scholarly journals The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats: the protective role of resveratrol

2018 ◽  
Vol 7 (3) ◽  
pp. 503-512 ◽  
Author(s):  
Erten Akbel ◽  
Damla Arslan-Acaroz ◽  
Hasan Huseyin Demirel ◽  
Ismail Kucukkurt ◽  
Sinan Ince
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Tissue Damage ◽  
Protective Role ◽  
Organophosphate Pesticide ◽  
Subchronic Exposure

The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks.

scholarly journals Cellular Apoptosis, Mitochondrial Swelling, Permeability and Cytochrome-C Level After (Fe3o4)-Nps Nanoparticles Exposure and Protective Role of Diferuloylmethane in Rats Liver

2020 ◽  
Vol 7 (1) ◽  
pp. 140-154
Author(s):  
Zina Bouteraa ◽  
Rachid Rouabhi ◽  
Fouad Menaceur ◽  
Salim Gasmi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protective Role ◽  
Mitochondrial Swelling ◽  
Male Rats ◽  
Glutathione S Transferase ◽  
Defensive Role ◽  
Cellular Apoptosis ◽  
Cyt C

AbstractDuring recent years the defensive role of diferuloylmethane against oxidative stress and apoptosis has been experimentally documented. Fe3O4-NPs can cause cellular death by inducing oxidative stress. Present study aimed to investigate whether diferuloylmethane could protect rats mitochondria against Fe3O4-NPs intoxication. Twenty adult male rats were randomly chosen and divided into four groups: control; treated with 10 mg/kg/d of Fe3O4-NPs; treated with diferuloylmethane at the dose 20 ml/kg/d; treated with Fe3O4-NPs (10 mg/kg/d) and diferuloylmethane (20 ml/kg/d) respectively for 28 days. The results showed that Fe3O4-NPs increased the Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxidation, mit-GSH (Glutathione), mit-CAT (Catalase), mit-GST (Glutathione S-transferase) and decreased mit-GPx (Glutathione peroxidase), with increased in mitochondrial swelling and permeability followed by the increasing level of plasmatic Cyt-c. The addition of diferuloylmethane (DFM) to these samples reduces or corrects the amount of the most of biomarkers. These findings have demonstrated that DFM can act as an antioxidant and antiapoptotic factor against damages induced by Fe3O4-NPs.

scholarly journals Effects of cisplatin on lipid peroxidation and the glutathione redox status in the liver of male rats: The protective role of selenium

2010 ◽  
Vol 62 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Ivana Trbojevic ◽  
Branka Ognjanovic ◽  
Natasa Djordjevic ◽  
Snezana Markovic ◽  
A.S. Stajn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Lipids ◽  
Redox Status ◽  
Protective Role ◽  
Male Rats ◽  
Albino Rats ◽  
Wistar Albino Rats ◽  
Glutathione Redox

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.

scholarly journals Role of vitamin C against bifenthrin induced oxidative damage in lungs of Wistar rats

2016 ◽  
Vol 8 (1) ◽  
pp. 346-349
Author(s):  
Muneer Ahmad Dar ◽  
Rajinder Raina ◽  
Arshad Hussain Mir ◽  
Pawan Kumar Verma ◽  
Mahrukh Ahmad
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin C ◽  
Protective Role ◽  
Group Iv ◽  
Control Value ◽  
Oxidative Stress Parameters ◽  
Group I ◽  
Stress Parameters

The aim of present study was to unravel the protective role of vitamin C on oxidative stress parameters in lung homogenates of bifenthrin intoxicated rats. Rats were divided into four groups. Group I served as control while group II animals were treated with bifenthrin @ 5.8mg/Kg/day. In group III, vitamin C was orally administered @ 60mg/Kg/day where as group IV received both vitamin C and bifenthrin @ 60mg/Kg/day and 5.8mg/Kg/day respectively. After 30th day of treatment, lung samples were taken and analysed for oxidative stress parameters. Significant (P<0.05) increase in lipid peroxidation was observed from control value of 4.80±0.39 to 7.90±0.50 in bifenthrin treated animals. Mean control values of SOD, GSH-Px and CAT were 0.55±0.05, 0.98±0.03 and 138.70±6.01 which were significantly (P<0.05) decreased to values of 0.27±0.0, 0.53±0.05 and 91.10±9.70 respectively in bifenthrin treated animals. The value of GST increased significantly (p<0.05) to 1.05±0.06 in bifenthrin administered animals from control value of 0.70±0.08. Pre-treatment with vitamin C in ameliorative group IV significantly restored the normal values of lipid peroxidation, SOD, GST and CAT but could not reverse the decreased values of GSH-Px. The present research is first of its type where in free radical generation due to bifenthrin –a commonly used insecticide was evaluated in lung homogenates when given orally which might be due to residues present in the lung. Besides it will be helpful in better understanding of toxicological profile of pyrethoids, the most commonly used insecticides.

scholarly journals Protective Role of Catechin and Quercetin in Sodium Benzoate-Induced Lipid Peroxidation and the Antioxidant System in Human ErythrocytesIn Vitro

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Gamze Yetuk ◽  
Dilek Pandir ◽  
Hatice Bas
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Sodium Benzoate ◽  
Protective Role ◽  
Food Additive ◽  
Human Erythrocytes ◽  
Low Concentrations ◽  
High Concentrations

The aim of this study was to evaluate the protective effect of catechin and quercetin in sodium benzoate- (SB-) induced oxidative stress in human erythrocytesin vitro. For this, the effects of SB (6.25, 12.5, 25, 50, and 100 μg/mL), catechin (10 μM), and quercetin (10 μM) on lipid peroxidation (LPO) and the activities of SOD, CAT, GPx, and GST were studied. Significantly higher LPO and lower activities of antioxidant enzymes were observed with the increasing concentrations of SB. Catechin or quercetin protected the erythrocytes against SB-induced toxicity only at low concentrations of SB. The presence of catechin or quercetin at 10 μM have no effect on SB-induced toxicity at high concentrations of SB (50 and 100 μg/mL). In conclusion, SB may cause oxidative stress as food additive in human erythrocytesin vitro. So, it appears that our findings provide evidence for the protection of erythrocytes from SB that could be considered for further studies.

scholarly journals Effect of salinity on Brassica rapa var. toria (BRSRT) under selenium defence: A trial to assess the protective role of selenium

2017 ◽  
Vol 109 (3) ◽  
pp. 577 ◽  
Author(s):  
Akanksha SAO ◽  
Priya SARAF ◽  
Divya BAGCHI
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Salt Stress ◽  
Glutathione Peroxidase ◽  
Brassica Rapa ◽  
Photosynthetic Pigments ◽  
Nacl Stress ◽  
Protective Role ◽  
Sodium Selenate

The present study assesses the role of selenium, an antioxidant in salt-stressed plants. A hydroponic trial of sodium selenate (Na<sub>2</sub>SeO<sub>4</sub>) on the growth, oxidative stress and antioxidant protection system of <em>Brassica rapa </em>var. <em>toria</em> (BRSRT) plant was studied. 40 µmol and 100 µmol of Na<sub>2</sub>SeO<sub>4 </sub>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 Na<sub>2</sub>SeO<sub>4 </sub>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 Na<sub>2</sub>SeO<sub>4</sub> 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.

Protective role of L-ascorbic acid against cypermethrin-induced oxidative stress and lipid peroxidation in Wistar rats

2010 ◽  
Vol 92 (5) ◽  
pp. 947-953 ◽  
Author(s):  
Rajinder Raina ◽  
Pawan K. Verma ◽  
Nrip K. Pankaj ◽  
Vinay Kant ◽  
Shahid Prawez
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Wistar Rats ◽  
Protective Role

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

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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