scholarly journals Melatonin ameliorates brain oxidative stress and upregulates senescence marker protein-30 and osteopontin in a rat model of vascular dementia

2018 ◽  
Vol 105 (1) ◽  
pp. 38-52 ◽  
Author(s):  
I Bin-Jaliah ◽  
HF Sakr
Keyword(s):  
Oxidative Stress ◽  
Vascular Dementia ◽  
Neuroprotective Effect ◽  
Thiobarbituric Acid ◽  
Cerebral Hypoperfusion ◽  
Male Rats ◽  
Marker Protein ◽  
Group Iii ◽  
Total Antioxidant ◽  
Brain Oxidative Stress

The aim of this study was to investigate the effect of melatonin on oxidative stress and senescence marker protein-30 (SMP30) as well as osteopontin (OPN) expression in the hippocampus of rats subjected to vascular dementia (VD). A total of 72 male rats were divided into six groups (n = 12 each) as follows: (i) untreated control (CON), (ii) sham-operated group, (iii) sham-operated + melatonin, (iv) rats exposed to VD induced by permanent bilateral occlusion of the common carotid arteries (BCCAO) leading to chronic cerebral hypoperfusion, (v) rats exposed to VD + melatonin, and (vi) rats exposed to VD + donepezil (DON). At the end of experiment, the hippocampal levels of acetylcholine (ACh), norepinephrine (NE), and dopamine (Dop) were measured. Expression of OPN was determined using immunohistochemistry, and SMP30 expression was determined using real-time PCR in the hippocampus. Hippocampal thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) were evaluated. The BCCAO group showed significantly decreased TAC (p < 0.05) and significantly increased in TBARS levels compared with the CON group. In addition, BCCAO significantly decreased (p < 0.05) the expression of both OPN and SMP30 and the levels of ACh, NE, and Dop in the hippocampus compared with CON treatment. Treatment with melatonin significantly increased OPN and SMP30 expression and ACh, NE, and Dop levels in the hippocampus with amelioration of the oxidative stress compared with BCCAO rats. Melatonin might produce a neuroprotective effect through its antioxidant action and by increasing the expression of SMP30 and OPN that is not comparable with that of DON.

scholarly journals NANOTUBS INCREASE TETRACHLOROMETHANE INDUCED OXIDATIVE STRESS

2017 ◽  
Author(s):  
N. Ya. Letniak ◽  
I. P. Kuzmak ◽  
M. M. Korda
Keyword(s):  
Oxidative Stress ◽  
Carbon Nanotubes ◽  
Chemical Properties ◽  
Thiobarbituric Acid ◽  
The Body ◽  
Male Rats ◽  
Total Antioxidant ◽  
Multi Walled Carbon Nanotubes ◽  
Physical And Chemical ◽  
Walled Carbon Nanotubes

Background. The unique physical and chemical properties of carbon nanotubes determine wide-ranging prospects for their use in biology and medicine. The capability of nanotubes to transport medicines and chemicals inside a cell makes the possibility of classical toxicants toxicity increase in case of their intake to the body with nanotubes, an urgent issue.Objective. The aim of the research was to study the effect of carbon nanotubes on the capability of the chemical toxicant tetrachloromethane (TCM) to induce oxidative stress in serum and liver of rats.Methods. The experiments were performed on outbred male rats, which were administered intraperitoneally with 0.5 ml of suspension of single-walled, multi-walled or multi-walled functionalized COOH nanotubes (60 mg/kg) only or together with TCM (2 ml/kg). The animals were taken out of the experiment in 3, 6 and 48 hours after the administration of the nanotubes and TCM. The activity of catalase, superoxide dismutase, the content of thiobarbituric acid reactive substances (TARS), reduced glutathione, ceruloplasmin and total antioxidant activity of serum were determined in serum and liver.Results. It was established that under the influence of multi-walled carbon nanotubes the studied parameters changed significantly. The administration of tetrachloromethane to rats caused significant changes in all indicators. Maximal changes in the rates were recorded in the group of animals that were administered with carbon nanotubes and tetrachloromethane togeather. In this case, a number of the studied parameters of blood and liver significantly changed compare to the similar indicators of the group of animals, which were administered with the chemical toxicant only.Conclusions. Carbon nanotubes increase the capability of the chemical toxicant tetrachloride to cause oxidative stress in liver and serum.

scholarly journals Increased Oxidative Stress in Acute Myeloid Leukemia Patients after Red Blood Cell Transfusion, but Not Platelet Transfusion, Results Mainly from the Oxidative/Nitrative Protein Damage: An Exploratory Study

2021 ◽  
Vol 10 (7) ◽  
pp. 1349
Author(s):  
Kamila Czubak-Prowizor ◽  
Jacek Trelinski ◽  
Paulina Stelmach ◽  
Piotr Stelmach ◽  
Agnieszka Madon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Myeloid Leukemia ◽  
Exploratory Study ◽  
Myeloid Leukemia ◽  
Thiobarbituric Acid ◽  
Red Blood Cell Transfusion ◽  
Packed Red Blood Cells ◽  
Chronic Oxidative Stress ◽  
Total Antioxidant ◽  
Acute Myeloid

Chronic oxidative stress (OS) can be an important factor of acute myeloid leukemia (AML) progression; however, there are no data on the extent/consequence of OS after transfusion of packed red blood cells (pRBCs) and platelet concentrates (PCs), which are commonly used in the treatment of leukemia-associated anemia and thrombocytopenia. We aimed to investigate the effects of pRBC/PC transfusion on the OS markers, i.e., thiol and carbonyl (CO) groups, 3-nitrotyrosine (3-NT), thiobarbituric acid reactive substances (TBARS), advanced glycation end products (AGE), total antioxidant capacity (TAC), SOD, GST, and LDH, in the blood plasma of AML patients, before and 24 h post-transfusion. In this exploratory study, 52 patients were examined, of which 27 were transfused with pRBCs and 25 with PCs. Age-matched healthy subjects were also enrolled as controls. Our results showed the oxidation of thiols, increased 3-NT, AGE levels, and decreased TAC in AML groups versus controls. After pRBC transfusion, CO groups, AGE, and 3-NT significantly increased (by approximately 30, 23, and 35%; p < 0.05, p < 0.05, and p < 0.01, respectively) while thiols reduced (by 18%; p < 0.05). The PC transfusion resulted in the raise of TBARS and AGE (by 45%; p < 0.01 and 31%; p < 0.001), respectively). Other variables showed no significant post-transfusion changes. In conclusion, transfusion of both pRBCs and PCs was associated with an increased OS; however, transfusing the former may have more severe consequences, since it is associated with the irreversible oxidative/nitrative modifications of plasma proteins.

scholarly journals Are insulin-resistance and oxidative stress cause or consequence of aging

2020 ◽  
Vol 245 (14) ◽  
pp. 1260-1267
Author(s):  
Sylwia Dzięgielewska-Gęsiak ◽  
Dorota Stołtny ◽  
Alicja Brożek ◽  
Małgorzata Muc-Wierzgoń ◽  
Ewa Wysocka
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Antioxidant Status ◽  
Antioxidant Defense ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Elderly Individuals ◽  
Total Antioxidant ◽  
Antioxidant Defense Systems ◽  
Antioxidant Markers

Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r =  0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.

Nephrotoxicity and its prevention by catechin in ferric nitrilotriacetate promoted oxidative stress in rats

2004 ◽  
Vol 23 (3) ◽  
pp. 137-143 ◽  
Author(s):  
Kanwaljit Chopra ◽  
Devinder Singh ◽  
Vikas Chander
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Renal Dysfunction ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Morphological Alterations ◽  
Group Iii ◽  
Ferric Nitrilotriacetate ◽  
Group I ◽  
Rats And Mice

Intraperitoneal injection of ferric nitrilotriacetate (Fe-NTA) to rats and mice results in iron-induced free radical injury and cancer in kidneys. This study was designed to investigate the effect of catechin, a bioflavonoid with antioxidant potential, on Fe-NTA-induced nephrotoxicity in rats. Four groups were employed in the present study. Group I served as control group, Group II animals received Fe-NTA (8 mg iron/kg body weight i.p.), Group III animals were given 40 mg/kg catechin p.o. twice a day for 4 days and on the 5th day Fe-NTA was challenged, and Group IV animals received catechin alone for 4 days. Renal function was assessed by measuring plasma creatinine and blood urea nitrogen. The oxidative stress was measured by renal malondialdehyde levels, reduced glutathione levels and by enzymatic activity of catalase, glutathione reductase and superoxide dismutase. One hour after a single intraperitoneal (i.p.) injection of Fe-NTA (8 mg iron/kg), a marked deterioration of renal architecture, renal function and severe oxidative stress was observed. Pretreatment of animals with catechin markedly attenuated renal dysfunction, reduced elevated thiobarbituric acid reacting substances (TBARS), restored the depleted renal antioxidant enzymes and normalized the renal morphological alterations. These results clearly demonstrate the role of oxidative stress and its relation to renal dysfunction, and suggest a protective effect of catechin on Fe-NTA-induced nephrotoxicity in rats.

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.

scholarly journals Effect of concurrent exposure of toxic concentrations of lead and endosulfan on oxidative stress indices in rats

2021 ◽  
Vol 10 (3) ◽  
pp. 192-195
Author(s):  
Ranganathan V ◽  
◽  
Malik JK ◽  
Rao GS ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reduced Glutathione ◽  
Group Iv ◽  
Male Rats ◽  
Technical Grade ◽  
Stress Indices ◽  
Group Iii ◽  
Group I ◽  
Male Wistar Rats ◽  
Toxic Concentrations

The effect of concurrent exposure of toxic concentrations of lead and endosulfan were evaluated on oxidative stress parameters in male wistar rats. Group I served as untreated control whereas Group II received drinking water containing lead as lead acetate @1000 ppm (Pb1000). Group III was exposed to feed containing technical grade endosulfan @ 100 ppm (E100). Group IV was exposed to Pb (1000) +E (100). All the treatments were given daily for 28 days. Combination of lead and endosulfan modified the indices of oxidative stress in the parameters such as lipid peroxidation, reduced glutathione, superoxide dismutase and catalase in rats as compared to their individual compounds. The results suggest that the combination of these individual compounds may have the potential to modify oxidative stress produced by single compounds in male rats

scholarly journals Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Christonikos Leventelis ◽  
Nikolaos Goutzourelas ◽  
Aikaterini Kortsinidou ◽  
Ypatios Spanidis ◽  
Georgia Toulia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Redox Status ◽  
Protein Carbonyls ◽  
Healthy Individuals ◽  
Thiobarbituric Acid Reactive Substances ◽  
Antioxidant Defence ◽  
Total Antioxidant ◽  
Beneficial Action ◽  
The Impact

Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n=21) and the methadone (n=21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n=29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.

scholarly journals Protective Role of Ce Nanoparticles Against the Hepatotoxicity Induced by Exposure to Paraquat

2018 ◽  
Vol 6 (2) ◽  
pp. 37-43
Author(s):  
Hamid Heidary Dartoti ◽  
Farzin Firozian ◽  
Sara Soleimani Asl ◽  
Akram Ranjbar
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Role ◽  
Male Rats ◽  
Hepatic Tissue ◽  
Control Group ◽  
Serum Samples ◽  
Tissue Samples ◽  
Total Antioxidant ◽  
Group 2

Objectives: The present study aimed to investigate the antioxidant activity of cerium oxide nanoparticles (CeNPs) against paraquat (PQ)-induced liver injury in rats. Methods: Thirty-two male rats were divided into four 8-member groups and treated intraperitoneally with PQ and/or CeNPs for 14 days. Group 1 received PQ (5 mg/kg/d), group 2 received CeNPs (15, 30, and 60 mg/kg/d), group 3 received a combination of PQ (5 mg/kg/d) and CeNPs (15, 30, and 60 mg/kg/d), and group 4 (control group) received saline solution. Serum samples along with liver tissue samples were collected from all the rats. Oxidative stress (OS) biomarkers including total antioxidant capacity, lipid peroxidation, total thiol groups, DNA damage, and nitric oxide levels were determined. Histological samples were also analyzed using hematoxylin and eosin staining slides. Results: Levels of oxidative stress and hepatic tissue damage were significantly higher in the PQ group compared to the control group. CeNPs at a dose of 15 mg/kg showed the antioxidant activity and compromised the PQ-induced damage. Conclusion: In the scenario tested in this study, CeNPs could reduce the levels of OS, as well as hepatic damage induced by PQ.

scholarly journals Effect of Curcumin on Oxidative Stress in a Model of Turpentine Induced Acute Experimental Inflammation

2017 ◽  
Vol 45 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Andrei CONEAC ◽  
Meda Sandra ORASAN ◽  
Daniel Corneliu LEUCUTA ◽  
Nicoleta DECEA ◽  
Miuta FILIP ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
High Performance ◽  
Control Group ◽  
Group Iii ◽  
Group I ◽  
Total Antioxidant ◽  
Experimental Inflammation ◽  
Group Ii

Curcumin, a natural phenolic compound is an anti-tumor agent with anti-inflammatory and anti-oxidant properties. The aim of this research was to evaluate oxidative stress levels, the antioxidant activity and Curcumin concentrations by high performance liquid chromatography (HPLC) in an acute experimental inflammation induced by Turpentine oil (intramuscular 0.6 mg kg-1 body weight) and to compare a prophylactic versus a therapeutic regimen of Curcumin (oral suspension of 150 mg Curcumin kg-1 rat weight). Sixteen adult male Wistar rats were assigned to four groups: Control, Group I (Curcumin only), Group II (Curcumin administration, then induced inflammation after 1 hour) and Group III (induced inflammation then Curcumin administration after 2 hours). Oxidative stress was assessed by measuring serum malondialdehide and carbonylated proteins, while systemic and local total antioxidant capacity was determined by ABTS. Local tissue changes (muscle, kidney, liver) were analysed using histopathology. Results showed that acute inflammation significantly increased lipid peroxidation in Groups II and III compared to Control and Group I. A significantly reduced total antioxidant capacity (ATBS) was present in serum and kidney in Group II, also in muscle and kidney in Group III. ABTS levels were significantly increased only in the liver tissue of the animals in Groups II and III with induced inflammation as compared to Group I. This study proved the potential of Curcumin in reducing oxidative stress in both prophylactic and therapeutic regimens.

Alteration of hepatic cells glucose metabolism as a non-cholinergic detoxication mechanism in counteracting diazinon-induced oxidative stress

2006 ◽  
Vol 25 (12) ◽  
pp. 697-703 ◽  
Author(s):  
Fatemeh Teimouri ◽  
Nasim Amirkabirian ◽  
Hadi Esmaily ◽  
Azadeh Mohammadirad ◽  
Atousa Aliahmadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Glucose ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Liver Lipid ◽  
Liver Homogenate ◽  
Thiobarbituric Acid ◽  
Predisposing Factor ◽  
Cholinergic Mechanism ◽  
Hepatic Cells ◽  
Total Antioxidant

The aim of this study was to evaluate effects of acute exposure to various doses of diazinon, a widely used synthetic organophosphorus (OP) insecticide on plasma glucose, hepatic cells key enzymes of glycogenolysis and gluconeogenesis, and oxidative stress in rats. Diazinon was administered by gavage at doses of 15, 30 and 60 mg/kg. The liver was perfused and removed under anaesthesia. The activities of glycogen phosphorylase (GP), phosphoenolpyruvate carboxykinase (PEPCK), thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) were analysed in liver homogenate. Administration of diazinon (15, 30 and 60 mg/kg) increased plasma glucose concentrations by 101.43% (P=0.001), 103.68% (P=0.000) and 160.65% (P=0.000) of control, respectively. Diazinon (15, 30 and 60 mg/kg) increased hepatic GP activity by 43.5% (P=0.05), 70.3% (P=0.00) and 117.2% (P=0.02) of control, respectively. In addition, diazinon (30 and 60 mg/kg) increased hepatic PEPCK by 77.3% (P=0.000) and 93.5% (P=0.000) of control, respectively. Diazinon (30 and 60 mg/kg) decreased liver TAC by 38% (P=0.046) and 48% (P=0.000) of control, respectively. Also diazinon (30 and 60 mg/kg) increased hepatic cell liver lipid peroxidation by 77% (P=0.05) and 280% (P=0.000) of control. The correlations between plasma glucose and hepatic cells TBARS (r2=0.537, P=0.02), between plasma glucose and ChE activity (r2=0.81, P=0.049) and between plasma glucose and hepatic cells GP activity (r2=0.833, P=0.04) were significant. It is concluded that the liver cells are a site of toxic action of diazinon. Diazinon increases glucose release from liver into blood through activation of glycogenolysis and gluconeogenesis as a detoxication non-cholinergic mechanism to overwhelm diazinon-induced toxic stress. The results are in accordance with the hypothesis that OPs are a predisposing factor of diabetes.

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