nitric oxide (NO) released by tumor cells
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How is the Immune System Suppressed by Cancer - 1 views
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Excellent work by Prof de Groot of Essen, indicated by adding exogenous xanthine oxidase ( XO) in hepatoma cells, hydrogen peroxide was produced to destroy the hepatoma cells
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The other important influence of NO is in its inhibition of the proapoptoic caspases cascade. This in turn protects the cells from intracellular preprogrammed death.
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nitric oxide in immune suppression in relation to oxygen radicals is its inhibitory effect on the binding of leukocytes (PMN) at the endothelial surface
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NO from the tumor cells actually suppresses the iNOS, and in addition it reduces oxygen radicals to stop the formation of peroxynitrite in these cells. But NO is not the only inhibitor of iNOS in cancer.
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Prostaglandin E2, released from tumor cells is also an inhibitor of iNOS, as well as suppressing the immune system
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Th-1 subset of T-cells. These cells are responsible for anti-viral and anti-cancer activities, via their cytokine production including Interleukin-2, (IL-2), and Interleukin-12 which stimulates T-killer cell replication and further activation and release of tumor fighting cytokines.
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Th1 cells stimulate NK and other tumor fighting macrophages via IL-2 and IL-12; In contrast, Th2, which is stimulated in allergies and parasitic infections, produce IL-4 and IL-10. IL-4 and IL-10 inhibit TH-1 activation and the histamine released from mast cell degranulation upregulates T suppressor cells to further immune suppression.
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Th-2 subset of lymphocytes, on the other hand are activated in allergies and parasitic infections to release Interleukin-4 and Interleukin-10
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Mast cells contain histamine which when released increases the T suppressor cells, to lower the immune system and also acts directly on many tumor Histamine receptors to stimulate tumor growth
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Tumor cells release IL-10, and this is thought to be one of the important areas of Th-1 suppression in cancer patients
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IL-10 is also a central regulator of cyclooxygenase-2 expression and prostaglandin production in tumor cells stimulating their angiogenesis and NO production
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nitric oxide in tumor cells even prevents the activation of caspases responsible for apoptosis
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early stages of carcinogenesis, which we call tumor promotion, one needs a strong immune system, and fewer oxygen radicals to prevent mutations but still enough to destroy the tumor cells should they develop
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later stages of cancer development, the oxygen radicals are decreased around the tumors and in the tumor cells themselves, and the entire cancer fighting Th-1 cell replication and movement are suppressed. The results are a decrease in direct toxicity and apoptosis, which is prevented by NO, a suppression of the macrophage and leukocyte toxicity and finally, a suppression of the T-cell induced tumor toxicity
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elevated lactic acid which neutralizes the toxicity and activity of Lymphocyte immune response and mobility
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The lactic acid is also feeding fungi around tumors and that leads to elevated histamine which increases T-suppressor cells. Histamine alone stimulates many tumor cells.
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last but not least, the Lactic acid from tumor cells and acidic diets shifts the lymphocyte activity to reduce its efficacy against cancer cells and pathogens in addition to altering the bacteria of the intestinal tract.
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intestinal tract bacteria in cancer cells release sterols that suppress the immune system and down regulate anticancer activity from lymphocytes.
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In addition to the lactic acid, adenosine is also released from tumors. Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state
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Adenosine is a purine nucleoside found within the interstitial fluid of solid tumors at concentrations that are able to inhibit cell-mediated immune responses to tumor cells
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Adenosine appears to up-regulate the PD1 receptor in T-1 Lymphocytes and inhibits the immune system further
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Mast cells with their release of histamine lower the immune system and also stimulate tumor growth and activate the metalloproteinases involved in angiogenesis and metastases
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Cimetidine, an antihistamine has been actually shown to increase in apoptosis in MDSC via a separate mechanism than the antihistamine effect
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In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha)
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these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target
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Equine Estrogens Impair Nitric Oxide Production and Endothelial Nitric Oxide ... - 0 views
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This is the perfect study to compare synthetic, unnatural hormones with bioidentical hormones. Premarin was compared with bioidentical estradiol. Premarin reduced the endothelial NO synthase transcription and activity by 30-50% compared to Estradiol. Thus, premarin results in a lower NO production and thus greater endothelial dysfunction compared to Estradiol.
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Interaction of 5-methyltetrahydrofolate and tetrah... [Am J Physiol Heart Circ Physiol.... - 0 views
www.ncbi.nlm.nih.gov/...12003825
5-methyltetrahydrofolate tetrahydropbiopterin NO endothelial vascular function cardiovascular disease
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We demonstrate that 5-methyltetrahydrofolate binds the active site of nitric oxide synthase and mimics the orientation of tetrahydrobiopterin
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5-methyltetrahydrofolate attenuates superoxide production (induced by inhibition of tetrahydrobiopterin synthesis) and improves endothelial function
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e suggest that 5-methyltetrahydrofolate directly interacts with nitric oxide synthase to promote nitric oxide (vs. superoxide) production and improve endothelial function
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5-Methyltetrahydrofolate may represent an important strategy for intervention aimed at improving tetrahydrobiopterin bioavailability.
Nitric Oxide and Cancer Therapy: The Emperor has NO Clothes - 0 views
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Toxicity of the spike protein of COVID-19 is a redox shift phenomenon: A novel therapeu... - 0 views
www.sciencedirect.com/...S0891584923005014
COVID19 COVID-19 cancer inflammation SARS-CoV-2 spike proteins COVID spikeopathy
shared by Nathan Goodyear on 01 Sep 23
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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cell division is the most sophisticated way to release entropy
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redox signaling plays an important role in regulating immune function and inflammation, and disruptions in this signaling can lead to excessive cytokine production and immune system activation
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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People at high risk are the elderly, patients suffering from metabolic syndrome such as obesity, or those suffering from chronic diseases such as cancer or inflammation
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COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
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oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
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inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
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persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
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IL-2 is highly up-regulated in Covid-19 patients [37], and IL-2 is known to significantly stimulate the generation of NO in patients
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Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
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vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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viral reactivation in varicella-zoster virus [55] or hepatitis [56], coagulopathy and resulting stroke and myocarditis following both DNA-based vaccines [57] and RNA-based vaccines
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characteristic of the Warburg effect is present in almost every disease and appears to be a central feature in most of the hallmarks of cancer
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inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
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As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
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Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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Cancer, inflammation, Alzheimer's, and Parkinson's diseases share a common peculiarity, the inability of the cell to export entropy outside the body in the harmless form of heat
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
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MeB + can take a pair of electrons (of H atoms) and MeBH can release this pair easily, so that MeB is partially recycled like a catalyst
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MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
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As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
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ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
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Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
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Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism
Targeting Nitric Oxide: Say NO to Metastasis | Clinical Cancer Research | American Asso... - 0 views
aacrjournals.org/...rgeting-Nitric-Oxide-Say-NO-to
iNOS TME cancer NO tumor microenvironment nitric oxide
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American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views
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Although currently no drugs that specifically target mitochondrial biogenesis in HF are available, acceleration of this process through adenosine monophosphate–activated kinase (AMPK), endothelial nitric oxide synthase (eNOS), and other pathways may represent a promising therapeutic approach
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Mitochondrial biogenesis can be enhanced therapeutically with the use of adenosine monophosphate kinase (AMPK) agonists, stimulants of nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway (including phosphodiesteraes type 5 inhibitors), or resveratrol
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Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis
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BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy
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folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity
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Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function
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Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis
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epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men
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post-menopausal women
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The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III
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Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.
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cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly
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Testosterone: a vascular hormone in health and disease - 0 views
joe.endocrinology-journals.org/...R47.full
testosterone hormone health disease hormones men male cardiovascular disease CVD
shared by Nathan Goodyear on 13 May 13
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Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
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In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
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testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
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Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
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there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
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bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
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Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
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It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
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no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
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free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
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Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
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Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
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Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
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In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
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the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
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Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
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acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
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Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
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non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
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increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
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Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
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Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
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TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
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testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
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Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
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Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
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decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
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The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
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Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
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As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
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prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
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DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
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(Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
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TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
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3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
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This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
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The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
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There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
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The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
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trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
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Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
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The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
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the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
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Astaxanthin Inhibits Nitric Oxide Production and Inflammatory Gene Expression... - 0 views
www.cyanotech.com/...batl03.pdf
astaxanthin inflammation NF-KappaB NO nitric oxide antioxidant antioxidants
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Beyond the male sex hormone: deciphering the metabolic and vascular actions of testoste... - 0 views
joe.endocrinology-journals.org/...C1.full
AR androgen receptors androgen receptor testosterone androgen receptors Diabetes metabolic syndrome MetS CVD cardiovascular disease men hormone hormones male
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androgen deprivation therapy results in unfavorable changes in body composition, insulin resistance, and dyslipidemia and predisposes men to develop atherosclerosis and an increased risk of cardiovascular mortality
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The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs testosterone levels by increasing the aromatization of testosterone to estradiol, while low testosterone levels promote increased fat deposition
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adipocytokines contribute to low testosterone levels as well as to the processes underlying metabolic syndromes and type 2 diabetes
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The presence of estradiol and the adipocytokines TNF-α, IL6, and leptin (as a result of leptin resistance in obesity) inhibits the hypothalamic–pituitary–testicular axis response to decreasing androgen levels
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An increasing number of studies have illustrated the potential for applying metabolomics to the field of androgen research
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As early as the 1940s, the therapeutic use of testosterone was reported to improve angina pectoris in men with coronary artery disease
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most of the epidemiological studies reported increased cardiovascular risk and mortality in men with low testosterone levels
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long-term testosterone replacement appears to be a safe and effective means of treating hypogonadal elderly men
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a recent interventional trial showed that testosterone treatment was associated with decreased mortality when compared with no testosterone treatment in an observational cohort of men with low testosterone levels
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a number of short-term studies conducted support the notion that testosterone therapy reduces the cardiovascular risk
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The majority of animal studies support the hypothesis that the actions of testosterone on vascular relaxation are both endothelium-dependent and -independent vasodilatory effects
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Endothelial-dependent actions of testosterone increase the expression or activity of endothelial nitric oxide synthase and enhance nitric oxide production, which in turn activates cyclic guanosine monophosphate to induce vasorelaxation in smooth muscle cells
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Endothelial-independent mechanisms of testosterone are believed to occur primarily via inhibition of voltage-operated Ca2+ channels and/or activation of K+ channels in smooth muscle cells
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Testosterone may also inhibit intracellular Ca2+ influx via store-operated Ca2+ channels by blocking the response to prostaglandin F2α
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testosterone has demonstrated anti-inflammatory effects to protect against atherogenesis in animal studies
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both genomic AR activation to modulate gene transcription and non-genomic activation to modulate the rapid intracellular signaling pathways of ion channels may mediate testosterone effects on vascular function and inflammation.
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Butenandt & Ruzicka first showed how testosterone is synthesized and responsible for masculine characteristics in the early 1930s
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Does vitamin C enhance nitric oxide bioavailability in a tetrahydrobiopterin-dependent ... - 0 views
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Ascorbic Acid Enhances Endothelial Nitric-oxide Synthase Activity by Increasing Intrace... - 0 views
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Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activit... - 0 views
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Effects of Cocaine on Nitric Oxide Production in Bovine Coronary Artery Endothelial Cells - 0 views
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Diverse Influences of Androgen-Disrupting Chemi... [Inflammation. 2013] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...24287822
Bisphenol-A bisphenol A BPA EDC endocrine disrupting chemicals NO inflammation
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International Journal of Impotence Research - Mechanisms of action of PDE5 inhibition i... - 0 views
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Nitric oxide (NO) is produced from oxygen and L-arginine under the control of Nitric oxide synthase (NOS)
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Effects of testosterone on neuronal nitric oxide synthase and tyrosine hydroxylase. - P... - 0 views
www.ncbi.nlm.nih.gov/...10415408
Testosterone low T low Testosterone NO nitric oxide NOS ED male hormones
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Nitric oxide mediated erectile activity is a testosterone dependent event: a rat erecti... - 0 views
www.ncbi.nlm.nih.gov/...8770664
low T low Testosterone NO NOS nitric oxide Testosterone ED men male hormones
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Purple Carrot Anthocyanins Decrease LPS Stimulated Nitric Oxide Production - 0 views
www.fasebj.org/...A731.4.short
anthocyanin NO iNOS LPS lipopolysaccharides nitric oxide inflammation
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