scholarly journals Evaluating the Protective Effect of a Combination of Curcumin and Selenium-L-Methionine on Radiation Induced Dual Oxidase Upregulation

2018 ◽  
Vol 24 (4) ◽  
pp. 340-345 ◽  
Author(s):  
Peyman Amini ◽  
Saeed Rezapoor ◽  
Dheyauldeen Shabeeb ◽  
Ahmed Eleojo Musa ◽  
Masoud Najafi ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Atomic Bomb ◽  
Heart Diseases ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Left Breast ◽  
Interleukin 4 ◽  
Breast Cancer Patients ◽  
Radiation Induced

Background: Epidemiological studies have shown an increased incidence of heart diseases among survivors of Chernobyl disaster as well as Hiroshima and Nagasaki atomic bomb explosion. Similar results were observed for lung and left breast cancer patients. Experimental studies have proposed the chronic upregulation of some pro-inflammatory and pro-fibrotic cytokines. Recent studies have shown that upregulation of pro-oxidant enzymes play a key role in the development of late effects of ionizing radiation such as fibrosis. Interleukin-4 (IL-4) and Interleukin-13 (IL-13) are two important cytokines that have shown ability to induce production of free radicals through dual oxidases (Duox) i.e. Duox1 and Duox2. In this study, we aimed to detect the expression of IL-4 receptor-a1 (IL-4Ra1), IL-13 receptor-a2 (IL-13Ra2), Duox1 and Duox2 genes following irradiation of rat’s heart. In addition, we evaluated the possible role of the combination of curcumin and selenium-L-methionine on the regulation of these genes. Methods: Twenty rats were divided into 4 groups as follows; G1: control; G2: treatment with the combination of curcumin and selenium-L-methionine; G3: radiation; G4: radiation plus treatment with the combination of curcumin and selenium-L-methionine. Rats were sacrificed 10 weeks after irradiation for detecting the expression of IL-4Ra1, IL-13Ra2, Duox1 and Duox2. Results: Results showed that exposure to ionizing radiation caused upregulation of IL-4Ra1 by more than 4-fold as well as Duox1 and Duox2 by more than 5-fold. However, results showed no detectable expression for IL-13Ra2. Treatment with the combination of curcumin and selenium-L-methionine could attenuate the upregulation of all genes. Conclusion: This study has shown that exposing rat’s heart tissues to radiation leads to chronic upregulation of IL-4Ra1, Duox1 and Duox2 as well as pro-oxidant enzymes. Treatment with the combination of curcumin and selenium-L-methionine showed ability to attenuate the upregulation of these genes.

Potential Role of Inflammation in Associations between Particulate Matter and Heart Failure

2018 ◽  
Vol 24 (3) ◽  
pp. 341-358 ◽  
Author(s):  
Xiaotong Ji ◽  
Yingying Zhang ◽  
Guangke Li ◽  
Nan Sang
Keyword(s):  
Heart Failure ◽  
Particulate Matter ◽  
Inflammatory Response ◽  
Heart Diseases ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Inflammatory Mechanism ◽  
High Concentrations ◽  
Future Work ◽  
The Relationship

Recently, numerous studies have found that particulate matter (PM) exposure is correlated with increased hospitalization and mortality from heart failure (HF). In addition to problems with circulation, HF patients often display high expression of cytokines in the failing heart. Thus, as a recurring heart problem, HF is thought to be a disorder characterized in part by the inflammatory response. In this review, we intend to discuss the relationship between PM exposure and HF that is based on inflammatory mechanism and to provide a comprehensive, updated evaluation of the related studies. Epidemiological studies on PM-induced heart diseases are focused on high concentrations of PM, high pollutant load exposure in winter, or susceptible groups with heart diseases, etc. Furthermore, it appears that the relationship between fine or ultrafine PM and HF is stronger than that between HF and coarse PM. However, fewer studies paid attention to PM components. As for experimental studies, it is worth noting that coarse PM may indirectly promote the inflammatory response in the heart through systematic circulation of cytokines produced primarily in the lungs, while ultrafine PM and its components can enter circulation and further induce inflammation directly in the heart. In terms of PM exposure and enhanced inflammation during the pathogenesis of HF, this article reviews the following mechanisms: hemodynamics, oxidative stress, Toll-like receptors (TLRs) and epigenetic regulation. However, many problems are still unsolved, and future work will be needed to clarify the complex biologic mechanisms and to identify the specific components of PM responsible for adverse effects on heart health.

scholarly journals Investigating New Therapeutic Strategies Targeting Hyperinsulinemia's Mitogenic Effects in a Female Mouse Breast Cancer Model

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1701-1710 ◽  
Author(s):  
Ran Rostoker ◽  
Keren Bitton-Worms ◽  
Avishay Caspi ◽  
Zila Shen-Orr ◽  
Derek LeRoith
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Experimental Studies ◽  
Tumor Development ◽  
Treated Group ◽  
Tumor Growth Rate ◽  
Breast Cancer Patients ◽  
Mitogenic Effect

Abstract Epidemiological and experimental studies have identified hyperinsulinemia as an important risk factor for breast cancer induction and for the poor prognosis in breast cancer patients with obesity and type 2 diabetes. Recently it was demonstrated that both the insulin receptor (IR) and the IGF-IR mediate hyperinsulinemia's mitogenic effect in several breast cancer models. Although IGF-IR has been intensively investigated, and anti-IGF-IR therapies are now in advanced clinical trials, the role of the IR in mediating hyperinsulinemia's mitogenic effect remains to be clarified. Here we aimed to explore the potential of IR inhibition compared to dual IR/IGF-IR blockade on breast tumor growth. To initiate breast tumors, we inoculated the mammary carcinoma Mvt-1 cell line into the inguinal mammary fat pad of the hyperinsulinemic MKR female mice, and to study the role of IR, we treated the mice bearing tumors with the recently reported high-affinity IR antagonist-S961, in addition to the well-documented IGF-IR inhibitor picropodophyllin (PPP). Although reducing IR activation, with resultant severe hyperglycemia and hyperinsulinemia, S961-treated mice had significantly larger tumors compared to the vehicle-treated group. This effect maybe secondary to the severe hyperinsulinemia mediated via the IGF-1 receptor. In contrast, PPP by partially inhibiting both IR and IGF-IR activity reduced tumor growth rate with only mild metabolic consequences. We conclude that targeting (even partially) both IR and IGF-IRs impairs hyperinsulinemia's effects in breast tumor development while simultaneously sparing the metabolic abnormalities observed when targeting IR alone with virtual complete inhibition.

scholarly journals Role of Ferulic Acid in the Amelioration of Ionizing Radiation Induced Inflammation: A Murine Model

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97599 ◽  
Author(s):  
Ujjal Das ◽  
Krishnendu Manna ◽  
Mahuya Sinha ◽  
Sanjukta Datta ◽  
Dipesh Kr Das ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Ferulic Acid ◽  
Murine Model ◽  
Radiation Induced

Flavonoids, the Family of Plant-derived Antioxidants making inroads into Novel Therapeutic Design against IR-induced Oxidative Stress in Parkinson’s Disease

2021 ◽  
Vol 19 ◽  
Author(s):  
Tapan Behl ◽  
Gagandeep Kaur ◽  
Aayush Sehgal ◽  
Gokhan Zengin ◽  
Sukhbir Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ionizing Radiation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Radiation Induced ◽  
Novel Therapeutic

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.

Exposure to environmental chemicals and type 1 diabetes: an update

2019 ◽  
Vol 73 (6) ◽  
pp. 483-488 ◽  
Author(s):  
Sarah G Howard
Keyword(s):  
Type 1 Diabetes ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Environmental Chemicals ◽  
Exposure Level ◽  
Environmental Chemical ◽  
Timing Of Exposure

This narrative review summarises recently published epidemiological and in vivo experimental studies on exposure to environmental chemicals and their potential role in the development of type 1 diabetes mellitus (T1DM). These studies focus on a variety of environmental chemical exposures, including to air pollution, arsenic, some persistent organic pollutants, pesticides, bisphenol A and phthalates. Of the 15 epidemiological studies identified, 14 include measurements of exposures during childhood, 2 include prenatal exposures and 1 includes adults over age 21. Together, they illustrate that the role of chemicals in T1DM may be complex and may depend on a variety of factors, such as exposure level, timing of exposure, nutritional status and chemical metabolism. While the evidence that these exposures may increase the risk of T1DM is still preliminary, it is critical to investigate this possibility further as a means of preventing T1DM.

scholarly journals Potential Role of the Chemokine Macrophage Inflammatory Protein 1α in Human and Experimental Schistosomiasis

2005 ◽  
Vol 73 (4) ◽  
pp. 2515-2523 ◽  
Author(s):  
Adriano L. S. Souza ◽  
Ester Roffê ◽  
Vanessa Pinho ◽  
Danielle G. Souza ◽  
Adriana F. Silva ◽  
...  
Keyword(s):  
Potential Role ◽  
Severe Disease ◽  
Experimental Studies ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Deficient Mice

ABSTRACT In human schistosomiasis, the concentrations of the chemokine macrophage inflammatory protein 1α (MIP-1α/CCL3) is greater in the plasma of patients with clinical hepatosplenic disease. The objective of the present study was to confirm the ability of CCL3 to detect severe disease in patients classified by ultrasonography (US) and to evaluate the potential role of CCL3 in Schistosoma mansoni-infected mice. CCL3 was measured by enzyme-linked immunosorbent assay in the plasma of S. mansoni-infected patients. CCL3-deficient mice were infected with 25 cercariae, and various inflammatory and infectious indices were evaluated. The concentration of CCL3 was higher in the plasma of S. mansoni-infected than noninfected patients. Moreover, CCL3 was greater in those with US-defined hepatosplenic than with the intestinal form of the disease. In CCL3-deficient mice, the size of the granuloma and the liver eosinophil peroxidase activity and collagen content were diminished compared to wild-type mice. In CCL3-deficient mice, the worm burden after 14 weeks of infection, but not after 9 weeks, was consistently smaller. The in vitro response of mesenteric lymph node cells to antigen stimulation was characterized by lower levels of interleukin-4 (IL-4) and IL-10. CCL3 is a marker of disease severity in infected humans, and experimental studies in mice suggest that CCL3 may be a causative factor in the development of severe schistosomiasis.

Radical yields in DNA exposed to ionizing radiation: Role of energy and charge transfer

1990 ◽  
Vol 68 (9) ◽  
pp. 962-966 ◽  
Author(s):  
John H. Miller ◽  
Charles E. Swenberg
Keyword(s):  
Charge Transfer ◽  
Ionizing Radiation ◽  
Mechanistic Model ◽  
Experimental Studies ◽  
High Mobility ◽  
Orientation Dependence ◽  
Model Calculations ◽  
Insight Into ◽  
High Linear Energy Transfer

Theoretical and experimental studies of free-radical yields in oriented DNA samples exposed to ionizing radiation with high linear energy transfer at 77 K are discussed. The dependence of radical yields on the orientation of DNA chains relative to the particle flux is being investigated to gain insight into the role of intramolecular energy and charge transfer processes in radical production and decay. Model calculations based on a thermal-spike approximation are presented and their limitations for predicting the orientation dependence of radical yields observed after neutron irradiation (see C. M. Arroyo et al. Int. J. Radiat. Biol. 50, 789 (1986)) are discussed. A more mechanistic model based on the high mobility of excess electrons in hydrated DNA (D. van Lith et al. J. Chem. Soc. Faraday Trans. 1, 82, 2933 (1986)) is outlined.

scholarly journals Role of pregnancy and female sex steroids on aneurysm formation, growth, and rupture: a systematic review of the literature

2019 ◽  
Vol 47 (1) ◽  
pp. E8 ◽  
Author(s):  
Milli Desai ◽  
Arvin R. Wali ◽  
Harjus S. Birk ◽  
David R. Santiago-Dieppa ◽  
Alexander A. Khalessi
Keyword(s):  
Pregnant Women ◽  
Cerebral Aneurysm ◽  
Sex Steroids ◽  
Experimental Studies ◽  
Cerebral Aneurysms ◽  
Epidemiological Studies ◽  
Female Sex ◽  
The Relationship ◽  
In Pregnancy

OBJECTIVEWomen have been shown to have a higher risk of cerebral aneurysm formation, growth, and rupture than men. The authors present a review of the recently published neurosurgical literature that studies the role of pregnancy and female sex steroids, to provide a conceptual framework with which to understand the various risk factors associated with cerebral aneurysms in women at different stages in their lives.METHODSThe PubMed database was searched for “(“intracranial” OR “cerebral”) AND “aneurysm” AND (“pregnancy” OR “estrogen” OR “progesterone”)” between January 1980 and February 2019. A total of 392 articles were initially identified, and after applying inclusion and exclusion criteria, 20 papers were selected for review and analysis. These papers were then divided into two categories: 1) epidemiological studies about the formation, growth, rupture, and management of cerebral aneurysms in pregnancy; and 2) investigations on female sex steroids and cerebral aneurysms (animal studies and epidemiological studies).RESULTSThe 20 articles presented in this study include 7 epidemiological articles on pregnancy and cerebral aneurysms, 3 articles reporting case series of cerebral aneurysms treated by endovascular therapies in pregnancy, 3 epidemiological articles reporting the relationship between female sex steroids and cerebral aneurysms through retrospective case-control studies, and 7 experimental studies using animal and/or cell models to understand the relationship between female sex steroids and cerebral aneurysms. The studies in this review report similar risk of aneurysm rupture in pregnant women compared to the general population. Most ruptured aneurysms in pregnancy occur during the 3rd trimester, and most pregnant women who present with cerebral aneurysm have caesarean section deliveries. Endovascular treatment of cerebral aneurysms in pregnancy is shown to provide a new and safe form of therapy for these cases. Epidemiological studies of postmenopausal women show that estrogen hormone therapy and later age at menopause are associated with a lower risk of cerebral aneurysm than in matched controls. Experimental studies in animal models corroborate this epidemiological finding; estrogen deficiency causes endothelial dysfunction and inflammation, which may predispose to the formation and rupture of cerebral aneurysms, while exogenous estrogen treatment in this population may lower this risk.CONCLUSIONSThe aim of this work is to equip the neurosurgical and obstetrical/gynecological readership with the tools to better understand, critique, and apply findings from research on sex differences in cerebral aneurysms.

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