The effects of endometritis on the establishment of pregnancy in cattle

2012 ◽  
Vol 24 (1) ◽  
pp. 252 ◽  
Author(s):  
Robert O. Gilbert
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Post Partum ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Breeding Period ◽  
Increased Risk ◽  
Factor Α ◽  
And Function

Endometritis is common in post partum dairy cows and is associated with impaired reproductive performance reflected in reduced first service conception, reduced hazard of pregnancy over the breeding period and increased risk of reproductive culling. The observed effects may be mediated directly by bacterial products, such as lipopolysaccharide (LPS, endotoxin), or indirectly by inflammatory mediators, such as cytokines, eicosanoids, nitric oxide and oxidative stress affecting sperm, ovarian, uterine and embryonic function. An inflammatory milieu in the uterus has been associated with changes in sperm motility and function as well as increased sperm phagocytosis. Zygotes resulting from fertilisation of oocytes with sperm subjected to oxidative stress are less likely to develop to the blastocyst stage. In addition, LPS and tumour necrosis factor-α (TNFα) impair follicular steroidogenesis, growth and ovulation. Oocytes exposed to LPS or prostaglandin (PG) F2α during maturation are less likely to develop to blastocyst stage after fertilisation. Embryos exposed to inflammatory mediators during development have fewer trophoectoderm cells. Nitric oxide impairs development of preimplantation embryos and TNFα increases blastomere apoptosis. Endometritis in women has been associated with higher rates of implantation failure. Extragenital inflammation (e.g. mastitis) is also associated with an increased rate of embryonic loss in cattle. These observations make it clear that direct and indirect effects of endometritis, and inflammation in general, can interrupt successful reproduction at several crucial stages.

scholarly journals Nitric oxide synthase 3 deficiency limits adverse ventricular remodeling after pressure overload in insulin resistance

2011 ◽  
Vol 301 (5) ◽  
pp. H2093-H2101 ◽  
Author(s):  
Baptiste Kurtz ◽  
Helene B. Thibault ◽  
Michael J. Raher ◽  
John R. Popovich ◽  
Sharon Cawley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Insulin Resistance ◽  
Mitochondrial Respiration ◽  
Pressure Overload ◽  
Lv Remodeling ◽  
Stress Levels ◽  
Nitric Oxide Synthase 3 ◽  
And Function ◽  
Oxide Synthase

Insulin resistance (IR) and systemic hypertension are independently associated with heart failure. We reported previously that nitric oxide synthase 3 (NOS3) has a beneficial effect on left ventricular (LV) remodeling and function after pressure-overload in mice. The aim of our study was to investigate the interaction of IR and NOS3 in pressure-overload-induced LV remodeling and dysfunction. Wild-type (WT) and NOS3-deficient (NOS3−/−) mice were fed either a standard diet (SD) or a high-fat diet (HFD) to induce IR. After 9 days of diet, mice underwent transverse aortic constriction (TAC). LV structure and function were assessed serially using echocardiography. Cardiomyocytes were isolated, and levels of oxidative stress were evaluated using 2′,7′-dichlorodihydrofluorescein diacetate. Cardiac mitochondria were isolated, and mitochondrial respiration and ATP production were measured. TAC induced LV remodeling and dysfunction in all mice. The TAC-induced decrease in LV function was greater in SD-fed NOS3−/− mice than in SD-fed WT mice. In contrast, HFD-fed NOS3−/− developed less LV remodeling and dysfunction and had better survival than did HFD-fed WT mice. Seven days after TAC, oxidative stress levels were lower in cardiomyocytes from HFD-fed NOS3−/− than in those from HFD-fed WT. Nω-nitro-l-arginine methyl ester and mitochondrial inhibitors (rotenone and 2-thenoyltrifluoroacetone) decreased oxidative stress levels in cardiomyocytes from HFD-fed WT mice. Mitochondrial respiration was altered in NOS3−/− mice but did not worsen after HFD and TAC. In contrast with its protective role in SD, NOS3 increases LV adverse remodeling after pressure overload in HFD-fed, insulin resistant mice. Interactions between NOS3 and mitochondria may be responsible for increased oxidative stress levels in HFD-fed WT mice hearts.

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

scholarly journals Metabolic Syndrome Is Associated with Oxidative Stress and Proinflammatory State

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 236 ◽  
Author(s):  
Margalida Monserrat-Mesquida ◽  
Magdalena Quetglas-Llabrés ◽  
Xavier Capó ◽  
Cristina Bouzas ◽  
David Mateos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Vascular Function ◽  
Mononuclear Cells ◽  
Antioxidant Defenses ◽  
Peripheral Blood Mononuclear ◽  
Protein Levels ◽  
Inflammatory Parameters ◽  
Increased Risk ◽  
Factor Α

Metabolic syndrome (MetS) is associated with increased risk of developing diabetes and cardiovascular diseases. MetS is also characterized by an increase of oxidative stress which contributes to impaired inflammation, vascular function, and atherosclerosis. The aim was to assess the oxidative stress and inflammatory markers in plasma and PBMCs in adults with or without MetS. Antioxidant and inflammatory parameters were measured in peripheral blood mononuclear cells (PBMCs) of 80 men and 80 women over 55 to 80-years-old residing in the Balearic Islands without previously documented cardiovascular disease. Circulating leukocytes, neutrophils, lymphocytes, basophils, and monocytes were higher in MetS subjects with respect to those without MetS. Plasma levels of malondialdehyde, tumor necrosis factor α (TNFα), and interleukin 6 (IL-6) levels were higher in MetS subjects in both genders, but the superoxide dismutase activity was lower. The myeloperoxidase plasma activity was higher in the MetS male subjects. Higher activities and protein levels of catalase and glutathione reductase in PBMCs were observed in MetS subjects in both genders. Obtained data show that MetS is associated with oxidative stress and a proinflammatory state and with high antioxidant defenses in PBMCs probably derived from a pre-activation state of immune cells.

Catechins attenuate eccentric exercise-induced inflammation and loss of force production in muscle in senescence-accelerated mice

2011 ◽  
Vol 111 (6) ◽  
pp. 1654-1663 ◽  
Author(s):  
Satoshi Haramizu ◽  
Noriyasu Ota ◽  
Tadashi Hase ◽  
Takatoshi Murase
Keyword(s):  
Oxidative Stress ◽  
Eccentric Exercise ◽  
Inflammatory Mediators ◽  
Reductase Activity ◽  
Force Production ◽  
Monocyte Chemoattractant Protein 1 ◽  
Downhill Running ◽  
Exercise Induced ◽  
Factor Α

Catechins have a great variety of biological actions. We evaluated the potential benefits of catechin ingestion on muscle contractile properties, oxidative stress, and inflammation following downhill running, which is a typical eccentric exercise, in senescence-accelerated prone mice (SAMP). Downhill running (13 m/min for 60 min; 16° decline) induced a greater decrease in the contractile force of soleus muscle and in Ca2+-ATPase activity in SAMP1 compared with the senescence-resistant mice (SAMR1). Moreover, compared with SAMR1, SAMP1 showed greater downhill running-induced increases in plasma CPK and LDH activity, malondialdehyde, and carbonylated protein as markers of oxidative stress; and in protein and mRNA expression levels of the inflammatory mediators such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in muscle. SAMP1 exhibited aging-associated vulnerability to oxidative stress and inflammation in muscle induced by downhill running. Long-term (8 wk) catechin ingestion significantly attenuated the downhill running-induced decrease in muscle force and the increased inflammatory mediators in both plasma and gastrocnemius muscle. Furthermore, catechins significantly inhibited the increase in oxidative stress markers immediately after downhill running, accompanied by an increase in glutathione reductase activity. These findings suggest that long-term catechin ingestion attenuates the aging-associated loss of force production, oxidative stress, and inflammation in muscle after exercise.

scholarly journals Role of oxidative stress in multiparity-induced endothelial dysfunction

2008 ◽  
Vol 295 (4) ◽  
pp. H1736-H1742 ◽  
Author(s):  
Huda E. Tawfik ◽  
Jonathan Cena ◽  
Richard Schulz ◽  
Susan Kaufman
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Coronary Arteries ◽  
Vascular Tissue ◽  
Fold Increase ◽  
Oxidase Inhibitor ◽  
Maximal Response ◽  
Protein Levels ◽  
Increased Risk

Multiparity is associated with increased risk of cardiovascular disease. We tested whether multiparity induces oxidative stress in rat vascular tissue. Coronary arteries and thoracic aorta were isolated from multiparous and age-matched virgin rats. Relaxation to ACh and sodium nitroprusside (SNP) was measured by wire myography. We also tested the effect of the superoxide dismutase mimetic MnTE2PyP (30 μM), the NADPH oxidase inhibitor apocynin (10 μM), and the peroxynitrite scavenger FeTPPs (10 μM) on ACh-mediated relaxation in coronary arteries. Vascular superoxide anion was measured using the luminol derivative L-012 and nitric oxide (NO) generation by the Griess reaction. Multiparity reduced maximal response and sensitivity to ACh in coronary arteries [maximal relaxation (Emax): multiparous 49 ± 3% vs. virgins 95% ± 3%; EC50: multiparous 135 ± 1 nM vs. virgins 60 ± 1 nM], and in aortic rings (Emax: multiparous 38 ± 3% vs. virgins 79 ± 4%; EC50: multiparous 160 ± 2 nM vs. virgins 90 ± 3 nM). Coronary arteries from the two groups relaxed similarly to SNP. Superoxide anions formation was significantly higher in both coronary arteries (2.8-fold increase) and aorta (4.1-fold increase) from multiparous rats compared with virgins. In multiparous rats, incubation with MnTE2PyP, apocynin, and FeTPPs improved maximal relaxation to ACh (MnTE2PyP: 74 ± 5%; vehicle: 41 ± 5%; apocynin: 73 ± 3% vs. vehicle: 41 ± 3%; FeTPPs: 72 ± 3% vs. vehicle: 46 ± 3%) and increased sensitivity (EC50: MnTE2PyP: 61 ± 0.5 nM vs. vehicle: 91 ± 1 nM; apocynin: 45 ± 3 nM vs. vehicle: 91 ± 6 nM; FeTPP: 131 ± 2 nM vs. vehicle: 185 ± 1 nM). Multiparity also reduced total nitrate/nitrite levels (multiparous: 2.5 ± 2 μmol/mg protein vs. virgins: 7 ± 1 μmol/mg protein) and endothelial nitric oxide synthase protein levels (multiparous: 0.53 ± 0.1 protein/actin vs. virgins: 1.0 ± 0.14 protein/actin). These data suggest that multiparity induces endothelial dysfunction through decreased NO bioavailability and increased reactive oxygen species formation.

scholarly journals Vascular Ageing and Exercise: Focus on Cellular Reparative Processes

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Mark D. Ross ◽  
Eva Malone ◽  
Geraint Florida-James
Keyword(s):  
Oxidative Stress ◽  
Prolonged Exposure ◽  
The Body ◽  
Noncommunicable Diseases ◽  
Regular Exercise ◽  
Vascular Ageing ◽  
Increased Risk ◽  
And Function ◽  
Endothelial Homeostasis ◽  
Endothelial Precursors

Ageing is associated with an increased risk of developing noncommunicable diseases (NCDs), such as diabetes and cardiovascular disease (CVD). The increased risk can be attributable to increased prolonged exposure to oxidative stress. Often, CVD is preceded by endothelial dysfunction, which carries with it a proatherothrombotic phenotype. Endothelial senescence and reduced production and release of nitric oxide (NO) are associated with “vascular ageing” and are often accompanied by a reduced ability for the body to repair vascular damage, termed “reendothelialization.” Exercise has been repeatedly shown to confer protection against CVD and diabetes risk and incidence. Regular exercise promotes endothelial function and can prevent endothelial senescence, often through a reduction in oxidative stress. Recently, endothelial precursors, endothelial progenitor cells (EPC), have been shown to repair damaged endothelium, and reduced circulating number and/or function of these cells is associated with ageing. Exercise can modulate both number and function of these cells to promote endothelial homeostasis. In this review we look at the effects of advancing age on the endothelium and these endothelial precursors and how exercise appears to offset this “vascular ageing” process.

scholarly journals Oxidative Stress and Neuronal Injury After Cannabis and Ketamine Administration

2021 ◽  
Vol 18 ◽  
pp. 126-135
Author(s):  
Omar M. E. Abdel-Salam ◽  
Eman R. Youness ◽  
Amany Ameen Sleem ◽  
Enayat A. Omara
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Mediators ◽  
Cannabis Sativa ◽  
Paraoxonase 1 ◽  
Saline Control ◽  
Control Group ◽  
Neuronal Necrosis ◽  
Tnf Α ◽  
Markers Of Oxidative Stress ◽  
Factor Α

Cannabis sativa and ketamine are common substances of abuse causing psychotic events and neurodegeneration. In this study, the effect of pretreatment with Cannabis sativa extract on oxidative stress, inflammatory mediators and brain damage induced by ketamine was investigated. Rats were treated with subcutaneous injections of cannabis extract (10, 20, 30 or 40 mg/kg; expressed as Δ9-THC content) daily for three weeks and then in combination with ketamine (15 mg/kg, intraperitoneally) for another 5 days. Rats were tested for biochemical markers of oxidative stress including malondialdehyde (MDA) reduced glutathione (GSH), and nitric oxide (NO) concentrations in brain. Paraoxonase-1 (PON-1) activity, and levels of the proinflammatory cytokines, interleukin-1β (IL-1β), and tumour necrosis factor-α (TNF-α) in brain were also determined at the end of treatment period. Results indicated that compared with the saline control group, ketamine induced significant elevation in brain MDA and NO, which was accompanied by depletion of GSH and inhibition of PON-1 activity. Ketamine also significantly increased brain IL-1β and TNF-α and induced neuronal necrosis, apoptosis and vacuolation. Cannabis sativa (20-40 mg/kg) pretreated rats showed lower levels of oxidative stress and inflammation and doses of 30 or 40 mg/kg slightly reduced neuronal apoptosis and necrosis. These findings suggest that cannabis constituents do not enhance the neurotoxic effects of ketamine and might partly counteract the effects of ketamine-induced NMDA antagonism by reducing the release of free radicals and inflammatory mediators in brain

scholarly journals Intracellular Antioxidant Activity and Inhibition of Bee Pollens on the Production of Inflammatory Mediators (P06-081-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Je-Hyuk Lee
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Antioxidant Activity ◽  
Inflammatory Mediators ◽  
Pollen Extract ◽  
Bee Pollen ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Ethanol Extracts ◽  
Intracellular Oxidative Stress

Abstract Objectives The purpose of this study is to present scientific evidences for health promotion of bee pollens through the investigation of the antioxidant and the anti-inflammatory effect. Methods The intracellular antioxidant activity of bee pollen ethanol extracts was investigated by DCFH-DA assay for the oxidative stress induced by lipopolysaccharide (LPS) in mitochondria of macrophages. Inhibition of nitric oxide (NO) and prostaglandin E2 (PGE2) production were confirmed by the addition of bee pollen extracts. Inhibition of transcription/expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and the inflammatory mediators-production were investigated by adding the bee pollen extracts. Results Intracellular oxidative stress by LPS was inhibited at approximately 53% by 0.25 and 3 mg/ml of the Darae-bee pollen extract. It was found that the Acorn- and Mixed bee pollen extract (3 mg/ml) reduced the intracellular oxidative stress at approximately 26.3 and 41.3%, respectively. For anti-inflammatory activity, all three bee pollen extracts (3 g/ml) inhibited effectively the production of NO to an equal to or rather lower than basal level in macrophages. Bee pollen extracts decreased the LPS-induced PGE2 production depending on the amount added, regardless of the kind of bee pollen added. Gene transcription and expression of iNOS and COX-2, an enzyme producing NO and PGE2, respectively, was suppressed by bee pollen extracts and confirmed by RT-PCR and western blot. Additionally, the production of IL-1b, IL-6 and TNF-α, which are inflammatory mediators in macrophages, were inhibited by Darae-, Acorn- and Mixed bee pollen extract. Conclusions The ethanol extracts of Darae-, Acorn- and Mixed bee pollen were verified to have the intracellular antioxidant activity and the inhibitory activity on the production of several anti-inflammatory mediators in macrophage cells. Funding Sources N/A.

Surfactant protein A enhances mycobacterial killing by rat macrophages through a nitric oxide-dependent pathway

2000 ◽  
Vol 279 (2) ◽  
pp. L216-L223 ◽  
Author(s):  
Laura F. Weikert ◽  
Joseph P. Lopez ◽  
Rasul Abdolrasulnia ◽  
Zissis C. Chroneos ◽  
Virginia L. Shepherd
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Protein A ◽  
Surfactant Protein ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Tnf Α ◽  
Presence And Absence ◽  
Factor Α ◽  
Oxide Synthase

Surfactant-associated protein A (SP-A) is involved in surfactant homeostasis and host defense in the lung. We have previously demonstrated that SP-A specifically binds to and enhances the ingestion of bacillus Calmette-Guerin (BCG) organisms by macrophages. In the current study, we investigated the effect of SP-A on the generation of inflammatory mediators induced by BCG and the subsequent fate of ingested BCG organisms. Rat macrophages were incubated with BCG in the presence and absence of SP-A. Noningested BCG organisms were removed, and the release of tumor necrosis factor-α (TNF-α) and nitric oxide were measured at varying times. TNF-α and nitric oxide production induced by BCG were enhanced by SP-A. In addition, SP-A enhanced the BCG-induced increase in the level of inducible nitric oxide synthase protein. Addition of antibodies directed against SPR210, a specific macrophage SP-A receptor, inhibited the SP-A-enhanced mediator production. BCG in the absence of SP-A showed increased growth over a 5-day period, whereas inclusion of SP-A dramatically inhibited BCG growth. Inhibition of nitric oxide production blocked BCG killing in the presence and absence of SP-A. These results demonstrate that ingestion of SP-A-BCG complexes by rat macrophages leads to production of inflammatory mediators and increased mycobacterial killing.

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