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Abstract:

Acute and chronic treatments of mice with the glutathione-depleting agent, L-buthionine-(SR)-sulfoximine (BSO), impaired the mineralocorticoid receptor (MR)-dependent biological response by inhibiting aldosterone binding. This steroid-binding inhibition was fully reversed when reducing agents were added to kidney cytosol obtained from mice treated for 5 h, but it was only partially reversed in cytosol obtained from mice treated for 10 days. Although the oligomeric structure of the MR-hsp90 heterocomplex was always unaffected, a decreased amount of MR protein was evidenced after the long term treatment. Such a deleterious effect was correlated with a post-translational modification of MR, as demonstrated by an increased level of receptor carbonylation. In addition, a failure at the elongation/termination step was also observed during the receptor translation process in a reticulocyte lysate system. Thus, a high polyribosomes/monomers ratio and both increased proteolysis and decreased ADP-ribosylatable concentration of elongation factor 2 (EF-2) were shown. Importantly, similar observations were also performed in vivo after depletion of glutathione. Notwithstanding the EF-2 functional disruption, not all renal proteins were equally affected as the MR. Interestingly, both EF-2 and MR expressed in old mice were similarly affected as in L-buthionine-(SR)-sulfoximine-treated young mice. We therefore propose that a dramatic depletion of glutathione in kidney cells mimics the cumulative effect of aging which, at the end, may lead to a renal mineralocorticoid dysfunction.

Registro:

Documento: Artículo
Título:Impairment of mineralocorticoid receptor (MR)-dependent biological response by oxidative stress and aging: Correlation with post-translational modification of MR and decreased ADP-ribosylatable level of elongation factor 2 in kidney cells
Autor:Piwien-Pilipuk, G.; Ayala, A.; Machado, A.; Galigniana, M.D.
Filiación:Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Ciudad Universitaria, 1428 Buenos Aires, Argentina
Departamento de Bioquímica, Bromatología y Toxicología, Facultad de Farmacia, Universidad de Sevilla, 41012 Sevilla, Spain
1301 Medical Science Research Bldg. III, Dept. of Pharmacology, University of Michigan Medical School, Ann Arbor, MI 48109, United States
Palabras clave:Biological organs; Carbonylation; Cells; Monomers; Oligomers; Proteins; Oxidative stress; Biochemistry; buthionine sulfoximine; elongation factor 2; mineralocorticoid receptor; adenosine diphosphate ribosylation; aging; animal cell; animal model; article; controlled study; correlation analysis; cytosol; hormone binding; inhibition kinetics; male; mouse; nonhuman; oxidative stress; priority journal; protein degradation; protein depletion; protein expression; protein modification; protein processing; protein structure; structure analysis; translation initiation; ADP-Ribosylation Factors; Aging; Animals; Antimetabolites; Buthionine Sulfoximine; Cytosol; Enzyme Inhibitors; Glutathione; HSP90 Heat-Shock Proteins; Kidney; Male; Mice; Mice, Inbred BALB C; Oxidation-Reduction; Oxidative Stress; Oxygen; Peptide Elongation Factor 2; Polyribosomes; Precipitin Tests; Protein Binding; Protein Biosynthesis; Protein Processing, Post-Translational; Receptors, Mineralocorticoid; Reticulocytes; Time Factors; Transcription, Genetic; Animalia
Año:2002
Volumen:277
Número:14
Página de inicio:11896
Página de fin:11903
DOI: http://dx.doi.org/10.1074/jbc.M109530200
Título revista:Journal of Biological Chemistry
Título revista abreviado:J. Biol. Chem.
ISSN:00219258
CODEN:JBCHA
CAS:ADP-Ribosylation Factors, EC 3.6.5.2; Antimetabolites; Buthionine Sulfoximine, 5072-26-4; Enzyme Inhibitors; Glutathione, 70-18-8; HSP90 Heat-Shock Proteins; Oxygen, 7782-44-7; Peptide Elongation Factor 2; Receptors, Mineralocorticoid
PDF:https://bibliotecadigital.exactas.uba.ar/download/paper/paper_00219258_v277_n14_p11896_PiwienPilipuk.pdf
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v277_n14_p11896_PiwienPilipuk

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Citas:

---------- APA ----------
Piwien-Pilipuk, G., Ayala, A., Machado, A. & Galigniana, M.D. (2002) . Impairment of mineralocorticoid receptor (MR)-dependent biological response by oxidative stress and aging: Correlation with post-translational modification of MR and decreased ADP-ribosylatable level of elongation factor 2 in kidney cells. Journal of Biological Chemistry, 277(14), 11896-11903.
http://dx.doi.org/10.1074/jbc.M109530200
---------- CHICAGO ----------
Piwien-Pilipuk, G., Ayala, A., Machado, A., Galigniana, M.D. "Impairment of mineralocorticoid receptor (MR)-dependent biological response by oxidative stress and aging: Correlation with post-translational modification of MR and decreased ADP-ribosylatable level of elongation factor 2 in kidney cells" . Journal of Biological Chemistry 277, no. 14 (2002) : 11896-11903.
http://dx.doi.org/10.1074/jbc.M109530200
---------- MLA ----------
Piwien-Pilipuk, G., Ayala, A., Machado, A., Galigniana, M.D. "Impairment of mineralocorticoid receptor (MR)-dependent biological response by oxidative stress and aging: Correlation with post-translational modification of MR and decreased ADP-ribosylatable level of elongation factor 2 in kidney cells" . Journal of Biological Chemistry, vol. 277, no. 14, 2002, pp. 11896-11903.
http://dx.doi.org/10.1074/jbc.M109530200
---------- VANCOUVER ----------
Piwien-Pilipuk, G., Ayala, A., Machado, A., Galigniana, M.D. Impairment of mineralocorticoid receptor (MR)-dependent biological response by oxidative stress and aging: Correlation with post-translational modification of MR and decreased ADP-ribosylatable level of elongation factor 2 in kidney cells. J. Biol. Chem. 2002;277(14):11896-11903.
http://dx.doi.org/10.1074/jbc.M109530200