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.

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.

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.

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.

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.

scholarly journals Effect of Aloe Vera Extract on Reducing Aflatoxin B1 in Eggs of Laying Hen and Egg Yolk Oxidative Stability

2021 ◽  
Vol 11 (5) ◽  
pp. 12680-12688
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Stability ◽  
Aflatoxin B1 ◽  
Aloe Vera ◽  
Egg Yolk ◽  
Positive Control ◽  
Laying Hen ◽  
Positive Control Group ◽  
Control Group ◽  
Control Groups

Aloe vera extract's effect on Aflatoxin B1 (AFB1) residue and yolk oxidative stability was examined in yolk samples. The results indicated that residue of AB1 in AF-Aloe (100 and 300 ppm) treated groups were lower than the control groups on day 14 and was not detected on day 28. The lipid peroxidation level in all groups was significantly (p<0.05) lower than the positive control group. The weight, production, and carotenoid of eggs were not statistically significant between the groups. These results indicate that Aloe vera extract can be effective in diminishing AFB1.

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.

Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats

2007 ◽  
Vol 26 (6) ◽  
pp. 527-534 ◽  
Author(s):  
P. Murugavel ◽  
L. Pari
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Protective Efficacy ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Vital Role ◽  
Glutathione S Transferase ◽  
Glucose 6 Phosphate Dehydrogenase

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver. Human & Experimental Toxicology(2007) 26, 527—534

Protective effects of casein-derived peptide VLPVPQK against hydrogen peroxide–induced dysfunction and cellular oxidative damage in rat osteoblastic cells

2017 ◽  
Vol 36 (9) ◽  
pp. 967-980 ◽  
Author(s):  
SB Mada ◽  
S Reddi ◽  
N Kumar ◽  
S Kapila ◽  
R Kapila
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Osteoblastic Cells ◽  
Antioxidant Enzyme Activities ◽  
Protective Agent ◽  
Protective Effects ◽  
Differentiation Markers

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from β-casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50–200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide–positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress–related diseases such as osteoporosis.

scholarly journals Assessment of Hepatoprotective Effect of Chokeberry Juice in Rats Treated Chronically with Carbon Tetrachloride

Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1268
Author(s):  
Hanna Piotrowska-Kempisty ◽  
Michał Nowicki ◽  
Jadwiga Jodynis-Liebert ◽  
Monika Kurpik ◽  
Małgorzata Ewertowska ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Liver Fibrosis ◽  
Messenger Rna ◽  
Positive Control ◽  
Histological Evaluation ◽  
Protective Effects ◽  
Hepatic Lipid Peroxidation ◽  
Chokeberry Juice ◽  
Mrna Expression Levels

The aim of this study was to compare the protective effects of chokeberry juice and silymarin against chemical-induced liver fibrosis in rats. Liver fibrosis was induced by CCl4 administered two days a week for six weeks. Two groups of rats were co-treated with chokeberry juice, 10 mL/kg/day. or silymarin as a positive control, 100 mg/kg/day for six weeks. Hepatic lipid peroxidation was suppressed by 50% and the activity of hepatic antioxidant enzymes was increased by 19%–173% in rats co-treated with CCl4 and substances tested as compared to rats administered CCl4 alone. Hepatic hydroxyproline was decreased by 24% only in rats treated with silymarin. The messenger RNA (mRNA) expression levels of fibrosis-related molecules, procollagen I, α-SMA, TIMP-1, TGFβ, and TNFα, which were significantly increased in the liver of CCl4-treated rats, were not modulated by substances tested. Histological evaluation revealed a slight protective effect of silymarin against fibrosis. However, in CCl4 + chokeberry-treated rats, the density of vacuolated hepatocytes was significantly lower than that in silymarin administered animals. Chokeberry juice did not demonstrate an antifibrotic effect in the applied experimental model of fibrosis, and the effect of the known antifibrotic agent, silymarin, was very limited.

scholarly journals Cumulative Protective Effect of Melatonin and Indole-3-Propionic Acid against KIO3—Induced Lipid Peroxidation in Porcine Thyroid

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 89
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Thyroid Cancer ◽  
Oxidative Damage ◽  
Propionic Acid ◽  
Membrane Lipids ◽  
Iodine Concentration ◽  
Protective Effects ◽  
Experimental Conditions ◽  
Salt Iodization

Iodine deficiency is the main environmental factor leading to thyroid cancer. At the same time iodine excess may also contribute to thyroid cancer. Potassium iodate (KIO3), which is broadly used in salt iodization program, may increase oxidative damage to membrane lipids (lipid peroxidation, LPO) under experimental conditions, with the strongest damaging effect at KIO3 concentration of ~10 mM (corresponding to physiological iodine concentration in the thyroid). Melatonin and indole-3-propionic acid (IPA) are effective antioxidative indoles, each of which protects against KIO3-induced LPO in the thyroid. The study aims to check if melatonin used together with IPA (in their highest achievable in vitro concentrations) reveals stronger protective effects against KIO3-induced LPO in porcine thyroid homogenates than each of these antioxidants used separately. Homogenates were incubated in the presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25; 0.0 mM) without/with melatonin (5 mM) or without/with IPA (10 mM) or without/with melatonin + IPA, and then, to further clarify the narrow range of KIO3 concentrations, against which melatonin + IPA reveal cumulative protective effects, the following KIO3 concentrations were used: 20; 18.75; 17.5; 16.25; 15; 13.75; 12.5; 11.25; 10; 8.75; 7.5; 0.0 mM. Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. Protective effects of melatonin + IPA were stronger than those revealed by each antioxidant used separately, but only when LPO was induced by KIO3 in concentrations from 18.75 mM to 8.75 mM, corresponding to physiological iodine concentration in the thyroid. In conclusion, melatonin and indole-3-propionic acid exert cumulative protective effects against oxidative damage caused by KIO3, when this prooxidant is used in concentrations close to physiological iodine concentrations in the thyroid. Therefore, the simultaneous administration of these two indoles should be considered to prevent more effectively oxidative damage (and thereby thyroid cancer formation) caused by iodine compounds applied in iodine prophylaxis.

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