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Ascorbic acid amyloidosis

Chih-Chien Sung, Yu-Chuan Hsu, Chun-Chi Chen, Yuh-Feng Lin, Chia-Chao Wu
Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids...
2013: Oxidative Medicine and Cellular Longevity
Adriano Spreafico, Lia Millucci, Lorenzo Ghezzi, Michela Geminiani, Daniela Braconi, Loredana Amato, Federico Chellini, Bruno Frediani, Elena Moretti, Giulia Collodel, Giulia Bernardini, Annalisa Santucci
OBJECTIVE: Alkaptonuria (AKU) is an ultra-rare autosomal recessive disease that currently lacks an appropriate therapy. Recently we provided experimental evidence that AKU is a secondary serum amyloid A (SAA)-based amyloidosis. The aim of the present work was to evaluate the use of antioxidants to inhibit SAA amyloid and pro-inflammatory cytokine release in AKU. METHODS: We adopted a human chondrocytic cell AKU model to evaluate the anti-amyloid capacity of a set of antioxidants that had previously been shown to counteract ochronosis in a serum AKU model...
September 2013: Rheumatology
No abstract text is available yet for this article.
June 1952: Annals of the Rheumatic Diseases
No abstract text is available yet for this article.
May 1951: Revue Canadienne de Biologie
No abstract text is available yet for this article.
January 1965: American Journal of Ophthalmology
No abstract text is available yet for this article.
September 1964: Archivio Per le Scienze Mediche
No abstract text is available yet for this article.
November 19, 1953: Nordisk Medicin
Francisco J Muñoz, Carlos Opazo, Gabriel Gil-Gómez, Gladys Tapia, Virginia Fernández, Miguel A Valverde, Nibaldo C Inestrosa
Amyloid beta-peptide (Abeta) fibril deposition on cerebral vessels produces cerebral amyloid angiopathy that appears in the majority of Alzheimer's disease patients. An early onset of a cerebral amyloid angiopathy variant called hereditary cerebral hemorrhage with amyloidosis of the Dutch type is caused by a point mutation in Abeta yielding Abeta(Glu22-->Gln). The present study addresses the effect of amyloid fibrils from both wild-type and mutated Abeta on vascular cells, as well as the putative protective role of antioxidants on amyloid angiopathy...
April 15, 2002: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
O B Suhr, K Lång, L Wikström, I Anan, Y Ando, M El-Salhy, G Holmgren, K Tashima
Since oxidative stress has been implicated in amyloid diseases, a study of scavenger treatment of hereditary transthyretin amyloidosis was undertaken on 23 familial amyloidotic polyneuropathy (FAP) patients. Nine patients had undergone a liver transplantation for the disease. Twenty patients completed the 6-month study period of scavenger treatment (vitamin C, 1 g, three times daily, vitamin E, 0.1 g, three times daily and acetylcysteine, 0.2 g three times daily). They were evaluated clinically and by immunohistochemical measurement of hydroxynonenal (HNE), a product of lipid peroxidation, in biopsy specimens...
February 2001: Scandinavian Journal of Clinical and Laboratory Investigation
R Habbal, M Noureddine, K Hachim, M Zahraoui, L Azzouzi, S Fadouach, D Zaid, N Chraibi
Amyloidosis results from protein infiltration of the extracellular space of organs and tissues. Several amyloidosis proteins have been identified. Protein AL, (deriving from immunoglobulin light chain), protein AA and prealbumin are the most involved in this disease. When AL amyloidosis involves the heart, the illness is often terminal. Most clinical symptoms are heart failure and arrhythmia or block conduction. This case was characterised by the unusual combination of hypertension and amyloidosis. The diagnosis suggested by the echocardiographic but was confirmed by the damaged organ's biopsy...
1997: Néphrologie
T Miyata, Y Wada, Z Cai, Y Iida, K Horie, Y Yasuda, K Maeda, K Kurokawa, C van Ypersele de Strihou
Recent studies have demonstrated a marked increase in the level of advanced glycation end products (AGEs) in the plasma, skin and amyloid fibrils of hemodialysis (HD) patients. The presence of AGEs in (beta2m) forming amyloid fibrils has been established in a previous immunochemical study relying on a monoclonal anti-AGE antibody. In the present study, Western blot analysis and immunohistochemistry reveal that the epitope recognized by this antibody is N epsilon-(carboxymethyl)lysine (CML) and that CML is one of the AGE structures present in amyloid fibrils...
April 1997: Kidney International
I Kedar, E Sohar, M Ravid
ADA of human serum was demonstrated and investigated with an agar gel diffusion technique using amyloid-impregnated agar plates. Sera of 20 healthy adults, 40 patients with AA-amyloidosis, and 86 nonamyloidotic patients were tested. The presence of an ADF, showing enzymatic properties and strongly bound to albumin, was demonstrated in normals and amyloidotic and nonamyloidotic patients. ADA in the serum of amyloidotic and cirrhotic patients was markedly decreased due to the presence of an inhibitor of ADF. ADA of amyloidotic sera was restored to normal by EDTA, citric acid, and ascorbic acid...
May 1982: Journal of Laboratory and Clinical Medicine
A P Alyabyeva, Muravyev YuV
No abstract text is available yet for this article.
1983: Annals of the New York Academy of Sciences
M L Baltz, D Caspi, B E Glatthaar, U Moser, M B Pepys
It has been claimed that ascorbic acid enhances the in vitro degradation of AA amyloid fibrils. This raises the possibility that ascorbic acid may be of benefit in systemic AA amyloidosis, a condition with serious morbidity and mortality for which there is as yet no specific treatment. The effect was therefore tested of oral or injected supplements of ascorbic acid on the induction of AA amyloidosis in mice. Amyloid was induced either by repeated injections of casein or by injection of 'amyloid enhancing factor' and silver nitrate...
September 1984: Clinical and Experimental Immunology
M N Volgarev
No abstract text is available yet for this article.
September 1971: Voprosy Pitaniia
P Mètais, J M Mantz, J Warter
No abstract text is available yet for this article.
1972: Annales de Biologie Clinique
M Drózdz, E Kucharz
No abstract text is available yet for this article.
August 1, 1974: Wiadomości Lekarskie: Organ Polskiego Towarzystwa Lekarskiego
S N Rizvi, P D Gulati, H Vaishnava
No abstract text is available yet for this article.
December 14, 1974: British Medical Journal (1857-1980)
J Warter, J M Mantz, P Metais, D Storck, F Oberling
No abstract text is available yet for this article.
May 14, 1972: La Semaine des Hôpitaux: Organe Fondé Par L'Association D'enseignement Médical des Hôpitaux de Paris
V A Odinokova, V F Kondalenko, A P Kalinin, V B Zaĭrat'iants
No abstract text is available yet for this article.
1970: Arkhiv Patologii
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