Protective role of exogenous nitric oxide against oxidative-stress induced by salt stress in barley (Hordeum vulgare)

The present study assesses the role of selenium, an antioxidant in salt-stressed plants. A hydroponic trial of sodium selenate (Na2SeO4) on the growth, oxidative stress and antioxidant protection system of Brassica rapa var. toria (BRSRT) plant was studied. 40 µmol and 100 µmol of Na2SeO4 were hydroponically applied to BRSRT roots with 50 mmol and 100 mmol sodium chloride (NaCl) for 12 days. Plant growth, biomass production and photosynthetic pigments at 100 mmol salt stress was inhibited while oxidative stress indicators, for example, hydrogen peroxide and lipid peroxidation were stimulated. Supplementation of 40 µmol Na2SeO4 with 50 mmol and 100 mmol NaCl improved growth, photosynthetic pigments and acted as an antioxidant by inhibiting lipid peroxidation and increasing superoxide dismutase, ascorbate peroxidase, catalase, glutathione peroxidase, glutathione reductase activities. The in-gel assays also showed enhanced activities of these enzymes. At 100 µmol concentration, selenium under salt stress, repressed growth and expression of antioxidant enzymes and stimulated oxidative stress with enhanced glutathione peroxidase activity. Under consolidated stress treatment, an addition of 40 µmol Na2SeO4 was the most effective for both NaCl concentrations. The finding reveals that the optimal selenium supplementation presents a promising potential for use in conditions of relatively high levels of NaCl stress for BRSRT seedlings.

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Protective Role of Perillic Acid Against Radiation−Induced Oxidative Stress, Cytokine Profile, DNA Damage, and Intestinal Toxicity in Mice

Journal of Environmental Pathology Toxicology and Oncology ◽

10.1615/jenvironpatholtoxicoloncol.v29.i3.40 ◽

2010 ◽

Vol 29 (3) ◽

pp. 199-212 ◽

Cited By ~ 11

Author(s):

P. Pratheeshkumar ◽

T.J. Raphael ◽

Girija Kuttan

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Protective Role ◽

Cytokine Profile ◽

Intestinal Toxicity ◽

Radiation Induced

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Protective Role of Glutathione in the Hippocampus after Brain Ischemia

International Journal of Molecular Sciences ◽

10.3390/ijms22157765 ◽

2021 ◽

Vol 22 (15) ◽

pp. 7765

Author(s):

Youichirou Higashi ◽

Takaaki Aratake ◽

Takahiro Shimizu ◽

Shogo Shimizu ◽

Motoaki Saito

Keyword(s):

Oxidative Stress ◽

Neuronal Death ◽

Excitatory Amino Acid ◽

Ischemia Reperfusion ◽

Thiol Group ◽

Protective Role ◽

Key Factor ◽

Rate Limiting ◽

Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

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