Protective effects of an aqueous extract of Welsh onion green leaves on oxidative damage of reactive oxygen and nitrogen species

2006 ◽  
Vol 98 (1) ◽  
pp. 149-157 ◽  
Author(s):  
B WANG ◽  
S LIN ◽  
W HSIAO ◽  
J FAN ◽  
L FUH ◽  
...  
2020 ◽  
Vol 16 (3) ◽  
pp. 265-283
Author(s):  
Kyriaki Hatziagapiou ◽  
George I. Lambrou

Background: Reactive oxygen species and reactive nitrogen species, which are collectively called reactive oxygen nitrogen species, are inevitable by-products of cellular metabolic redox reactions, such as oxidative phosphorylation in the mitochondrial respiratory chain, phagocytosis, reactions of biotransformation of exogenous and endogenous substrata in endoplasmic reticulum, eicosanoid synthesis, and redox reactions in the presence of metal with variable valence. Among medicinal plants there is a growing interest in Crocus sativus L. It is a perennial, stemless herb, belonging to Iridaceae family, cultivated in various countries such as Greece, Italy, Spain, Israel, Morocco, Turkey, Iran, India, China, Egypt and Mexico. Objective: The present study aims to address the anti-toxicant role of Crocus sativus L. in the cases of toxin and drug toxification. Materials and Methods: An electronic literature search was conducted by the two authors from 1993 to August 2017. Original articles and systematic reviews (with or without meta-analysis), as well as case reports were selected. Titles and abstracts of papers were screened by a third reviewer to determine whether they met the eligibility criteria, and full texts of the selected articles were retrieved. Results: The authors focused on literature concerning the role of Crocus Sativus L. as an anti-toxicant agent. Literature review showed that Saffron is a potent anti-toxicant agent with a plethora of applications ranging from anti-oxidant properties, to chemotherapy protective effects. Conclusion: Literature findings represented in current review herald promising results for using Crocus Sativus L. and/or its active constituents as anti-toxicant, chemotherapy-induced protection and toxin protection.


2008 ◽  
Vol 410 (2) ◽  
pp. 359-368 ◽  
Author(s):  
Lucía Piacenza ◽  
Gonzalo Peluffo ◽  
María Noel Alvarez ◽  
John M. Kelly ◽  
Shane R. Wilkinson ◽  
...  

There is increasing evidence that Trypanosoma cruzi antioxidant enzymes play a key immune evasion role by protecting the parasite against macrophage-derived reactive oxygen and nitrogen species. Using T. cruzi transformed to overexpress the peroxiredoxins TcCPX (T. cruzi cytosolic tryparedoxin peroxidase) and TcMPX (T. cruzi mitochondrial tryparedoxin peroxidase), we found that both cell lines readily detoxify cytotoxic and diffusible reactive oxygen and nitrogen species generated in vitro or released by activated macrophages. Parasites transformed to overexpress TcAPX (T. cruzi ascorbate-dependent haemoperoxidase) were also more resistant to H2O2 challenge, but unlike TcMPX and TcCPX overexpressing lines, the TcAPX overexpressing parasites were not resistant to peroxynitrite. Whereas isolated tryparedoxin peroxidases react rapidly (k=7.2×105 M−1·s−1) and reduce peroxynitrite to nitrite, our results demonstrate that both TcMPX and TcCPX peroxiredoxins also efficiently decompose exogenous- and endogenously-generated peroxynitrite in intact cells. The degree of protection provided by TcCPX against peroxynitrite challenge results in higher parasite proliferation rates, and is demonstrated by inhibition of intracellular redox-sensitive fluorescence probe oxidation, protein 3-nitrotyrosine and protein–DMPO (5,5-dimethylpyrroline-N-oxide) adduct formation. Additionally, peroxynitrite-mediated over-oxidation of the peroxidatic cysteine residue of peroxiredoxins was greatly decreased in TcCPX overexpressing cells. The protective effects generated by TcCPX and TcMPX after oxidant challenge were lost by mutation of the peroxidatic cysteine residue in both enzymes. We also observed that there is less peroxynitrite-dependent 3-nitrotyrosine formation in infective metacyclic trypomastigotes than in non-infective epimastigotes. Together with recent reports of up-regulation of antioxidant enzymes during metacyclogenesis, our results identify components of the antioxidant enzyme network of T. cruzi as virulence factors of emerging importance.


2014 ◽  
Vol 64 ◽  
pp. 618-625 ◽  
Author(s):  
Lilian R.B. Mariutti ◽  
Eliseu Rodrigues ◽  
Renan C. Chisté ◽  
Eduarda Fernandes ◽  
Adriana Z. Mercadante

2013 ◽  
Vol 138 (2-3) ◽  
pp. 751-756 ◽  
Author(s):  
Bor-Sen Wang ◽  
Guan-Jhong Huang ◽  
Ya-Hui Lu ◽  
Lee-Wen Chang

2010 ◽  
Vol 62 (6) ◽  
pp. 601-605 ◽  
Author(s):  
Mongi Saoudi ◽  
Mohamed Salah Allagui ◽  
Abdelwaheb Abdelmouleh ◽  
Kamel Jamoussi ◽  
Abdelfattah El Feki

2014 ◽  
Vol 5 (8) ◽  
pp. 1956-1965 ◽  
Author(s):  
Hui-Chun Kuo ◽  
Hung-Chi Chang ◽  
Wan-Cheng Lan ◽  
Fan-Hsuan Tsai ◽  
Jung-Chun Liao ◽  
...  

In this study, we demonstrate the antioxidant and protective properties of the aqueous extract of two commercial Polydiaceae plants –Drynaria fortuneiandPseudodrynaria coronans– against 6-hydroxydopamine-induced oxidative damage in B35 neuroblastoma cells.


2012 ◽  
Vol 214 (1) ◽  
pp. 11-20 ◽  
Author(s):  
P Newsholme ◽  
E Rebelato ◽  
F Abdulkader ◽  
M Krause ◽  
A Carpinelli ◽  
...  

Growing evidence indicates that the regulation of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels is essential for maintaining normal β-cell glucose responsiveness. While long-term exposure to high glucose induces oxidative stress in β cells, conflicting results have been published regarding the impact of ROS on acute glucose exposure and their role in glucose stimulated insulin secretion (GSIS). Although β cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione (GSH) peroxidase, other less known GSH-based antioxidant systems are expressed in β cells at higher levels. Herein, we discuss the key mechanisms of ROS/RNS production and their physiological function in pancreatic β cells. We also hypothesize that specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic β cells to oxidative damage. In addition, using a hypothetical metabolic model based on the data available in the literature, we emphasize the importance of amino acid availability for GSH synthesis and for the maintenance of β-cell function and viability during periods of metabolic disturbance before the clinical onset of diabetes.


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