scholarly journals Magnesium Sulfate Attenuates Lethality and Oxidative Damage Induced by Different Models of Hypoxia in Mice

2020 ◽  
Author(s):  
Hamidreza Mohammadi ◽  
Amir Shamshirian ◽  
Shafagh Eslami ◽  
Danial Shamshirian ◽  
Mohammad Ali Ebrahimzadeh
Keyword(s):  
Oxidative Damage ◽  
Brain Mitochondria ◽  
Positive Control ◽  
Protein Carbonyl ◽  
Experimental Models ◽  
Antihypoxic Activity ◽  
Protective Effects ◽  
Control Groups ◽  
Mice Brain ◽  
Prolonged Latency

AbstractMg2+ is an important cation in our body. It is an essential co-factor for many enzymes. Despite many works, nothing is known about the protective effects of MgSO4 against hypoxia-induced lethality and oxidative damage in brain mitochondria. In this study, antihypoxic and antioxidative activities of MgSO4 were evaluated by three experimental models of induced-hypoxia (asphyctic, haemic, and circulatory) in mice. Mitochondria protective effects of MgSO4 were evaluated in mice brain after induction of different models of hypoxia. Antihypoxic activity was especially pronounced in asphyctic hypoxia where MgSO4 at dose 600 mg/kg showed the same activity as phenytoin which used as a positive control (P< 0.001). In the haemic model, MgSO4 at all used doses significantly prolonged latency of death. In circulatory hypoxia, MgSO4 (600 mg/kg) doubles the survival time. MgSO4 significantly decreased Lipid peroxidation, protein carbonyl, and improved mitochondrial function and glutathione content in brain mitochondria compared to control groups. The results obtained in this study showed that MgSO4 administration has protective effects against lethality induced by different models of hypoxia and improves brain mitochondria oxidative damage.

scholarly journals Magnesium Sulfate Attenuates Lethality and Oxidative Damage Induced by Different Models of Hypoxia in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Hamidreza Mohammadi ◽  
Amir Shamshirian ◽  
Shafagh Eslami ◽  
Danial Shamshirian ◽  
Mohammad Ali Ebrahimzadeh
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Brain Mitochondria ◽  
Positive Control ◽  
Protein Carbonyl ◽  
Experimental Models ◽  
Antihypoxic Activity ◽  
Protective Effects ◽  
Control Groups ◽  
Prolonged Latency

Mg2+ is an important cation in our body. It is an essential cofactor for many enzymes. Despite many works, nothing is known about the protective effects of MgSO4 against hypoxia-induced lethality and oxidative damage in brain mitochondria. In this study, antihypoxic and antioxidative activities of MgSO4 were evaluated by three experimental models of induced hypoxia (asphyctic, haemic, and circulatory) in mice. Mitochondria protective effects of MgSO4 were evaluated in mouse brain after induction of different models of hypoxia. Antihypoxic activity was especially pronounced in asphyctic hypoxia, where MgSO4 at dose 600 mg/kg showed the same activity as phenytoin, which used as a positive control ( P < 0.001 ). In the haemic model, MgSO4 at all used doses significantly prolonged latency of death. In circulatory hypoxia, MgSO4 (600 mg/kg) doubles the survival time. MgSO4 significantly decreased lipid peroxidation and protein carbonyl and improved mitochondrial function and glutathione content in brain mitochondria compared to the control groups. The results obtained in this study showed that MgSO4 administration has protective effects against lethality induced by different models of hypoxia and improves brain mitochondria oxidative damage.

Protective effects of ethanolic extract of Lemon Beebrush (Aloysia citrodora) leaf against hypoxia-induced lethality in mice

2020 ◽  
Author(s):  
Mohammad Hossein Hosseinzadeh ◽  
Mohammad Ali Ebrahimzadeh
Keyword(s):  
Biological Activities ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Positive Control ◽  
Experimental Models ◽  
Total Phenolic ◽  
Control Group ◽  
Antihypoxic Activity ◽  
Significant Activity ◽  
Protective Effects

Lemon Beebrush, known as Lippia citroiodora and Aloysia citrodora is a known medicinal plant in Iran. Many biological activities have been reported from this plant. In spite of many works, nothing is known about protective effect of A. citrodora against hypoxia conditions. In this study, protective effects of A. citrodora leaf extract against hypoxia-induced lethality in mice were evaluated by three experimental models of hypoxia, asphyctic, haemic and circulatory. Its phenol and flavonoid contents and antioxidant activity were also evaluated. Statistically significant protective activities were established in some doses of extract in three models. Antihypoxic activity was especially pronounced in circulatory hypoxia where extract at 62.5 mg kg-1 prolonged the latency for death with respect to control group (p<0.01). The effect was dose dependent. At 250 mg kg-1, it prolonged the latency for death with the same activity of propranolol (20 mg kg-1), that used as positive control (p>0.05). Extract showed weak activity in haemic model. Only at the highest tested dose, 250 mg kg-1, it significantly prolonged latency for death with respect to control group (p<0.05). Extract at this dose showed the same activity of propranolol which used as positive control (p>0.05). In asphytic model, extract at the highest tested dose showed statistically significant activity respect to the control. At 250 mg kg-1, it significantly prolonged the latency for death (26.84 ± 4.11 vs. 19.45 ± 1.13 min, p = 0.0006). At 125 mg kg-1, it also prolonged survival time but this increase was not significantly different. Phenytoin that used as positive control kept mice alive for 29.60 ± 2.51 min (p<0.0001). Extract at 250 mg kg-1 showed the same activity of phenytoin (p>0.05). The total phenolic content was 342.9 ± 11.5 mg gallic acid equivalent/g of extract powder and flavonoid content was 90.2 ± 7.8 mg quercetin equivalent/g of extract powder. IC50 for DPPH radical-scavenging activity was 21.97 ± 2.4 mg/ml. The presence of polyphenols in this plant may be a proposal mechanism for reported antihypoxic activities.

Study of the Effects of L-tryptophane Nanoparticles on Motor Behavior in Alzheimer's Experimental Models

2019 ◽  
Vol 18 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Andressa L. Miri ◽  
Andressa P. Hosni ◽  
Jossinelma C. Gomes ◽  
Rubiana M. Mainardes ◽  
Najeh M. Khalil ◽  
...  
Keyword(s):  
Motor Behavior ◽  
Senile Plaques ◽  
Well Being ◽  
Positive Control ◽  
Negative Control ◽  
Experimental Models ◽  
Control Groups ◽  
Behavioral Reactions ◽  
Post Surgery ◽  
Physiological Alterations

Background: Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive and incapacitating decay of cognitive, neuropsychiatric, and behavioral manifestations. L-tryptophan is the precursor amino acid of serotonin, which is a neurotransmitter responsible for mood balance and the sense of well-being and can be administered in the form of nanoparticles. Objective: This study analyzed the effectiveness of L-tryptophan nanoparticles and L-tryptophan on behavioral physiological alterations resulting from AD in animal models. Methods: The sample consisted of 50 Rattus norvegicus rats, divided in 10 groups with 5 animals each: one negative control (NC), three positive control groups (C3, C7, and C21), three groups treated with L-tryptophan nanoparticles (T3N, T7N, and T21N) at the concentration of 1.5 mg, and three groups treated with L-tryptophan (T3L, T7L, and T21L) at the concentration of 1.5 mg. The rats underwent stereotactic surgery to induce AD through the injection of amyloid beta-amyloid peptide1-42 in the intracerebroventricular region. All rats were submitted to pre- and post-surgery and post-treatment motor behavior evaluation through the Later Water Maze (LWM) and elevated cross-labyrinth (ECL). Histological analysis was performed to verify the presence of senile plaques, and the statistical analysis used the unpaired T-test. Results: Significant intergroup differences were observed in some of the evaluated parameters between treated and untreated groups. Conclusion: It was concluded that the treatment with L-tryptophan nanoparticles was beneficial to improve behavioral reactions in the Alzheimer's model.

scholarly journals Protective Effects of Edaravone Against Hypoxia-Induced Lethality in Mice

2020 ◽  
Author(s):  
Fatemeh Shaki ◽  
Mina Mokhtaran ◽  
Amir Shamshirian ◽  
Shahram Eslami ◽  
Danial Shamshirian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cerebral Infarction ◽  
Experimental Models ◽  
The Other ◽  
Protective Effects ◽  
Control Groups ◽  
Glutathione Oxidation ◽  
Dose Dependent ◽  
And Oxidative Stress

AbstractEdaravone is used for the treatment of acute cerebral infarction in Japan. However, nothing is known about the protective effects of this drug against hypoxia-induced lethality. In this study, the protective effects of edaravone against hypoxia-induced lethality and oxidative stress in mice were evaluated by three experimental models of hypoxia, which are asphyctic, haemic, and circulatory. Statistically significant protective activities were established in all tested models of hypoxia. Antihypoxic activities were especially pronounced in asphytic and circulatory hypoxia. The effect was dose-dependent. Edaravone, at 5 mg kg-1, showed statistically significant activities respect to the control groups. It significantly prolonged the latency for death. At 2.5 mg kg-1, it also prolonged survival time (26.08 ± 5.26 min), but this effect was not statistically significant from the control (P>0.05). On the other hand, edaravone significantly inhibited hypoxia-induced oxidative stress (lipid peroxidation and glutathione oxidation) in three models of hypoxia. In conclusion, the results obtained in this study showed that Edaravone has very good protective effects against the hypoxia in all tested models.

Protection by pentoxifylline of malathion-induced toxic stress and mitochondrial damage in rat brain

2010 ◽  
Vol 29 (10) ◽  
pp. 851-864 ◽  
Author(s):  
Akram Ranjbar ◽  
Mohammad Hossein Ghahremani ◽  
Mohammad Sharifzadeh ◽  
Abolfazl Golestani ◽  
Mahmood Ghazi-Khansari ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Rat Brain ◽  
Manganese Superoxide Dismutase ◽  
Brain Homogenate ◽  
Brain Mitochondria ◽  
Alpha Tocopherol ◽  
Protective Effects ◽  
Whole Brain ◽  
Induced Changes

Objective: The objective of this study was to investigate the possible protective effects of pentoxifylline as a phosphodiesterase-5 inhibitor on malathion-induced oxidative damage to rat brain mitochondria. Methods: Rats received malathion (200 mg/kg/day) and pentoxifylline (PTX, 50 mg/kg/day) in combination or alone. Alpha-tocopherol (AT, 15 mg/kg/day) was used as a positive standard. After 1 week of treatment, blood, whole brain tissue, and brain mitochondria were isolated. The activity of enzymatic scavengers such as glutathione peroxidase (GPx), catalase (CAT), copper-zinc superoxide dismutase (Cu/ZnSOD), and manganese superoxide dismutase (MnSOD) were measured. The extents of cellular lipid peroxidation (LPO), nitrotyrosine (NOx), and the ratio of reduced versus oxidized glutathione (GSH/GSSG) were determined. The protein expression of MnSOD was determined in brain mitochondria. Results: Malathion stimulated activities of CAT, Cu/ZnSOD, GPx, and increased LPO and NOx, and decreased GSH/GSSG in whole brain homogenate. The changes in CAT, LPO, GPx, and GSH/GSSG were restored by PTX and AT. In plasma samples, malathion increased CAT, Cu/ZnSOD, and GPx activities, increased LPO, and decreased GSH/GSSG, while PTX and AT attenuated malathion-induced changes in GPx, Cu/ZnSOD, LPO, and GSH/GSSG. In brain mitochondria, malathion enhanced LPO, NOx, CAT, GPx, and MnSOD and decreased GSH/GSSG as compared to controls, whereas PTX and AT restored malathion-induced changes in GSH/GSSG, NOx, GPx, and CAT. Malathion noticeably enhanced expression of MnSOD protein as compared to controls. Malathion decreased viability of mitochondria that was recovered by AT. It is concluded that oxidative damage is at least in part the mechanism of toxicity of malathion in the mitochondria that can be recovered by PTX comparable to AT.

scholarly journals Chemical Profiling of Polyphenolics in Eucalyptus globulus and Evaluation of Its Hepato–Renal Protective Potential Against Cyclophosphamide Induced Toxicity in Mice

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 415 ◽  
Author(s):  
Mosad A. Ghareeb ◽  
Mansour Sobeh ◽  
Walaa H. El-Maadawy ◽  
Hala Sh. Mohammed ◽  
Heba Khalil ◽  
...  
Keyword(s):  
Benzoic Acid ◽  
Eucalyptus Globulus ◽  
Leaf Extract ◽  
Renal Toxicity ◽  
Immunosuppressive Agent ◽  
Positive Control ◽  
Protein Carbonyl ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protective Effects

Cyclophosphamide (CP) is a potent anti-neoplastic and immunosuppressive agent; however, it causes multi-organ toxicity. We elucidated the protective activities of Eucalyptus globulus (EG) leaf extract against CP-induced hepato–renal toxicity. Mice were treated with EG for 15 days plus CP on day 12 and 13 of the experiment. Using HPLC-DAD-ESI-MS/MS, 26 secondary metabolites were identified in EG leaf extract. Out of them, 4 polyphenolic compounds were isolated: (1) 4-(O-β-d-xylopyranosyloxy)-3,5-di-hydroxy-benzoic acid, (2) 4-(O-α-l-rhamnopyranosyloxy)-3,5-di-hydroxy-benzoic acid, (3) gallic acid, and (4) methyl gallate. Effects of EG extract on biochemical parameters, gene expression, and immune-histopathological changes were assessed in comparison to mesna positive control. Results showed that EG improved CP-increased serum ALT, AST, creatinine, and blood urea nitrogen levels. The hepatic and renal tissue levels of MDA, nitric oxide, protein carbonyl, TNF-α, IL-6, and immunohistochemical expression of nuclear factor kappa-B (NF-kB) and caspase-3 were reduced. Also, hepatic and renal GSH contents, and nuclear factor E2-related factor 2 (NRf2)/ hemoxygenase-1 (HO-1) signaling levels were increased. Histopathological findings supported our findings where hepatic and renal architecture were almost restored. Results revealed the protective effects of EG against CP-induced hepato–renal toxicity. These effects may be related to EG antioxidant, anti-inflammatory, and anti-apoptotic properties coupled with activation of Nrf2/HO-1 signaling.

scholarly journals Protective effects of methanolic extract of Vicia cracca against hypoxia-induced lethality in mice

2018 ◽  
Author(s):  
Razieh Shahnazi ◽  
Mohammad Ali Ebrahimzadeh
Keyword(s):  
Protective Effect ◽  
Survival Time ◽  
Biological Activities ◽  
Experimental Models ◽  
Prolonged Survival ◽  
Control Group ◽  
Antihypoxic Activity ◽  
Protective Effects ◽  
Circulatory Model ◽  
Vicia Cracca

Vicia genus has 45 species in Iran. Many protective and biological activities have been reported from these species. In spite of many works, nothing is known about protective effect of V. cracca against hypoxia conditions. In this study, protective effects of V. cracca extract against hypoxia-induced lethality in mice were evaluated by three experimental models of hypoxia, asphyctic, haemic and circulatory. Statistically significant protective activities were observed in some doses of extract in three models. Antihypoxic activity was especially pronounced in asphyctic model. Extract at 200 mg/kg prolonged survival time (27.37 ± 4.0 min) but was not comparable with that of phenytoin (39.80 ± 1.92). At 100 mg/kg it also prolonged survival time (24.76 ± 3.7 min) which was so higher than control group. In haemic model, V. cracca extract significantly and dose dependently prolonged survival time as compared to control group. At 200 mg/kg, extract was being capable of keeping the mice alive for 15.38 ± 1.93 min. It was also effective in circulatory model. V. cracca extract at 200 mg/kg prolonged survival time (16.84 ± 1.47 min) that was statistically significant as compared to control group (13.14 ± 0.51 min). V. cracca extract showed a very good protective effect against the hypoxia in some models. Specifically, they produced significant and dose-dependent effect on the model of asphytic and haemic hypoxia. The presence of polyphenols in this plant may be a proposal mechanism for reported antihypoxic activities of this plant.

scholarly journals Protective effects of quercetin from oxidative/nitrosative stress under intermittent hypobaric hypoxia exposure in the rat’s heart

2018 ◽  
Vol 105 (3) ◽  
pp. 233-246 ◽  
Author(s):  
IC Chiş ◽  
D Baltaru ◽  
A Dumitrovici ◽  
A Coseriu ◽  
BC Radu ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Nitrosative Stress ◽  
Heart Tissue ◽  
Protein Carbonyl ◽  
Free Radical Scavenger ◽  
Male Rats ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Control Groups ◽  
Hypoxia Exposure

Background Exposure to high altitude in hypobaric hypoxia (HH) is considered to be a physiological oxidative/nitrosative stress. Quercetin (Que) is an effective antioxidant and free radical scavenger against oxidative/nitrosative stress. Aims The aim of this study was to investigate the cardioprotective effects of Que in animals exposed to intermittent HH (IHH) and therefore exposed to oxidative/nitrosative stress. Materials and methods Wistar albino male rats were exposed to short-term (2 days) or long-term (4 weeks; 5 days/week) IHH in a hypobaric chamber (5,500 m, 8 h/day, 380 mmHg, 12% O2, and 88% N2). Half of the animals received natural antioxidant Que (body weight: 30 mg/kg) daily before each IHH exposure and the remaining rats received vehicle (carboxymethylcellulose solution). Control rats were kept under normobaric normoxia (Nx) and treated in a corresponding manner. One day after the last exposure to IHH, we measured the cardiac hypoxia-induced oxidative/nitrosative stress biomarkers: the malondialdehyde (MDA) level and protein carbonyl (PC) content, the activity of some antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)], the nitrite plus nitrate (NOx) production, and the inducible nitric oxide synthase (iNOS) protein expression. Results Heart tissue MDA and PC levels, NOx level, and iNOS expression of IHH-exposed rats had increased, and SOD and CAT activities had decreased compared with those of the Nx-exposed rats (control groups). MDA, CP, NOx, and iNOS levels had decreased in Que-treated IHH-exposed rats compared with IHH-exposed rats (control groups). However, Que administration increased SOD and CAT activities of the heart tissue in the IHH-exposed rats. Conclusion HH exposure increases oxidative/nitrosative stress in heart tissue and Que is an effective cardioprotective agent, which further supports the oxidative cardiac dysfunction induced by hypoxia.

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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