The Protective Effects of Acetylsalicylic Acid on Free Radical Production in Cisplatin Induced Nephrotoxicity: An Experimental Rat Model

2003 ◽  
Vol 26 (4) ◽  
pp. 259-270 ◽  
Author(s):  
Bahar Ulubaş ◽  
M. Y. Burak Çımen ◽  
Duygu Düşmez Apa ◽  
Emel Saritaş ◽  
Necatı Muşlu ◽  
...  
Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1876
Author(s):  
Peter F. Surai ◽  
Katie Earle-Payne ◽  
Michael T. Kidd

Natural antioxidants have received tremendous attention over the last 3 decades. At the same time, the attitude to free radicals is slowly changing, and their signalling role in adaptation to stress has recently received a lot of attention. Among many different antioxidants in the body, taurine (Tau), a sulphur-containing non-proteinogenic β-amino acid, is shown to have a special place as an important natural modulator of the antioxidant defence networks. Indeed, Tau is synthesised in most mammals and birds, and the Tau requirement is met by both synthesis and food/feed supply. From the analysis of recent data, it could be concluded that the direct antioxidant effect of Tau due to scavenging free radicals is limited and could be expected only in a few mammalian/avian tissues (e.g., heart and eye) with comparatively high (>15–20 mM) Tau concentrations. The stabilising effects of Tau on mitochondria, a prime site of free radical formation, are characterised and deserve more attention. Tau deficiency has been shown to compromise the electron transport chain in mitochondria and significantly increase free radical production. It seems likely that by maintaining the optimal Tau status of mitochondria, it is possible to control free radical production. Tau’s antioxidant protective action is of great importance in various stress conditions in human life, and is related to commercial animal and poultry production. In various in vitro and in vivo toxicological models, Tau showed AO protective effects. The membrane-stabilizing effects, inhibiting effects on ROS-producing enzymes, as well as the indirect AO effects of Tau via redox balance maintenance associated with the modulation of various transcription factors (e.g., Nrf2 and NF-κB) and vitagenes could also contribute to its protective action in stress conditions, and thus deserve more attention.


Diabetes ◽  
1984 ◽  
Vol 33 (2) ◽  
pp. 160-163 ◽  
Author(s):  
K. Asayama ◽  
D. English ◽  
A. E. Slonim ◽  
I. M. Burr

2020 ◽  
Vol 24 (1) ◽  
pp. 39-44
Author(s):  
E. V. Smirnova ◽  
E. V. Proskurnina ◽  
T. N. Krasnova

BACKGROUND. Oxidative status impairment plays a significant role in the pathogenesis of SLE and lupus nephritis (LN). The data about oxidative status in this disease are incomplete, that’s why it’s necessary to use a new approach to study it. THE AIM: To study oxidative status in SLE patients with kidney involvement. PATIENTS AND METHODS:53 patients with SLE were included in this prospective study, among them 40 patients with different severity of kidney involvement, control group were 87 healthy donors. Oxidative stress parameters were measured: antioxidant activity (AOA) of blood plasma and parameters, characterizing the state of the main source of reactive oxygen species (ROS) – neutrophils, more specifically: specific spontaneous neutrophil activity, specific stimulated activity (peak and integral), coefficient of respiratory burst attenuation, representing the rate of free radical production decrease after stimulation, the higher the value of this parameter, the slower is free radical production decrease. RESULTS. It was shown elevation of neutrophil free radical-producing activity parameters and elevation of blood plasma AOA in patients with LN, comparing to healthy controls. Immunosuppressive therapy with glucocorticosteroids (GCS) and cytostatics (CS) increased blood plasma AOA comparing to monotherapy with GCS. A correlation between oxidative status impairment and intensity of inflammatory reactions was found: correlation of respiratory burst attenuation coefficient with blood sedimentation rate was shown. Reduction of spontaneous free radical-producing neutrophil activity was found in LN patients with NS, which might be the result of neutrophil functional activity attenuation in high disease activity. CONCLUSION. The increased free radical-producing neutrophil activity was shown, which might be the cause of oxidative stress in SLE with LN. It seems warranted investigation of these parameters in samples of larger volume to search targets aimed at neutrophils. The necessity of antioxidant therapy in patients with SLE seems doubtful, as they show significant increase of blood plasma AOA, which might result from compensatory reaction of human organism to oxidative stress and therapy with GCS and CS.


1992 ◽  
Vol 55 ◽  
pp. 248
Author(s):  
H. Zhang ◽  
E. Agardh ◽  
C-D. Agardh

Glia ◽  
2004 ◽  
Vol 46 (3) ◽  
pp. 296-301 ◽  
Author(s):  
Arumugam R. Jayakumar ◽  
K.V. Rama Rao ◽  
Arne Schousboe ◽  
Michael D. Norenberg

2008 ◽  
Vol 295 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Krisztian Stadler ◽  
Marcelo G. Bonini ◽  
Shannon Dallas ◽  
Danielle Duma ◽  
Ronald P. Mason ◽  
...  

Diabetic patients frequently encounter ketosis that is characterized by the breakdown of lipids with the consequent accumulation of ketone bodies. Several studies have demonstrated that reactive species are likely to induce tissue damage in diabetes, but the role of the ketone bodies in the process has not been fully investigated. In this study, electron paramagnetic resonance (EPR) spectroscopy combined with novel spin-trapping and immunological techniques has been used to investigate in vivo free radical formation in a murine model of acetone-induced ketosis. A six-line EPR spectrum consistent with the α-(4-pyridyl-1-oxide)- N-t-butylnitrone radical adduct of a carbon-centered lipid-derived radical was detected in the liver extracts. To investigate the possible enzymatic source of these radicals, inducible nitric oxide synthase (iNOS) and NADPH oxidase knockout mice were used. Free radical production was unchanged in the NADPH oxidase knockout but much decreased in the iNOS knockout mice, suggesting a role for iNOS in free radical production. Longer-term exposure to acetone revealed iNOS overexpression in the liver together with protein radical formation, which was detected by confocal microscopy and a novel immunospin-trapping method. Immunohistochemical analysis revealed enhanced lipid peroxidation and protein oxidation as a consequence of persistent free radical generation after 21 days of acetone treatment in control and NADPH oxidase knockout but not in iNOS knockout mice. Taken together, our data demonstrate that acetone administration, a model of ketosis, can lead to protein oxidation and lipid peroxidation through a free radical-dependent mechanism driven mainly by iNOS overexpression.


2004 ◽  
Vol 91 (2) ◽  
pp. 327-336 ◽  
Author(s):  
Terence McManus ◽  
Matthew Sadgrove ◽  
Ashley K. Pringle ◽  
John E. Chad ◽  
Lars E. Sundstrom

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