Protective effect of molecular hydrogen against oxidative stress caused by peroxynitrite derived from nitric oxide in rat retina

2015 ◽  
Vol 43 (6) ◽  
pp. 568-577 ◽  
Author(s):  
Takashi Yokota ◽  
Naomi Kamimura ◽  
Tsutomu Igarashi ◽  
Hiroshi Takahashi ◽  
Shigeo Ohta ◽  
...  
Nitric Oxide ◽  
2008 ◽  
Vol 19 ◽  
pp. 56
Author(s):  
Harminder Pal Singh ◽  
Shalinder Kaur ◽  
Daizy Rani Batish ◽  
Ravinder K Kohli

2014 ◽  
Vol 37 (2) ◽  
pp. 136-141 ◽  
Author(s):  
Seyed Jafar Moosavi ◽  
Masoumeh Habibian ◽  
Maghsoud Peeri ◽  
Mohammad Ali Azarbayjani ◽  
Seyed Mohammad Nabavi ◽  
...  

2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.


2016 ◽  
Vol 34 (4) ◽  
pp. 777-786 ◽  
Author(s):  
K.S. SILVA ◽  
L.J. K. URBAN ◽  
A. BALBINOT ◽  
F.S. GNOCATO ◽  
N.D. KRUSE ◽  
...  

ABSTRACT The nitric oxide acts on the antioxidant system of plants and can discontinue the damage of herbicides elicitors of oxidative stress that cause the disruption of membranes and leakage of cellular contents. In order to evaluate the protective effect of nitric oxide in electrolytes leakage, leaf segments of the Puita INTA CL rice cultivar were incubated with 0, 5, 50, 500 and 5,000 μM clomazone (360 g a.i. L-1), oxadiazon (250 g a.i. L-1), oxyfluorfen (240 g a.i. L-1) and the formulated mixture of paraquat (200 g a.i. L-1) + diuron (100 g a.i. L-1) to obtain the maximum potential conductivity of 50% (MPC50). Subsequently, leaf segments were pre-treated with 0, 200 and 2,000 μM of sodium nitroprusside (SNP) for four hours and further incubated for 48 hours with 0, 0.5, 1, 2 and 4 times the concentration of the herbicide that caused the CMP50, and the protective effect was reassessed in the presence of nitric oxide scavenger, cPTIO. The MPC50 was caused by exposure to 188.9, 273.4, 410.2 + 205.1 and 917.0 μM of Oxadiazon, Oxyfluorfen, Paraquat + Diuron and Clomazone. Pretreatment with 200 μM of SNP reduced electrolyte leakage in leaf segments exposed to 2 and 4 times the MPC50 to oxadiazon and paraquat + diuron, while 2,000 μM reduced the damage caused by oxyfluorfen, at the same concentrations. Also, 200 and 2,000 μM of SNP were efficient for clomazone, and the protection was confirmed by cPTIO in all cases.


2014 ◽  
Vol 92 (9) ◽  
pp. 717-724 ◽  
Author(s):  
Ayman M. Mahmoud

The most important reason for the non-approval and withdrawal of drugs by the Food and Drug Administration is hepatotoxicity. Therefore, this study was undertaken to evaluate the protective effects of hesperidin against cyclophosphamide (CYP)-induced hepatotoxicity in Wistar rats. The rats received a single intraperitoneal dose of CYP of 200 mg/kg body mass, followed by treatment with hesperidin, orally, at doses of 25 and 50 mg/kg for 11 consecutive days. CYP induced hepatic damage, as evidenced by the significantly elevated levels of serum pro-inflammatory cytokines, serum transaminases, liver lipid peroxidation, and nitric oxide. As a consequence, there was reduced glutathione content, and the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were markedly reduced. In addition, CYP administration induced a considerable downregulation of peroxisome proliferator activated receptor gamma (PPARγ) and upregulation of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) mRNA expression. Hesperidin, in a dose-dependent manner, rejuvenated the altered markers to an almost normal state. In conclusion, hesperidin showed a potent protective effect against CYP-induced oxidative stress and inflammation leading to hepatotoxicity. The study suggests that hesperidin exerts its protective effect against CYP-induced hepatotoxicity through upregulation of hepatic PPARγ expression and abrogation of inflammation and oxidative stress.


2016 ◽  
Vol 71 (1-2) ◽  
pp. 21-28 ◽  
Author(s):  
Mi Hwa Park ◽  
Jae-Won Ju ◽  
Mihyang Kim ◽  
Ji-Sook Han

AbstractEndothelial cell dysfunction is considered a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of daidzein, a natural isoflavonoid, against high-glucose–induced oxidative damage in human umbilical vein endothelial cells (HUVECs). Treatment with a high concentration of glucose (30 mM) induced oxidative stress in the endothelial cells, against which daidzein protected the cells as demonstrated by significantly increased cell viability. In addition, lipid peroxidation, intracellular reactive oxygen species (ROS) generation, and indirect nitric oxide levels induced by the high glucose treatment were significantly reduced in the presence of daidzein (0.02–0.1 mM) in a dose-dependent manner. High glucose levels induced the overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and NF-κB proteins in HUVECs, which was suppressed by treatment with 0.04 mM daidzein. These findings indicate the potential of daidzein to reduce high glucose-induced oxidative stress.


Nitric Oxide ◽  
2005 ◽  
Vol 13 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Suyun Shi ◽  
Gang Wang ◽  
Yading Wang ◽  
Lingang Zhang ◽  
Lixin Zhang

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