Role of antioxidant activity of taurine in diabetesThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 91-99 ◽  
Author(s):  
Stephen W. Schaffer ◽  
Junichi Azuma ◽  
Mahmood Mozaffari

The unifying hypothesis of diabetes maintains that reactive oxygen species (ROS) generated in the mitochondria of glucose-treated cells promote reactions leading to the development of diabetic complications. Although the unifying hypothesis attributes the generation of oxidants solely to impaired glucose and fatty acid metabolism, diabetes is also associated with a decline in the levels of the endogenous antioxidant taurine in a number of tissues, raising the possibility that changes in taurine status might also contribute to the severity of oxidant-mediated damage. There is overwhelming evidence that taurine blocks toxicity caused by oxidative stress, but the mechanism underlying the antioxidant activity remains unclear. One established antioxidant action of taurine is the detoxification of hypochlorous acid. However, not all of the antioxidant actions of taurine are related to hypochlorous acid because they are detected in isolated cell systems lacking neutrophils. There are a few studies showing that taurine either modulates the antioxidant defenses or blocks the actions of the oxidants, but other studies oppose this interpretation. Although taurine is incapable of directly scavenging the classic ROS, such as superoxide anion, hydroxyl radical, and hydrogen peroxide, there are numerous studies suggesting that it is an effective inhibitor of ROS generation. The present review introduces a novel antioxidant hypothesis, which takes into consideration the presence of taurine-conjugated tRNAs in the mitochondria. Because tRNA conjugation is required for normal translation of mitochondrial-encoded proteins, taurine deficiency reduces the expression of these respiratory chain components. As a result, flux through the electron transport chain decreases. The dysfunctional respiratory chain accumulates electron donors, which divert electrons from the respiratory chain to oxygen, forming superoxide anion in the process. Restoration of taurine levels increases the levels of conjugated tRNA, restores respiratory chain activity, and increases the synthesis of ATP at the expense of superoxide anion production. The importance of this and other actions of taurine in diabetes is discussed.

Agric ◽  
2016 ◽  
Vol 26 (1) ◽  
pp. 85
Author(s):  
Sri Kasmiyati ◽  
Sucahyo

<p>Increased production of reactive oxygen species or ROS is one of the common responses to a wide range of biotic and abiotic stresses. Increased production of ROS is outstripping endogenous antioxidant defense systems has been referred to as oxidative stress. Heavy metals are known to initiate ROS generation which is implicated as a oxidative stress. Cr is a toxic heavy metal that can generate ROS like H2O2 and O2 - which cause oxidative stress. In this study, chromium toxicity was studied to detect the oxidative stress on Sonchus oleraceus weed plants by the detection of superoxide anion and H2O2. Superoxide anion was detected by staining techniques with nitroblue tetrazolium (NBT) and hydrogen peroxide by Diaminobenzidine tetrahydrochloride (DAB) staining. Results indicated that the plants were grown in sand media generate the highest (0.89 A/g FW and 3.23 mol/g FW) than in soil media (0.23 A/g FW and 2.11 mol/g FW) superoxide anion (*O- 2) and H2O2 and soil containing textile sludge (0.18 A/g FW and 2.66 mol/g FW), respectively. At application of 10 mg Cr6+/L and 250 mg Cr3+/L, the production of *O- 2 and H2O2 in leaves of sonchus plants were significantly increased compared with the control plants. The highest production of H2O2 and *O- 2 were showed in the leaves of sonchus plants grown in sand media with Cr6+ application. In this study, either Cr3+ or Cr6+ caused oxidative stress in Sonchus oleraceus weed plants. The result also showed that sonchus plants esposed to toxic Cr can suffer from oxidative stress leading to reduction of its fresh and dry plants biomass. NBT and DAB in an appropriate probe and significant value for monitoring the formation of *O- 2 and H2O2 in plants.</p>


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yuri Lourenco-Gonzalez ◽  
Victor Fattori ◽  
Talita P. Domiciano ◽  
Ana C. Rossaneis ◽  
Sergio M. Borghi ◽  
...  

Clinically active drugs for the treatment of acute pain have their prescription limited due to the significant side effects they induce. An increase in reactive oxygen species (ROS) has been linked to several conditions, including inflammation and pain processing. Therefore, new or repurposed drugs with the ability of reducing ROS-triggered responses are promising candidates for analgesic drugs. Vinpocetine is a clinically used nootropic drug with antioxidant, anti-inflammatory, and analgesic properties. However, the effects of vinpocetine have not been investigated in a model with a direct relationship between ROS, inflammation, and pain. Based on that, we aimed to investigate the effects of vinpocetine in a model of superoxide anion-induced pain and inflammation using potassium superoxide (KO2) as a superoxide anion donor to trigger inflammation and pain. In the KO2 model, vinpocetine dose-dependently reduced pain-like behaviors (spontaneous pain and hyperalgesia), paw edema, and neutrophil and mononuclear cell recruitment to the paw skin (assessed by H&E staining, fluorescence, and enzymatic assays) and to the peritoneal cavity. Vinpocetine also restored tissue endogenous antioxidant ability and Nrf2 and Ho-1 mRNA expression and reduced superoxide anion production and gp91phox mRNA expression. We also observed the inhibition of IκBα degradation by vinpocetine, which demonstrates a reduction in the activation of NF-κB explaining the diminished production of IL-33, IL-1β, and TNF-α. Collectively, our data show that vinpocetine alleviates pain and inflammation induced by KO2, which is a mouse model with a direct role of ROS in triggering pain and other inflammatory phenomena. Thus, the results suggest the repurposing of vinpocetine as an anti-inflammatory and analgesic drug.


Circulation ◽  
1997 ◽  
Vol 96 (2) ◽  
pp. 614-620 ◽  
Author(s):  
Kamal M. Mohazzab-H. ◽  
Pawel M. Kaminski ◽  
Michael S. Wolin

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
Meera Ramanujam ◽  
Rengarajulu Puvanakrishnan

Neutrophil infiltration plays a major role in the pathogenesis of myocardial injury. Oxidative injury is suggested to be a central mechanism of the cellular damage after acute myocardial infarction. This study is pertained to the prognostic role of a tetrapeptide derivative PEP1261 (BOC-Lys(BOC)-Arg-Asp-Ser(tBu)-OtBU), a peptide sequence (39–42) of lactoferrin, studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation, lysosomal enzymes release, and enhanced expression of C proteins. The groundwork experimentation was concerned with the isolation of neutrophils from the normal and acute myocardial infarct rats to find out the efficacy of PEP1261 in the presence of a powerful neutrophil stimulant, phorbol 12-myristate 13 acetate (PMA). Stimulation of neutrophils with PMA resulted in an oxidative burst of superoxide anion and enhanced release of lysosomal enzymes and expression of complement proteins. The present study further demonstrated that the free radicals increase the complement factors in the neutrophils confirming the role of ROS. PEP1261 treatment significantly reduced the levels of superoxide anion and inhibited the release of lysosomal enzymes in the stimulated control and infarct rat neutrophils. This study demonstrated that PEP1261 significantly inhibited the effect on the ROS generation as well as the mRNA synthesis and expression of the complement factors in neutrophils isolated from infarct heart.


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