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

7-Chloro-4-(phenylselanyl) quinoline reduces renal oxidative stress induced by oxaliplatin in mice

2021 ◽  
Author(s):  
Ketlyn P. da Motta ◽  
Briana B. Lemos ◽  
Jaini J. Paltian ◽  
Angélica S Reis ◽  
Gustavo B. Blödorn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Aminolevulinic Acid ◽  
Therapeutic Potential ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Glutathione S Transferase ◽  
Protein Thiol ◽  
The Relationship

Purpose: evaluating the relationship between oxidative damage oxaliplatin (OXA)-induced and the therapeutic potential of 7-chloro-4-(phenylselanyl) quinoline (4-PSQ) in kidney of mice. Methods: Mice received OXA (10 mg/kg) or vehicle by intraperitoneal route (days 0 and 2). Oral administration of 4-PSQ (1 mg/kg) or vehicle was performed on days 2 to 14. On day 15, the animals were euthanized, and the kidneys and blood collected. The effect of OXA and/or 4-PSQ on urea, thiobarbituric acid reactive species (TBARS), non-protein thiol (NPSH) and protein carbonyl (PC) levels were investigated. Moreover, renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), δ-aminolevulinic acid dehydratase (δ-ALA-D) and Na+, K+ ATPase activities were evaluated. Results: Our findings revealed an increase on urea levels and a significant renal oxidative damage in OXA-induced mice. OXA exposure increased SOD, GPx and GST activities and caused a reduction on NPSH levels, CAT and GR activities. Na+, K+ ATPase and -ALA-D activities were reduced by OXA. 4-PSQ decreased plasmatic urea levels and renal oxidative damage. SOD, GPx, CAT, GR and Na+, K+ ATPase activities were restored by 4-PSQ. Conclusion: 4-PSQ may be a good prototype for the treatment of OXA-induced renal injury.

Melatonin protects against cadmium-induced oxidative damage in different tissues of rat: a mechanistic insight

2019 ◽  
Vol 2 (2) ◽  
pp. 1-21 ◽  
Author(s):  
Elina Mitra ◽  
Bharati Bhattacharjee ◽  
Palash Kumar Pal ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Oxidative Damage ◽  
Protein Carbonyl ◽  
Environmental Pollutant ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
Wide Range ◽  
Liver And Kidney ◽  
Nadh Cytochrome ◽  
Cd Exposure

Cadmium (Cd) is a notorious environmental pollutant known for its wide range of toxicities to organisms. Thus, the present study is designed to examine whether melatonin, a potent antioxidant, protects against Cd-induced oxidative damage in the heart, liver and kidney of rats. Cd treatment at a dose of 0.44 mg/kg for 15 days caused severe damage in all these organs. These included significantly increased activities of SGPT, SGOT, lactate dehydrogenase- 1 and 5 and ALP and levels of total lactate, creatinine, lipid peroxidation, protein carbonyl content and reduced glutathione while the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase along with mitochondrial pyruvate dehydrogenase, isocitrate dehydrogenase, α-keto glutarate dehydrogenase, succinate dehydrogenase, NADH-cytochrome-c-oxidoreductase and cytochrome-c-oxidase were significantly reduced by Cd. However, if melatonin was given orally 30 min before Cd injection, all these alterations induced by Cd were significantly preserved by melatonin. Histological observations also demonstrated that Cd exposure caused cellular lesions, promoting necrotic or apoptotic changes. Notably, all these changes were significantly protected by melatonin. The results suggest that melatonin is a beneficial molecule to ameliorate Cd-induced oxidative damage in the heart, liver and kidney tissues of rats with its powerful antioxidant capacity, heavy metal chelating activity and competition of binding sites with Cd to the GSH and catalase.

scholarly journals Modafinil Effects on Behavior and Oxidative Damage Parameters in Brain of Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Open Field ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Behavioral Changes ◽  
Protein Damage ◽  
Behavioral Parameters ◽  
Carbonyl Formation ◽  
The Brain

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

scholarly journals TUALANG HONEY ATTENUATES KAINIC ACID-INDUCED OXIDATIVE STRESS IN RAT CEREBELLUM AND BRAINSTEM

2017 ◽  
Vol 9 (12) ◽  
pp. 155 ◽  
Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen ◽  
Mustapha Muzaimi ◽  
Mummedy Swamy ◽  
Mohd Asnizam Asari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Multiple Time ◽  
Rat Cerebellum ◽  
Total Antioxidant ◽  
Multiple Time Points ◽  
Tualang Honey

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property.

Antioxidant defenses and metabolic depression in a pulmonate land snail

1995 ◽  
Vol 268 (6) ◽  
pp. R1386-R1393 ◽  
Author(s):  
M. Hermes-Lima ◽  
K. B. Storey
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Thiobarbituric Acid ◽  
Land Snail ◽  
Land Snails ◽  
Antioxidant Defenses ◽  
Glutathione S Transferase ◽  
Hypometabolic State

During arousal from estivation oxygen consumption by land snails (Otala lactea) increases severalfold. To determine whether snails prepared for an accompanying rise in the rates of oxyradical generation by altering their antioxidant defense mechanisms, changes in the activities of antioxidant enzymes and lipid peroxidation products were quantified in foot and hepatopancreas of control, 30-day estivating, and aroused snails. Compared with controls, estivating O. lactea showed significant increases in the activities of foot muscle superoxide dismutase (SOD) (increasing by 56-67%), catalase (51-72%), and glutathione S-transferase (79-108%), whereas, in hepatopancreas, SOD (57-78%) and glutathione peroxidase (93-144%) increased. Within 40 min after arousal began, hepatopancreas glutathione peroxidase activity had returned to control values, but SOD showed a further 70% increase in activity but then returned to control levels by 80 min. Estivation had no effect on total glutathione (GSH + 2 GSSG) concentrations in tissues, but GSSG content had increased about twofold in both organs of 30-day dormant snails. Lipid peoxidation (quantified as thiobarbituric acid reactive substances) was significantly enhanced at the onset of arousal from dormancy, indicating that oxidative stress and tissue damage occurred at this time. The data suggest that antioxidant defenses in snail organs are increased while snails are in the hypometabolic state as a preparation for oxidative stress during arousal.

Lipid Peroxidation, Protein Oxidation, Gelatinases, and Their Inhibitors in a Group of Adults with Obesity

2019 ◽  
Vol 51 (06) ◽  
pp. 389-395 ◽  
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Maria Montana ◽  
Caterina Urso ◽  
Vincenzo Calandrino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
The Body ◽  
Control Group ◽  
The Matrix ◽  
Markers Of Oxidative Stress ◽  
Obese Subjects

AbstractThe association between obesity and cardiovascular diseases has a multifactorial pathogenesis, including the synthesis of inflammatory molecules, the increase in oxidative stress and the dysregulation of the matrix metalloprotease (MMP) concentration and activity. In a group of adults with obesity, divided in 2 subgroups according to the body mass index (BMI), we examined lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), protein oxidation, expressed as protein carbonyl groups (PCs), plasma gelatinases (MMP-2 and MMP-9), and their tissue inhibitors (TIMP-1 and TIMP-2). In the whole group, as well as in the 2 subgroups (with BMI 30–35 or BMI>35) of obese subjects, we observed an increase in TBARS, PCs, MMP-2, and MMP-9, and also TIMP-1 and TIMP-2 in comparison with the control group. A positive correlation between TBARS and PCs emerged in obese subjects and persisted after dividing obese subjects according to BMI. The correlation between MMP-2 and TIMP-2 was not statistically significant, while a significant correlation was present between MMP-9 and TIMP-1. The correlations between the markers of oxidative stress (TBARS and PCs) and those of the MMP/TIMP profile indicated a more marked influence of protein oxidation on MMPs and TIMPs in comparison with TBARS. The innovative aspect of our study was the simultaneous evaluation of oxidative stress markers and MMP/TIMP profile in adult obese subjects. We observed significant alterations and correlations that may negatively influence the clinical course of the disease.

scholarly journals Silicon Alleviates Copper Toxicity in Flax Plants by Up-Regulating Antioxidant Defense and Secondary Metabolites and Decreasing Oxidative Damage

2020 ◽  
Vol 12 (11) ◽  
pp. 4732 ◽  
Author(s):  
Hossam S. El-Beltagi ◽  
Mahmoud R. Sofy ◽  
Mohammed I. Aldaej ◽  
Heba I. Mohamed
Keyword(s):  
Lipid Peroxidation ◽  
Plant Growth ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Growth Yield ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Total Chlorophyll ◽  
Yield Attributes ◽  
Cu Toxicity

In recent years, nutrient management has gained much attention as a way to mitigate heavy metal stress. Silicon (Si) promotes plant defense responses against toxic metal stresses. In this study, we evaluated the effects of silicon (Si) on copper (Cu) toxicity in two flax genotypes (Sakha 1 and Sakha 2) as it relates to plant growth, yield attributes, total chlorophyll, nucleic acid content, enzymatic and non-enzymatic antioxidants, oxidative damage, lipid peroxidation, copper and silicon content, and fatty acid composition. The results showed that Cu (100 and 200 µM) inhibited plant growth and increased Cu accumulation in soil, roots, and shoots. Cu significantly decreased the yield attributes, total chlorophyll by 9.5% and 22% in Sakha 1 and by 22.5% and 29% in Sakha 2, and enhanced the accumulation of non-enzymatic (tocopherol), enzymatic antioxidants such as superoxide dismnutase, peroxidase, ascorbate peroxidase and catalase) and secondary metabolites (phenol and flavonoids). The DNA content significantly decreased in stressed plants with 100 and 200 µM Cu about 22% and 44%, respectively, in Sakha 1 and about 21.6% and 34.7% in Sakha 2, and RNA content also decreased by about 20% and 29%, respectively, in Sakha 1 and by about 2% and 13% in Sakha 2 compared to the control plant. Furthermore, Cu stress accelerated the generation of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and induced cellular oxidative injury caused by lipid peroxidation. In parallel, Cu induced a change in the composition of fatty acids, resulting in lower unsaturated fatty acid levels and increased saturated fatty acids (increased saturation/unsaturation ratio for both genotypes). Treating the flax plants with irrigation three times with Si protected the plants from Cu toxicity. Si treatment decreased the uptake and the transport of Cu to the shoots and harvested seeds and promoted plant growth, yield attributes, and antioxidant defense systems by reducing Cu accumulation, lipid peroxidation, and the generation of H2O2. In addition, the alleviation of Cu toxicity correlated with increased Si accumulation in the roots and shoots. In conclusion, Si can be used to improve the resistance of flax plants to Cu toxicity by up-regulating the antioxidant defense system such as superoxide dismutase (SOD), peroxidase (POD), ascorbate peroxidase (APX) and catalase (CAT) and decreasing the oxidative damage caused by reactive oxygen species (ROS).

The effects of oral glutamine on cyclophosphamide-induced nephrotoxicity in rats

2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Renal Damage ◽  
Neutrophil Infiltration ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Glutathione Depletion ◽  
Myeloperoxidase Activity ◽  
Protein Carbonyl Content

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.

scholarly journals Effect of Running Exercise on Oxidative Stress Biomarkers: A Systematic Review

2021 ◽  
Vol 11 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Ukadike C. Ugbolue ◽  
Yuhuan He ◽  
Yao Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Enzymatic Antioxidants ◽  
Oxidative Stress Biomarkers ◽  
Running Exercise ◽  
Exercise Induced ◽  
The Individual ◽  
Meta Analyses

Background: Exercise induced health benefits are limited by the overaccumulation of reactive oxygen species (ROS). ROS and further oxidative stress could potentially induce muscle damage which could result in poor exercise performance. However, predicting ROS induced oxidative stress in response to endurance training has several limitations in terms of selecting biomarkers that are used to measure oxidative stress.Objective: The purpose of this study was to systematically investigate the suitable biomarkers that predict oxidative stress status among runners.Methods: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, a search for relevant articles was carried out on PubMed/Medline, ISI Web of Science, and Google Scholar using related search terms such as oxidative damage, ROS, exercise, physical training, running, marathon, and ultramarathon.Results: Outcomes included (1) running programs like a half-marathon, ultramarathon, and iron-man race, (2) measuring biochemical assessment of oxidative damage markers such as malondialdehyde (MDA), protein carbonyl (PC), total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), 8-Oxo-2'-deoxyguanosine (8-OH-dG), 4-hydroxynonenal (HNE), and F1-isoprostones, and enzymatic and non-enzymatic antioxidants level.Conclusions: This study concluded that a running exercise does not elicit a response to specific biomarkers of oxidative stress, instead, oxidative damage markers of lipids, proteins, and various enzymatic and non-enzymatic antioxidants are expressed according to the training status of the individual.

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