scholarly journals Ameliorating Effect of Pentadecapeptide Derived from Cyclina sinensis on Cyclophosphamide-Induced Nephrotoxicity

Marine Drugs ◽  
2020 ◽  
Vol 18 (9) ◽  
pp. 462
Author(s):  
Xiaoxia Jiang ◽  
Zhexin Ren ◽  
Biying Zhao ◽  
Shuyao Zhou ◽  
Xiaoguo Ying ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Anticancer Drug ◽  
Tissue Damage ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Cyclina Sinensis ◽  
Apoptotic Pathways

Cyclophosphamide (CTX) is a widely used anticancer drug with severe nephrotoxicity. The pentadecapeptide (RVAPEEHPVEGRYLV) from Cyclina sinensis (SCSP) has been shown to affect immunity and to protect the liver. Hence, the purpose of this study was to investigate the ameliorating effect of SCSP on CTX-induced nephrotoxicity in mice. We injected male ICR mice with CTX (80 mg/kg·day) and measured the nephrotoxicity indices, levels of antioxidant enzymes, malondialdehyde (MDA), inflammatory factors, as well as the major proteins of the NF-κB and apoptotic pathways. Cyclophosphamide induced kidney injury; the levels of kidney-injury indicators and cytokines recovered remarkably in mice after receiving SCSP. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) increased, while there was a significant decrease in MDA levels. The kidney tissue damage induced by CTX was also repaired to a certain extent. In addition, SCSP significantly inhibited inflammatory factors and apoptosis by regulating the NF-κB and apoptotic pathways. Our study shows that SCSP has the potential to ameliorate CTX-induced nephrotoxicity and may be used as a therapeutic adjuvant to ameliorate CTX-induced nephrotoxicity.

Immunolocalization of antioxidant enzymes in testis of rams submitted to long-term heat stress

Zygote ◽  
2019 ◽  
Vol 27 (6) ◽  
pp. 432-435
Author(s):  
Thais Rose dos Santos Hamilton ◽  
Gabriela Esteves Duarte ◽  
José Antonio Visintin ◽  
Mayra Elena Ortiz D’Ávila Assumpção
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Heat Stress ◽  
Glutathione Peroxidase ◽  
Cell Types ◽  
Treated Group ◽  
Oxidative Balance ◽  
Testicular Cells

SummaryLong-term heat stress (HS) induced by testicular insulation generates oxidative stress (OS) on the testicular environment; consequently activating antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GPx). The aim of this work was to immunolocalize antioxidant enzymes present in different cells within the seminiferous tubule when rams were submitted to HS. Rams were divided into control (n = 6) and treated group (n = 6), comprising rams subjected to testicular insulation for 240 h. After the testicular insulation period, rams were subjected to orchiectomy. Testicular fragments were submitted to immunohistochemistry for staining against SOD, GR and GPx enzymes. We observed immunolocalization of GPx in more cell types of the testis after HS and when compared with other enzymes. In conclusion, GPx is the main antioxidant enzyme identified in testicular cells in an attempt to maintain oxidative balance when HS occurs.

scholarly journals Effect of Cross-Sex Hormonal Replacement on Antioxidant Enzymes in Rat Retroperitoneal Fat Adipocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Enzymatic Activities ◽  
Glutathione S Transferase ◽  
Control Groups ◽  
Intact Female ◽  
Hormonal Replacement

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.

scholarly journals The activity of antioxidant enzymes in colorectal adenocarcinoma and corresponding normal mucosa.

2012 ◽  
Vol 59 (4) ◽  
Author(s):  
Joanna Katarzyna Strzelczyk ◽  
Tomasz Wielkoszyński ◽  
Łukasz Krakowczyk ◽  
Brygida Adamek ◽  
Marzena Zalewska-Ziob ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Colorectal Adenocarcinoma ◽  
Average Distance ◽  
Normal Mucosa ◽  
Colorectal Carcinogenesis ◽  
Tissue Homogenates

Oxidative stress is one of several factors which contribute to the development of colorectal carcinogenesis. The aim of the study was an assessment of the activity of antioxidant enzymes in tumour and corresponding normal distal mucosa in a group of patients with colorectal adenocarcinoma. Samples of tumour and corresponding normal mucosa were obtained during a resection of colorectal cancer from 47 patients aged between 26 and 82 years. The average distance of corresponding normal distal mucosa from the tumour was 4.49 cm. Activities of antioxidant enzymes: superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST), and catalase (CAT) were measured in tissue homogenates. The patients were grouped according to the tumour stage (Duke's staging), grading, localization, and size of tumour, as well as age and sex. Statistical analysis was performed. The activity of SOD and GPx was considerably increased, while the activity of GST decreased significantly in tumour as compared with normal mucosa. GR activity in colorectal cancer was evidently higher in tumours of proximal location compared with the distal ones. The distance of corresponding normal distal mucosa from the tumour was analyzed and related to all assayed parameters. A decreased GST activity was observed in corresponding normal mucosa more than 5 cm distant from the tumour in patients with CD Duke's stage. The higher activity of superoxide dismutase and glutathione peroxidase in tumour compared to corresponding normal mucosa could indicate higher oxidative stress in colorectal adenocarcinoma cells.

scholarly journals Evaluation of Salivary Antioxidant Enzymes among Smokers and Nonsmokers

2012 ◽  
Vol 3 (1) ◽  
pp. 18-21 ◽  
Author(s):  
KMK Masthan ◽  
Tajinder Kaur Saggu ◽  
Mahesh Pundaleek Dudanakar ◽  
Shams UI Nisa
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Cigarette Smoke ◽  
Biological Fluid ◽  
Antioxidant Defense System ◽  
Mean Value ◽  
Oral Diseases ◽  
Unstimulated Saliva ◽  
Smoking Group

ABSTRACT Background Cigarette smoke contains various oxygen-free radicals which are considered as the main causes of damage to biomolecules when exposed to cigarette smoke. Saliva is the first biological fluid that encounters inhaled cigarette smoke (CS) and has an antioxidant defense system able to counter toxic activities of free radical species. So, the aim of this study was to compare the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in saliva of smokers and nonsmokers. Materials and methods Unstimulated saliva of 200 males (100 smokers and 100 nonsmokers) was collected. The saliva was centrifuged and the activity of salivary superoxide dismutase and glutathione peroxidase was measured according to a specific assay. Results The mean value of superoxide dismutase activity was significantly higher in the smoking group than in the nonsmoker group, while the levels of GSH-Px activity was significantly higher in the nonsmoking group than in the smoking group. Conclusion Cigarette smoke leads to an alteration in salivary antioxidant activity. Evaluating the variations in the level of antioxidant enzymes (SOD and GSH-Px) in smoker's saliva might be useful for estimating the level of oxidative stress caused by cigarette smoke. Thus, it may help in patient's education regarding the ill-effects of smoking and determining the evolution and progress of various oral diseases. How to cite this article Saggu TK, Masthan KMK, Dudanakar MP, Nisa SUI, Patil S. Evaluation of Salivary Antioxidant Enzymes among Smokers and Nonsmokers. World J Dent 2012;3(1):18-21.

Response of antioxidant enzymes to intermittent and continuous hyperbaric oxygen

1990 ◽  
Vol 69 (1) ◽  
pp. 328-335 ◽  
Author(s):  
A. L. Harabin ◽  
J. C. Braisted ◽  
E. T. Flynn
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Hyperbaric Oxygen ◽  
Enzyme Activities ◽  
Guinea Pigs ◽  
Exposure Duration ◽  
Biochemical Variables ◽  
Time Required

Rats and guinea pigs were exposed to O2 at 2.8 ATA (HBO) delivered either continuously or intermittently (repeated cycles of 10 min of 100% O2 followed by 2.5 min of air). The O2 time required to produce convulsions and death was increased significantly in both species by intermittency. To determine whether changes in brain and lung superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx) correlated with the observed tolerance, enzyme activities were measured after short or long HBO exposures. For each exposure duration, one group received continuous and one intermittent HBO; O2 times were matched. HBO had marked effects on these enzymes: lung SOD increased (guinea pigs 47%, rats 88%) and CAT and GSHPx activities decreased (33%) in brain and lung. No differences were seen in lung GSHPx or brain CAT in rats or brain SOD in either species. In guinea pigs, but less so in rats, the observed changes in activity were usually modulated by intermittency. Increases in hematocrit, organ protein, and lung DNA, which may also reflect ongoing oxidative damage, were also slowed with intermittency in guinea pigs. Intermittency benefited both species by postponing gross symptoms of toxicity, but its modulation of changes in enzyme activities and other biochemical variables was more pronounced in guinea pigs than in rats, suggesting that there are additional mechanisms for tolerance.

Pathophysiology of Acute Kidney Injury, Repair, and Regeneration

2014 ◽  
Author(s):  
Ching-Wei Tsai ◽  
Sanjeev Noel ◽  
Hamid Rabb
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Critical Role ◽  
Recovery Period ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Phase Cell ◽  
M2 Macrophage ◽  
Renal Stem Cells

Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

Absence of Modulating Effects of Cytokines on Antioxidant Enzymes in Peritoneal Mesothelial Cells

1997 ◽  
Vol 17 (5) ◽  
pp. 455-466 ◽  
Author(s):  
Jinn-Yang Chen ◽  
An-Hang Yang ◽  
Yao-Ping Lin ◽  
Jen-Kou Lin ◽  
Wu-Chang Yang ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Human Liver ◽  
Mesothelial Cells ◽  
Superoxide Dismutase Activity ◽  
Antioxidant Enzyme Activities ◽  
Peritoneal Mesothelial Cells ◽  
Liver And Kidney ◽  
Human Peritoneal Mesothelial Cells

Objective To investigate the modulation of superoxide dismutase, glutathione peroxidase, and catalase by cytokines and endotoxin in human peritoneal mesothelial cells. Design Cultured human peritoneal mesothelial cells were treated with various concentrations of interleu kin-1 α, tumor necrosis factor-α(TNFα), interleukin-6, interleukin-8, transforming growth factor-β (TGFβ), and lipopolysaccharide. Cell morphology was observed and the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed. The antioxidant enzyme activities of human peritoneal mesothelial cells were also compared with those of human liver and kidney tissues. Results Interleukin-1α, TNFα, TGFβ, and lipopolysaccharide caused dose-dependent cytotoxicities in mesothelial cells. The activities of these three antioxidant enzymes did not change after treatment with cytokines and endotoxin. The total superoxide dismutase activity of confluent human peritoneal mesothelial cells was found to be greater than that of human liver and kidney tissues and was composed mostly of manganese superoxide dismutase activity. Furthermore, glutathione peroxidase and catalase activities of human peritoneal mesothelial cells were lower than those of human liver and kidney tissues. Conclusion In human peritoneal mesothelial cells, lack of induction of antioxidant enzymes by inflammatory cytokines, as well as high superoxide dismutase activity accompanied by insufficient glutathione peroxidase and catalase activities may both contribute to the susceptibility of these cells to oxidative damage. Therefore, appropriate management to decrease oxidative injury to the peritoneum should be taken into consideration when treating long-term continuous ambulatory peritoneal dialysis patients.

scholarly journals The Inhibitory Impact of Schisandrin Against LPS-Induced Acute Kidney Injury in Vitro and in Vivo

2021 ◽  
Author(s):  
Weifeng Li ◽  
Qiuxia Huang ◽  
Jinjin Yu ◽  
Jiabao Yu ◽  
Yajie Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Immunohistochemical Analysis ◽  
Inflammatory Factors ◽  
Raw264.7 Macrophages ◽  
Bioactive Component

Abstract Schisandrin (Sch) is a main bioactive component of Schisandra sphenanthera Rehd.et Wils. It has been reported that Sch could regulate inflammatory disease. This study evaluated the anti-inflammatory and anti-oxidant effects effect of Sch on lipopolysaccharide (LPS)-induced macrophages activation and acute kidney injury mice. Male Kunming mice were intraperitoneally injected with LPS (15 mg/kg) after administration of Sch (12.5, 25, 50 mg/kg) seven days for developing acute kidney injury vivo model. RAW264.7 macrophages were pretreatment Sch (10, 20, 40 µM) and administrated LPS (1 µg/ml) to create an in vitro injury model. ELISA results found that Sch administration reduced the production of inflammatory factors induced by LPS in kidney tissues and RAW264.7 macrophages. It has been observed that Sch alleviated oxidative stress by reducing the levels of reactive oxygen species, myeloperoxidase and malondialdehyde, and increasing the activity of superoxide dismutase and glutathione peroxidase. Hematoxylin-eosin staining data suggested that Sch administration significantly reduced inflammatory cell infiltration and the kidney tissue damage induced by LPS. The blood urea nitrogen and creatinine levels were also reduced by Sch treatment. In addition, Western blot and immunohistochemical analysis showed that Sch up-regulated the expression of Nrf2 and HO-1, and decreased the expression of p-p38, p-JNK, p-ERK1/2, p-IκBα, p-NF-κBp65 and TLR4. The current research showed that Sch reduced LPS-induced acute kidney injury by inhibiting inflammation and oxidative stress, and provided insights into potential ways to treat AKI.

scholarly journals Ulinastatin improves renal microcirculation by protecting endothelial cells and inhibiting autophagy in a septic rat model

2022 ◽  
Author(s):  
Tian Li ◽  
Xiaojun Ji ◽  
Jingfeng Liu ◽  
Xinjie Guo ◽  
Ran Pang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Rat Model ◽  
Cecal Ligation ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sprague Dawley ◽  
Male Adult ◽  
Renal Microcirculation

Introduction: Increased permeability of the renal capillaries is a common consequence of sepsis-associated acute kidney injury. Vascular endothelial (VE)-cadherin is a strictly endothelial-specific adhesion molecule that can control the permeability of the blood vessel wall. Additionally, autophagy plays an important role in maintaining cell stability. Ulinastatin, a urinary trypsin inhibitor, attenuates the systemic inflammatory response and visceral vasopermeability. However, it is uncertain whether ulinastatin can improve renal microcirculation by acting on the endothelial adhesion junction. Methods: We observed the effect of ulinastatin in a septic rat model using contrast-enhanced ultrasonography (CEUS) to evaluate the perfusion of the renal cortex and medulla. Male adult Sprague-Dawley rats were subjected to cecal ligation and puncture and divided into the sham, sepsis, and ulinastatin groups. Ulinastatin (50,000 U/kg) was injected into the tail vein immediately after the operation. The CEUS was performed to evaluate the renal microcirculation perfusion at 3, 6, 12, and 24 hours after the operation. Histological staining was used to evaluate kidney injury scores. Western blot (WB) was used to quantify the expression of VE-cadherin, LC3II, and inflammatory factors [interleukin -1β (IL-1β), interleukin -6 (IL-6), and tumor necrosis factor-α (TNF-α)] in kidney tissue, and enzyme-linked immunosorbent assay (ELISA) detected serum inflammatory factors and kidney function and early kidney injury biomarker levels. Results: Compared with the sham group, ulinastatin reduced the inflammatory response, inhibited autophagy, maintained the expression of VE-cadherin, and meliorated cortical and medullary perfusion. Conclusion: Ulinastatin effectively protects the adhesion junction and helps ameliorate the perfusion of kidney capillaries during sepsis by the inhibition of autophagy and the expression of inflammatory factors.

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