Protective effects of catechin and quercetin on antioxidant status, lipid peroxidation and testis-histoarchitecture induced by chlorpyrifos in male rats

2012 ◽  
Vol 33 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Yusuf Kalender ◽  
Sinan Kaya ◽  
Dilek Durak ◽  
Fatma Gokce Uzun ◽  
Filiz Demir
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Status ◽  
Male Rats ◽  
Protective Effects

Influence of cadmium ions on the antioxidant status and lipid peroxidation in mouse liver: protective effects of zinc and selenite ions

2012 ◽  
Vol 29 (04) ◽  
pp. 137-142 ◽  
Author(s):  
Rasa Bernotiene ◽  
Laima Ivanoviene ◽  
Ilona Sadauskiene ◽  
Arunas Liekis ◽  
Leonid Ivanov
Keyword(s):  
Lipid Peroxidation ◽  
Mouse Liver ◽  
Antioxidant Status ◽  
Protective Effects ◽  
Cadmium Ions

Orange pulp improves antioxidant status and suppresses lipid peroxidation in orchidectomized male rats

Nutrition ◽  
2007 ◽  
Vol 23 (7-8) ◽  
pp. 617-621 ◽  
Author(s):  
Farzad Deyhim ◽  
Arnulfo Villarreal ◽  
Kristi Garcia ◽  
Ryan Rios ◽  
Claudia Garcia ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Status ◽  
Male Rats ◽  
Orange Pulp

scholarly journals Antiperoxidative and anti-apoptotic effects of lycopene and ellagic acid on cyclophosphamide-induced testicular lipid peroxidation and apoptosis

2010 ◽  
Vol 22 (4) ◽  
pp. 587 ◽  
Author(s):  
Gaffari Türk ◽  
Ali Osman Çeribaşi ◽  
Fatih Sakin ◽  
Mustafa Sönmez ◽  
Ahmet Ateşşahin
Keyword(s):  
Lipid Peroxidation ◽  
Ellagic Acid ◽  
Combined Treatment ◽  
Sperm Concentration ◽  
Testicular Tissue ◽  
Male Rats ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Sprague Dawley

The present study was conducted to investigate the possible protective effects of lycopene (LC) and ellagic acid (EA) on cyclophosphamide (CP)-induced testicular and spermatozoal toxicity associated with the oxidative stress and apoptosis in male rats. Forty-eight healthy adult male Sprague-Dawley rats were divided into six groups of eight rats each. The control group was treated with placebo; the LC, EA and CP groups were given LC (10 mg kg–1), EA (2 mg kg–1) and CP (15 mg kg–1), respectively, alone; the CP+LC group was treated with a combination of CP (15 mg kg–1) and LC (10 mg kg–1); and the CP+EA group was treated with a combination of CP (15 mg kg–1) and EA (2 mg kg–1). All treatments were maintained for 8 weeks. At the end of the treatment period, bodyweight and the weight of the reproductive organs, sperm concentration and motility, testicular tissue lipid peroxidation, anti-oxidant enzyme activity and apoptosis (i.e. Bax and Bcl-2 proteins) were determined. Administration of CP resulted in significant decreases in epididymal sperm concentration and motility and significant increases in malondialdehyde levels. Although CP significantly increased the number of Bax-positive (apoptotic) cells, it had no effect on the number of Bcl-2-positive (anti-apoptotic) cells compared with the control group. However, combined treatment of rats with LC or EA in addition to CP prevented the development of CP-induced lipid peroxidation and sperm and testicular damage. In conclusion, CP-induced lipid peroxidation leads to structural and functional damage, as well as apoptosis, in spermatogenic cells of rats. Both LC and EA protect against the development of these detrimental effects.

scholarly journals Punicalagin Exerts Protective Effects against Ankylosing Spondylitis by Regulating NF-κB-TH17/JAK2/STAT3 Signaling and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Xinzhe Feng ◽  
Qinyuan Yang ◽  
Chen Wang ◽  
Wenwen Tong ◽  
Weidong Xu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ankylosing Spondylitis ◽  
Inflammatory Mediators ◽  
Antioxidant Status ◽  
Serum Levels ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Protective Effects ◽  
Stat3 Signaling

Background. Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by sacroiliitis and spinal rigidity of the axial joints. The role of oxidative stress and increased proinflammatory cytokines is well documented in AS pathogenesis. Punicalagin (2,3-hexahydroxydiphenoyl-gallagyl-D-glucose), an ellagitannin widely present in pomegranates, is found to exhibit potent anti-inflammatory, antiproliferative, and antioxidative effects. The present study was undertaken to investigate the effects of punicalagin in a rodent model of AS. Methods. BALB/c mice induced spondylitis were sacrificed 24 h after the last injection of proteoglycan extract. Histological scoring was done to assess the degree of the disease. The expression of JAK2/STAT3 proteins and proteins of the nuclear factor-κB (NF-κB) pathway was determined by immunoblotting. Serum levels of inflammatory mediators—TNF-α, IL-1β, IL-6, IL-17A, and IL-23—were assessed. Levels of lipid peroxidation and reactive oxygen species (ROS) were quantified. Antioxidant status as a measure of activities of antioxidant enzymes—catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)—was determined. Results. Punicalagin effectively improved antioxidant status and decreased lipid peroxidation, ROS production, and serum levels of inflammatory mediators. NF-κB pathway and JAK2/STAT3 signaling were significantly (p<0.05) downregulated. Punicalagin effectively regulated the production of cytokines by the Th17 cells and the IL-17A/IL-23 axis. Conclusion. The observations suggest that punicalagin exerts a protective role in AS via reducing oxidative stress and regulating NF-κB/TH17/JAK2/STAT3 signal. Punicalagin thus could be explored further as a potent candidate compound in the treatment of AS.

scholarly journals Protective Effect of N-Acetylcysteine Against Toxicity on the Rat Blood After Chronic Exposure to Carbosulfan

2015 ◽  
Vol 01 ◽  
pp. 18 ◽  
Author(s):  
Ines El-Bini Dhouib ◽  
Alya Annabi ◽  
Aicha Jrad ◽  
Najoua Gharbi ◽  
Mohamed Montassar Lasram ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Cells ◽  
Chronic Exposure ◽  
Antioxidant Status ◽  
Male Rats ◽  
Transferase Activity ◽  
Protective Effects ◽  
Significant Elevation ◽  
And Oxidative Stress ◽  
Tsh Levels

The present study investigated the protective effects of N-acetylcysteine (NAC), is widely known as an antidote to acetaminophen overdose, on carbosulfan (CB)-induced hematotoxicity and oxidative stress in male rats. CB was administered at a dose of 25 mg/kg or simultaneously administered with NAC (2 g/l) for 30 days. Results of hematological examination showed that red blood cells, hematocrite, hemoglobin, and reticulocytes levels were significantly lower in CB-exposed rats compared with those in the control. Administration of CB caused a significant increase in the superoxide dismutase and catalase activities. However, the glutathione (GSH) and thiols group (TSH) levels were significantly increased as well as GSH S-transferase activity and levels of glutathione peroxidase on erythrocytes of males rats compared with those in the control. Also, CB-treated rats showed significant elevation in lipid peroxidation (LPO) and acetylcholinesterase (AChE) on erythrocytes in comparison with the control. Co-administration with NAC exhibited chemoprotective effects against CB-mediated hematotoxicity, augmented erythrocyte antioxidant status, and prevented the induction of anemia.

Procyanidinere therapy of pulmonary fibrosis induced by CdSe nanorods with pulmonary instillation

2020 ◽  
Author(s):  
Qixing Zhou ◽  
Zongkai Yue ◽  
Qingzhao Li ◽  
Ruiren Zhou ◽  
Lu Liu
Keyword(s):  
Lipid Peroxidation ◽  
Pulmonary Fibrosis ◽  
Inflammatory Responses ◽  
Early Stage ◽  
Male Rats ◽  
Histopathological Analysis ◽  
Protective Effects ◽  
Photoelectric Conversion ◽  
Pulmonary Instillation ◽  
Cdse Nanorods

Abstract Background: The CdSe nanorod as a one-dimensional nanostructure has an excellent performance in photoelectric conversion, biological labeling and environmental protection. Thus, it is crucial to investigate its potential adverse health effects at an early stage. Methods: Sprague-Dawley (SD) male rats were exposed to 15 mg/kg CdSe and 200 mg/kg procyanidine (OPC) for 30, 60 and 90 days. Lung tissues were collected on days 30, 60 and 90. Oxidation damages, histopathological analysis, transmission electron microscopy and hydroxyproline level were measured. Results: The lung tissue would be the main target organ after CdSe nanorods entering into biological bodies. Pulmonary instillation of CdSe nanorods could decrease vitality of T-SOD and T-AOC in lung tissues of a rat, increase MDA and hydroxyproline levels and lipid peroxidation products, induce mitochondrial cristae broken and vacuolization, cause inflammatory responses, and finally induce pulmonary fibrosis. The oral administration of procyanidinere could significantly increase the content of antioxidant enzymes, scavenge free radicals, reduce the lipid peroxidation and have protective effects on CdSe nanorods-induced pulmonary fibrosis. Conclusions: CdSe nanorods could induce an extensive inflammatory response, elevate ROS, induce pulmonary fibrosis and reveal time accumulation appearance. OPC has a protective effect on lung injury induced by CdSe nanorods, which might be related to anti-oxidative and anti-inflammatory properties.

Melatonin modulates 900 MHz microwave-induced lipid peroxidation changes in rat brain

2006 ◽  
Vol 22 (5) ◽  
pp. 211-216 ◽  
Author(s):  
Halis Köylü ◽  
Hakan Mollaoglu ◽  
Fehmi Ozguner ◽  
Mustafa Nazýroölu ◽  
Namýk Delibap
Keyword(s):  
Lipid Peroxidation ◽  
Brain Cortex ◽  
Treated Group ◽  
Male Rats ◽  
Control Group ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Melatonin Administration ◽  
Anti Oxidant ◽  
The Brain

Microwaves (MW) from cellular phones may affect biological systems by increasing free radicals, which may enhance lipid peroxidation levels of the brain, thus leading to oxidative damage. Melatonin is synthesized in and secreted by the pineal gland at night and exhibits anti-oxidant properties. Several studies suggest that supplementation with anti-oxidant can influence MW-induced brain damage. The present study was designed to determine the effects of MW on the brain lipid peroxidation system, and the possible protective effects of melatonin on brain degeneration induced by MW. Twenty-eight Sprague-Dawley male rats were randomly divided into three groups as follows: (1) sham-operated control group (N-8); (2) study 900-MHz MW-exposed group (N-8); and (3) 900-MHz MW-exposed-melatonin (100 mg/kg sc before daily MW exposure treated group) (N-10). Cortex brain and hippocampus tissues were removed to study the levels of lipid peroxidation as malonyl dialdehyde. The levels of lipid peroxidation in the brain cortex and hippocampus increased in the MW group compared with the control group, although the levels in the hippocampus were decreased by MW-melatonin administration. The brain cortex lipid peroxidation levels were unaffected by melatonin treatment. We conclude that melatonin may prevent MW-induced oxidative changes in the hippocampus by strengthening the anti-oxidant defense system, by reducing oxidative stress products.

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