyl radicals were bound. The sera of alcoholic cirrhotics also contained antibodies directed against acetaldehyde-modified albumin. However, the reaction of alcoholic sera with hydroxyethyl radical epitopes was not inhibited by increasing concentrations of acetaldehyde-modified albumin produced under either reducing or nonreducing conditions.
Conclusions: The results indicate that a new group of antigens that do not cross-react with antibodies against acetaldehyde-derived epitopes is formed by the alkylation of protein by hydroxyethyl radicals and is involved in the development of immunologic reactions in alcoholic patients.
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http://dx.doi.org/10.1016/0016-5085(95)90025-x | DOI Listing |
Pharmaceutics
January 2025
CDL Research, University Medical Center Utrecht, 3584CX Utrecht, The Netherlands.
Background/objectives: Glioblastoma is the most common and lethal primary brain tumor. Patients often suffer from tumor- and treatment induced vasogenic edema, with devastating neurological consequences. Intracranial edema is effectively treated with dexamethasone.
View Article and Find Full Text PDFDiscov Nano
January 2025
Institute of Science, Department of Chemistry, Firat University, 23200, Elazığ, Turkey.
In this study, firstly chitin was reacted with chloracetyl chloride to synthesize the macroinitiator chitinchloroacetate (Ch.ClAc). Then, graft copolymers of methacrylamide (MAM), diacetone acrylamide (DAAM), N-(4-nitrophenyl)acrylamide (NPA), and 2-hydroxyethyl methacrylate (HEMA) monomers were synthesized by atom transfer radical polymerization (ATRP).
View Article and Find Full Text PDFJ Am Chem Soc
January 2025
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, and MoE Frontiers Science Center for Precision Oncology, University of Macau, Taipa, Macau SAR 999078, China.
Despite the development of various controlled release systems for antitumor therapies, off-target side effects remain a persistent challenge. In situ therapeutic synthesis from biocompatible substances offers a safer and more precise alternative. This study presents a hypoxia-initiated supramolecular free radical system capable of inducing intracellular polymerization, thereby disrupting the cytoskeleton and organelles within 4T1 cells.
View Article and Find Full Text PDFPolymers (Basel)
December 2024
Departamento de Química, Facultad de Ciencias Naturales, Matemáticas y Medio Ambiente, Universidad Tecnológica Metropolitana (UTEM), J. P. Alessandri 1242, Santiago 7800002, Chile.
A series of hydrophilic copolymers were prepared using 2-hydroxyethyl methacrylate (HEMA) and itaconic acid (IA) from free radical polymerization at different feed monomer ratios using ammonium persulfate (APS) initiators in water at 70 °C. The herbicide 2,4-dichlorophenoxy acetic acid (2,4-D) was grafted to Poly(HEMA--IA) by a condensation reaction. The hydrolysis of the polymeric release system, Poly(HEMA--IA)-2,4-D, demonstrated that the release of the herbicide in an aqueous phase depends on the polymeric system's pH value and hydrophilic character.
View Article and Find Full Text PDFInt J Pharm
January 2025
Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC 27710; Department of Chemistry and Biochemistry, North Carolina Central University, Durham, NC 27707. Electronic address:
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