Testicular gametogenic and steroidogenic activities in chlorpyrifos insecticide-treated rats: a correlation study with testicular oxidative stress and role of antioxidant enzyme defence systems in Sprague-Dawley rats

Andrologia ◽  
2011 ◽  
Vol 44 (2) ◽  
pp. 102-115 ◽  
Author(s):  
T. K. Mandal ◽  
N. S. Das
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Correlation Study ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Ketab E. Al-Otaibi ◽  
Abdulrahman M. Al Elaiwi ◽  
Mohammad Tariq ◽  
Abdulrahman K. Al-Asmari
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Femoral Vein ◽  
Lipid Hydroperoxides ◽  
Sprague Dawley ◽  
Glycerol Injection ◽  
Sprague Dawley Rats ◽  
Structural Abnormalities ◽  
Nephroprotective Effect

Contrast media- (CM-) induced nephropathy is a serious complication of radiodiagnostic procedures. Available data suggests that the development of prophylaxis strategies is limited by poor understanding of pathophysiology of CM-induced nephropathy. Present study was designed to determine the role of oxidative stress, myeloperoxidase, and nitric oxide in the pathogenesis of iohexol model of nephropathy and its modification with simvastatin (SSTN). Adult Sprague Dawley rats were divided into seven groups. After 24 h of water deprivation, all the rats except in control and SSTN-only groups were injected (10 ml/kg) with 25% glycerol. After 30 min, SSTN (15, 30, and 60 mg/kg) was administered orally, daily for 4 days. Twenty-four hours after the glycerol injection, iohexol was infused (8 ml/kg) through femoral vein over a period of 2 min. All the animals were sacrificed on day 5 and blood and kidneys were collected for biochemical and histological studies. The results showed that SSTN dose dependently attenuated CM-induced rise of creatinine, urea, and structural abnormalities suggesting its nephroprotective effect. A significant increase in oxidative stress (increased lipid hydroperoxides and reduced glutathione levels) and myeloperoxidase (MPO) and decreased nitric oxide in CM group were reversed by SSTN. These findings support the use of SSTN to combat CM-induced nephrotoxicity.

scholarly journals Melatonin Attenuates Contrast-Induced Nephropathy in Diabetic Rats: The Role of Interleukin-33 and Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Didem Onk ◽  
Oruc Alper Onk ◽  
Kultigin Turkmen ◽  
Huseyin Serkan Erol ◽  
Tulin Akarsu Ayazoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Potential ◽  
Kidney Tissue ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
Contrast Induced Nephropathy ◽  
Interleukin 33 ◽  
Sprague Dawley Rats ◽  
And Oxidative Stress

Background.Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown.Methods.Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days.Results.We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p<0.05).Conclusion.Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.

scholarly journals Pharmacological Modulation of TRPM2 Channels via TRPM2 Pathway Leads to Neuroprotection in MPTP-induced Parkinson’s Disease in Sprague Dawley Rats

2021 ◽  
Author(s):  
Bhupesh Vaidya ◽  
Harpinder Kaur ◽  
Pavan Thapak ◽  
Shyam Sunder Sharma ◽  
Jitendra N Singh
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Deficits ◽  
Intraperitoneal Administration ◽  
Sprague Dawley ◽  
Therapeutic Benefits ◽  
Sprague Dawley Rats ◽  
Trpm2 Channels

Abstract Transient receptor potential melastatin-2 (TRPM2) channels are cation channels activated by oxidative stress and adenosine di-phosphate ribose (ADPR). Role of TRPM2 channels has been postulated in several neurological disorders, but, it has not been explored in animal models of Parkinson’s disease (PD). Thus, the role of TRPM2 and its associated poly (ADP-ribose) polymerase (PARP) signalling pathways were investigated in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD rat model using TRPM2 inhibitor, 2-aminoethyl diphenyl borinate (2-APB) and PARP inhibitor, N-(6-Oxo-5,6-dihydrophenanthridin-2-yl)-(N,N-dimethylamino) acetamide hydrochloride (PJ-34). PD was induced by using a bilateral intranigral administration of MPTP in Sprague-Dawley rats, and different parameters were evaluated. An increase in the oxidative stress was observed, leading to the locomotor and cognitive deficits in the PD rats. PD rats also showed an increased TRPM2 expression in striatum and mid brain accompanied by reduced expression of tyrosine-hydroxylase (TH) in comparison to sham animals. Intraperitoneal administration of 2-aminoethyl diphenyl borinate (2-APB) and N-(6-Oxo-5,6-dihydrophenanthridin-2-yl)-(N,N-dimethylamino) acetamide hydrochloride (PJ-34) led to an improvement in the locomotor and cognitive deficits in comparison to MPTP-induced PD rats. These improvements were accompanied by a reduction in the levels of oxidative stress and an increase in TH levels in striatum and mid brain. In addition, these pharmacological interventions also led to a decrease in the expression of TRPM2 in PD in striatum and mid brain. Our results provide a rationale for the development of potent pharmacological agents targeting TRPM2-PARP pathway to provide therapeutic benefits for the treatment of neurological disease like PD.

scholarly journals Methane Saline Ameliorates Traumatic Brain Injury through Anti-Inflammatory, Antiapoptotic, and Antioxidative Effects by Activating the Wnt Signalling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Meng Li ◽  
Weiman Gao ◽  
Le Ji ◽  
Jia Li ◽  
Wanting Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wnt Pathway ◽  
Wnt Signalling ◽  
Signalling Pathway ◽  
Sprague Dawley ◽  
Wnt Signalling Pathway ◽  
Sprague Dawley Rats ◽  
Antioxidative Effects ◽  
Anti Inflammatory

Objective. Methane saline (MS) can be used to treat many diseases via its anti-inflammatory, antiapoptotic, and antioxidative activities. However, to date, there is no published evidence as to whether MS has any effect on traumatic brain injury (TBI). The Wnt signalling pathway regulates cell proliferation, differentiation, migration, and apoptosis; however, whether the Wnt signalling pathway regulates any effect of MS on TBI is unknown. This study was designed to explore the role of MS in the treatment of TBI and whether the Wnt pathway is involved. Methods. Sprague-Dawley rats were randomly divided into five groups: sham, TBI, TBI+10 ml/kg MS, TBI+20 ml/kg MS, and TBI+30 ml/kg MS. After induction of TBI, MS was injected intraperitoneally once daily for seven consecutive days. Neurological function was evaluated by the Neurological Severity Score (NSS) at 1, 7, and 14 days after TBI. Haematoxylin-eosin (HE) staining, inflammatory factors, neuron-specific enolase (NSE) staining, oxidative stress, and cell apoptosis were measured and compared 14 d after TBI to identify the optimal dose of MS and to investigate the effect of MS on TBI. In the second experiment, Sprague-Dawley rats were randomly divided into four groups: sham, TBI, TBI+20 ml/kg MS, and TBI+20 ml/kg MS+Dickkopf-1 (DKK-1, a specific inhibitor of the Wnt pathway). NSE, caspase-3, superoxide dismutase (SOD), Wnt3a, and β-catenin were detected by real-time PCR and Western blotting. The results from each group were compared 14 d after TBI to determine the regulatory role of the Wnt pathway. Results. Methane saline significantly inhibited inflammation, oxidative stress, and cell apoptosis, thus protecting neurons within 14 days of TBI. The best treatment effect against TBI was obtained with 20 ml/kg MS. When the Wnt pathway was inhibited, the treatment effect of MS was impaired. Conclusion. Methane saline ameliorates TBI through its anti-inflammatory, antiapoptotic, and antioxidative effects via activation of the Wnt signalling pathway, which plays a part but is not the only mechanism underlying the effects of MS. Thus, MS may be a novel strategy for treating TBI.

scholarly journals Oxidative stress, DNA damage, and antioxidant enzyme activity induced by hexavalent chromium in Sprague-Dawley rats

2009 ◽  
Vol 24 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Anita K. Patlolla ◽  
Constance Barnes ◽  
Clement Yedjou ◽  
V. R. Velma ◽  
Paul B. Tchounwou
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Enzyme Activity ◽  
Antioxidant Enzyme ◽  
Hexavalent Chromium ◽  
Antioxidant Enzyme Activity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Inhibition of phospholipase C-γ1augments the decrease in cardiomyocyte viability by H2O2

2006 ◽  
Vol 291 (2) ◽  
pp. H854-H860 ◽  
Author(s):  
Rabban Mangat ◽  
Tushi Singal ◽  
Naranjan S. Dhalla ◽  
Paramjit S. Tappia
Keyword(s):  
Oxidative Stress ◽  
Phospholipase C ◽  
Mrna Level ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Inhibitory Peptide ◽  
Trypan Blue Exclusion ◽  
Kinase C ◽  
Sprague Dawley Rats

The present study was conducted to examine the role of a major cardiac phospholipase C (PLC) isozyme, PLC-γ1, in cardiomyocytes during oxidative stress. Left ventricular cardiomyocytes were isolated by collagenase digestion from adult male Sprague-Dawley rats (250–300 g) and treated with 20, 50, and 100 μM H2O2for 15 min. A concentration-dependent (up to 50 μM) increase in the mRNA level and membrane protein content of PLC-γ1was observed with H2O2treatment. Furthermore, PLC-γ1was activated in response to H2O2, as revealed by an increase in the phosphorylation of its tyrosine residues. There was a marked increase in the phosphorylation of the antiapoptotic protein Bcl-2 by H2O2; this change was attenuated by a PLC inhibitor, U-73122. Although both protein kinase C (PKC)-δ and -ε protein contents were increased in the cardiomyocyte membrane fraction in response to H2O2, PKC-ε activation, unlike PKC-δ, was attenuated by U-73122 (2 μM). Inhibition of PKC-ε with inhibitory peptide (0.1 μM) prevented Bcl-2 phosphorylation. Moreover, different concentrations (0.05, 0.1, and 0.2 μM) of this peptide augmented the decrease in cardiomyocyte viability in response to H2O2. In addition, a decrease in cardiomyocyte viability, as assessed by trypan blue exclusion, due to H2O2was also seen when cells were pretreated with U-73122 and was as a result of increased apoptosis. It is therefore suggested that PLC-γ1may play a role in cardiomyocyte survival during oxidative stress via PKC-ε and phosphorylation of Bcl-2.

scholarly journals Reestablishment of Ischemia-Reperfusion Liver Injury by N-Acetylcysteine Administration prior to a Preconditioning Iron Protocol

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Virginia Fernández ◽  
Romina Vargas ◽  
Valentina Castillo ◽  
Nicolás Cádiz ◽  
Daniela Bastías ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Ischemia Reperfusion ◽  
Protein Carbonyl ◽  
Glutathione Depletion ◽  
Sprague Dawley ◽  
Short Term ◽  
Sprague Dawley Rats ◽  
Hepatic Histology

The role of iron (Fe)-induced prooxidant status in Fe preconditioning against ischemia (1 h)-reperfusion (20 h) induced liver injury was assessed using N-acetylcysteine (NAC) (1 g/kg) before Fe (50 mg/kg), given to male Sprague Dawley rats on alternate days during 10 days. IR significantly increased serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, with drastic changes in liver histology, hepatic glutathione depletion, and nuclear factor-κB (NF-κB) p65 diminution (P<0.05) (ELISA). Fe-induced liver oxidative stress, as evidenced by higher protein carbonyl/glutathione content ratios (P<0.05) at days 11 and 12 after treatment, was abolished by NAC. Under these conditions, short-term Fe administration exerted significant protection against IR liver injury, as shown by 85% and 60% decreases in IR-induced serum AST and ALT (P<0.05), respectively, and normalization of hepatic histology, glutathione levels, and NF-κB activation, changes that were suppressed by NAC administration prior to Fe. Results of this study indicate that NAC administration prior to an iron protocol reestablishes IR liver injury, supporting the role of Fe-induced transient oxidative stress in hepatoprotection and its potential clinical application.

Angiotensin II type 1 receptor is involved in flow-induced vasomotor responses of isolated middle cerebral arteries. Role of oxidative stress

2021 ◽  
Author(s):  
Ivana Jukic ◽  
Zrinka Mihaljevic ◽  
Anita Matic ◽  
Martina Mihalj ◽  
Natasa Kozina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Arteries ◽  
Control Group ◽  
Ros Production ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Middle Cerebral Arteries ◽  
Losartan Group

This study aimed to determine the mechanosensing role of angiotensin II type 1 receptor (AT1R) in flow-induced dilation (FID) and oxidative stress production in middle cerebral arteries (MCA) of Sprague-Dawley rats. Eleven-weeks old, healthy male Sprague-Dawley rats on a standard diet were given the AT1R blocker losartan (1 mg/mL) in drinking water (losartan group) or tap water (control group) ad libitum for 7 days. Blockade of AT1R attenuated FID and acetylcholine-induced dilations was compared to control group. Nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) and cyclooxygenase inhibitor indomethacin (INDO) significantly reduced FID in control group. The attenuated FID in losartan group was further reduced by INDO only at ∆100 mmHg, whereas L-NAME had no effect. In losartan group, TEMPOL (a superoxide scavenger) restored dilatation, while TEMPOL+L-NAME together significantly reduced FID compared to restored dilatation with TEMPOL alone. Direct fluorescence measurements of NO and reactive oxygen species (ROS) production in MCA, in no-flow conditions revealed significantly reduced vascular NO levels with AT1R blockade compared to control group, while flow increased the NO and ROS production in losartan group and had no effect in control group. In losartan group, TEMPOL decreased ROS production in both no-flow and flow conditions. AT1R blockade elicited increased serum concentrations of AngII, 8-iso-PGF2α, and TBARS, and decreased antioxidant enzyme activity (SOD and CAT). These results suggest that in small isolated cerebral arteries: 1) AT1 receptor maintains dilations in physiological conditions; 2) AT1R blockade leads to increased vascular and systemic oxidative stress, which underlies impaired FID.

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