Protective effect of nitric oxide on iron deficiency-induced oxidative stress in maize (Zea mays)

Objective: This study aims to clarify the effects of intravenous iron supplementation on biomarkers for oxidative stress in women with iron deficiency anemia. Methods: This is a cross-sectional review of 40 healthy women and 40 women who underwent intravenous iron treatment due to anemia. Biochemical markers for oxidative stress were determined for both healthy controls and anemic patients. These markers were also evaluated at hour 1 and day 30 of intravenous iron treatment. Results: The patients with anemia had significantly higher catalase activity and total oxidant status (TOS) but significantly lower nitrate and total anti-oxidant status (TAS) than the healthy controls (p=0.0245, p<0.0001, p=0.0437 and p<0.0001 respectively). At hour 1 of intravenous iron treatment, nitrate, nitrite, nitric oxide, total thiol and TAS values were significantly lower and TOS values were significantly higher than those before the administration of treatment (p=0.0322, p=0.0003, p=0.0005, p<0.0001, p<0.0001 and p=0.004). At day 30 of intravenous iron treatment, catalase activity, nitrate, total thiol and TOS values were significantly lower than those before the administration of treatment (p=0.0332, p=0.0015, p=0.0391 and p<0.0001 respectively) and at hour 1 of treatment (p=0.0498, p<0.0001, p=0.0004 and p<0.0001 respectively). At day 30 of intravenous iron treatment, nitric oxide and TAS values were significantly higher than those before the administration of treatment (p=0.0480 and p=0.001 respectively) and at hour 1 of treatment (p<0.0001 for both). Conclusion: Intravenous iron replacement prompts oxidative stress at hour 1 of infusion in adults with anemia but this increase resolves partially in the following 30 days.

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Effects of Safranal on Tissue Oxidative Stress in Sub-Chronic Thinner-Addicted Rats

Journal of the Hellenic Veterinary Medical Society ◽

10.12681/jhvms.22942 ◽

2020 ◽

Vol 71 (1) ◽

pp. 1997

Author(s):

M. DÜZ ◽

A. F. FIDAN

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Protective Effect ◽

Total Antioxidant Capacity ◽

Reduced Glutathione ◽

Control Group ◽

Albino Rats ◽

Total Antioxidant ◽

Wistar Albino Rats ◽

And Oxidative Stress

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.

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Electrolyte Leakage and the Protective Effect of Nitric Oxide on Leaves of Flooded Rice Exposed to Herbicides

Planta Daninha ◽

10.1590/s0100-83582016340400018 ◽

2016 ◽

Vol 34 (4) ◽

pp. 777-786 ◽

Cited By ~ 3

Author(s):

K.S. SILVA ◽

L.J. K. URBAN ◽

A. BALBINOT ◽

F.S. GNOCATO ◽

N.D. KRUSE ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Protective Effect ◽

Sodium Nitroprusside ◽

Antioxidant System ◽

Electrolyte Leakage ◽

Rice Cultivar ◽

Flooded Rice ◽

Leaf Segments

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.

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Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARγ and abrogation of oxidative stress and inflammation

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0204 ◽

2014 ◽

Vol 92 (9) ◽

pp. 717-724 ◽

Cited By ~ 61

Author(s):

Ayman M. Mahmoud

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Protective Effect ◽

Liver Lipid ◽

Inos Mrna ◽

Peroxisome Proliferator ◽

Dependent Manner ◽

Protective Effects ◽

Peroxisome Proliferator Activated Receptor ◽

Intraperitoneal Dose

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.

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