scholarly journals CLA isomer t10,c12 induce oxidation and apoptosis in 3t3 adipocyte cells in a similar effect as omega-3 linolenic acid and DHA.

2017 ◽  
Vol 7 (2) ◽  
pp. 149 ◽  
Author(s):  
Jon Meadus ◽  
P. Vahmani ◽  
P. Duff ◽  
J.L. Zantinge ◽  
T.D. Turner ◽  
...  
Keyword(s):  
Linolenic Acid ◽  
Lipid Accumulation ◽  
Dairy Products ◽  
Caspase 3 ◽  
Lipid Hydroperoxide ◽  
Oxygen Species ◽  
Omega 3 ◽  
Anti Oxidant ◽  
Student’S T ◽  
One Way Anova

Background: Commercial conjugated linoleic acid (CLA) dietary supplements of contain an equal mixture of the C18:2 isomers, cis-9,trans-11 and trans-10,cis-12. CLA-c9t11 occurs naturally in meat and dairy products as the dominant CLA at 75%, whereas the CLA-t10c12 occurs at <1%. CLA-c9t11 generally promotes lipid accumulation but CLA-t10c12 inhibits lipid accumulation and may promote inflammation.Methods: Purified CLA-c9t11 and CLA-t10c12 were added to 3T3 mature adipocyte cultures at 100uM concentrations and compared with 100uM C18:3(n-3) (α-linolenic acid) and 50uM docosahexaenoic acid (DHA) to study their effect on growth, gene transcription and general oxidation. The results of 4 separate trials were averaged and compared for significance using one way ANOVA and Student’s t-test.Results: C18:3(n-3), DHA and CLA-t10c12 were inhibitory to 3t3 adipose cell growth and caused significant lipid hydro peroxide activity. CLA-t10c12 and c9t11 increased AFABP, FAS and ACOX1 mRNA expression but DHA and C18:3(n-3) decreased the same mRNAs. CLA-c9t11 but not the t10c12 stimulated adipoQ expression even though; c9t11 had only a slightly greater affinity for PPARγ than CLA- t10c12. The expression of the xenobiotic metabolism genes, aldo-keto reductase 1c1  (akr1c1), superoxide dismutase (SOD) and inflammation chemokine secretions of  eotaxin (CCL11), Rantes (CCL5), MIG (CCL9) and MCP-1 were increased by DHA, C18:3(n-3) and CLA-t10c12. This correlated with apoptosis factors, caspase 3, Bcl-2 and BAXs which were partially reduced by co-treatment with lipophilic anti-oxidant α-tocopherol.Conclusions: Based on this evidence, CLA-t10c12 promoted more reactive oxygen species (ROS) than CLAc9t11, in a similar effect as C18:3(n-3) and DHA. In response, cascades of genes are activated to deal with the potentially damaging effects of ROS through detoxification, inflammation or apoptosis.Keywords: CLA-t10c12, CLA-c9t11, gene expression, adipocyte lipid hydroperoxide, DHA,3T3 adipocytes, apoptosis.

scholarly journals Vanadium Derivative Exposure Promotes Functional Alterations of VSMCs and Consequent Atherosclerosis via ROS/p38/NF-κB-Mediated IL-6 Production

2019 ◽  
Vol 20 (24) ◽  
pp. 6115 ◽  
Author(s):  
Chang-Ching Yeh ◽  
Jing-Yiing Wu ◽  
Guan-Lin Lee ◽  
Hsiu-Ting Wen ◽  
Pinpin Lin ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Intranasal Administration ◽  
Fossil Fuels ◽  
Ros Generation ◽  
Oxygen Species ◽  
Pathological Effect ◽  
Atherosclerotic Lesions ◽  
Anti Oxidant ◽  
Differentiation Marker ◽  
Urinary Vanadium

Vanadium is a transition metal widely distributed in the Earth’s crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the vanadium derivative NaVO3 significantly increased plasma and urinary vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE−/−) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE−/− mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.

Danshensu Rescues Ischemia/Reperfusion Caused Human Hepatocyte Death

2018 ◽  
Vol 17 (2) ◽  
pp. 117-121
Author(s):  
Sun Maw-Sheng ◽  
Liang Chun-Ya ◽  
Hsieh Po-Chun ◽  
Kuo Chan-Yen
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Oxygen Species ◽  
Good Strategy ◽  
Ros Accumulation ◽  
Dichlorofluorescin Diacetate ◽  
Hepatocyte Damage ◽  
Hepatocyte Death

Apoptosis of hepatocyte, under ischemia/reperfusion (IR) conditions, has been identified as an essential process in the progression of liver transplantation. Under these conditions, mitochondria can become a threat to the cell because of their capacity to generate reactive oxygen species (ROS). Additionally, ROS overproduction may induce inflammation. As ROS accumulation appears to cause hepatocyte damage or death, there has been considerable interest in identifying the candidate natural products involved and in developing strategies to reduce oxidative stress. In this study, we use Danshensu as a candidate product to speculate whether has the protective effect on apoptotic hepatocyte upon IR. To speculate the apoptotic phenomena was reversed by Danshensu, we detected the p53, cleaved-caspase 3 expression by western blotting, as well as caspase-3 activity. Additionally, we analyzed the ROS levels by 2′,7′-dichlorofluorescin diacetate (DCF-DA) staining. We also detected the cell viability by WST-1. Results showed that Danshensu alleviated hypoxia-caused cell apoptosis via ROS overproduction. We suggested that Danshensu is a good strategy for treating hepatocyte damage upon IR.

scholarly journals Multifunctional Role of Chitosan Edible Coatings on Antioxidant Systems in Fruit Crops: A Review

2021 ◽  
Vol 22 (5) ◽  
pp. 2633
Author(s):  
Giuseppina Adiletta ◽  
Marisa Di Matteo ◽  
Milena Petriccione
Keyword(s):  
State Of The Art ◽  
Antioxidant Systems ◽  
Edible Coatings ◽  
Ros Production ◽  
Oxygen Species ◽  
Fruit Crops ◽  
Oxidative Damages ◽  
Film Forming ◽  
Anti Oxidant

Chitosan-based edible coatings represent an eco-friendly and biologically safe preservative tool to reduce qualitative decay of fresh and ready-to-eat fruits during post-harvest life due to their lack of toxicity, biodegradability, film-forming properties, and antimicrobial actions. Chitosan-based coatings modulate or control oxidative stress maintaining in different manner the appropriate balance of reactive oxygen species (ROS) in fruit cells, by the interplay of pathways and enzymes involved in ROS production and the scavenging mechanisms which essentially constitute the basic ROS cycle. This review is carried out with the aim to provide comprehensive and updated over-view of the state of the art related to the effects of chitosan-based edible coatings on anti-oxidant systems, enzymatic and non-enzymatic, evaluating the induced oxidative damages during storage in whole and ready-to-eat fruits. All these aspects are broadly reviewed in this review, with particular emphasis on the literature published during the last five years.

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