Oxidative stress mediated platelet activation in patients with congenital analbuminemia: effect of albumin infusion

2021 ◽  
Author(s):  
Francesco Baratta ◽  
Simona Bartimoccia ◽  
Roberto Carnevale ◽  
Lucia Stefanini ◽  
Francesco Angelico ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Activation ◽  
Albumin Infusion

scholarly journals Effects of heat-not-burn compared to combustible cigarettes on coronary flow, myocardial work index and vascular function

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
I Ikonomidis ◽  
K Katogiannis ◽  
D Vlastos ◽  
G Kostelli ◽  
K Kourea ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Activation ◽  
Vascular Function ◽  
Coronary Flow ◽  
Arterial Compliance ◽  
Chronic Phase ◽  
Protein Carbonyls ◽  
Flow Reserve ◽  
Work Index ◽  
Chronic Study

Abstract Funding Acknowledgements Type of funding sources: None. Aim/Introduction: Heat-not-burn cigarette (HNBC) constitutes a non-combustible smoke product. Purpose We compare the effects of heat-not-burn and conventional cigarettes on coronary flow, myocardial and vascular function, platelet activation and oxidative stress. Methods We compared the effects of HNBC to those of tobacco cigarette (TCig), on arterial stiffness, oxidative stress, and platelet activation, acutely and after 1 month of switching to HNBC, as well as on endothelial, myocardial, and coronary function after 1 month of switching to HNBC. In the acute study, 50 smokers were randomized into smoking a single Tcig or an HNBC and after 60 minutes were crossed over to the alternate smoking (HNBC or Tcig). For the chronic phase, 75 smokers were examined. Of those, 50 were switched to HNBC and 25 continued Tcig for 1 month. Pulse wave velocity (PWV) and biomarkers [malondialdehyde (MDA), protein carbonyls (PC), and thromboxane B2 (TXB2)] were assessed in the acute and chronic study. Myocardial deformation [global longitundinal strain (GLS), myocardial work index (GWI) and wasted myocardial work (GWW)], coronary flow reserve (CFR) by Doppler echocardiography, total arterial compliance (TAC), and flow-mediated dilation (FMD) were additionally assessed in the chronic study. Results Compared to baseline, TCig smoking acutely increased exhaled CO, PWV, MDA, and TxB2 (p < 0.05), while no changes were observed after HNBC. Compared to resuming Tcig smoking, switching to HNBC for 1 month improved CO (mean change: -55% vs -2.4%), FMD ( +55% vs +15%), CFR (+46% vs +4%), TAC (+9% vs -0.5%), GLS (+6% vs +1%), GWW (-19% vs +0.5%), MDA (-19% vs 1 %), and TxB2 (-12% vs 4%) (p < 0.05 for all comparisons). Conclusions HNBCs exert a less detrimental effect on vascular, cardiac and platelet function than combustible tobacco.

Effects of high-amount–high-intensity exercise on in vivo platelet activation: Modulation by lipid peroxidation and AGE/RAGE axis

2013 ◽  
Vol 110 (12) ◽  
pp. 1232-1240 ◽  
Author(s):  
Francesca Santilli ◽  
Natale Vazzana ◽  
Pierpaolo Iodice ◽  
Stefano Lattanzio ◽  
Rossella Liani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Exercise Training ◽  
Platelet Activation ◽  
High Intensity ◽  
Plasma Levels ◽  
High Intensity Exercise ◽  
Similar Amount ◽  
Activation Markers

SummaryPhysical activity is associated with cardiovascular risk reduction, but the effects of exercise on platelet activation remain controversial. We investigated the effects of regular high-amount, high intensity aerobic exercise on in vivo thromboxane (TX)-dependent platelet activation and plasma levels of platelet-derived proteins, CD40L and P-selectin, and whether platelet variables changes may be related to changes in high-density lipoprotein (HDL) and in the extent of oxidative stress and oxidative stress-related inflammation, as reflected by urinary isoprostane excretion and endogenous soluble receptor for advanced glycation end-products (esRAGE), respectively. Urinary excretion of 11-dehydro-TXB2 and 8-iso-prostaglandin (PG)F2α and plasma levels of P-selectin, CD40L and esRAGE were measured before and after a eight-week standardised aerobic high-amount–high-intensity training program in 22 sedentary subjects with low-to-intermediate risk. Exercise training had a clear beneficial effect on HDL cholesterol (+10%, p=0.027) and triglyceride (-27%, p=0.008) concentration. In addition, a significant (p<0.0001) decrease in urinary 11-dehydro-TXB2 (26%), 8-iso-PGF2α (21 %), plasma P-selectin (27%), CD40L (35%) and a 61% increase in esRAGE were observed. Multiple regression analysis revealed that urinary 8-iso-PGF2α [beta=0.33, SEM=0.116, p=0.027] and esRAGE (beta=-0.30, SEM=31.3, p=0.046) were the only significant predictors of urinary 11-dehydro-TXB2 excretion rate over the training period. In conclusion, regular high-amount–high-intensity exercise training has broad beneficial effects on platelet activation markers, paralleled and possibly associated with changes in the lipoprotein profile and in markers of lipid peroxidation and AGE/RAGE axis. Our findings may help explaining why a similar amount of exercise exerts significant benefits in preventing cardiovascular events.

scholarly journals Interplay between Nox2 Activity and Platelet Activation in Patients with Sepsis and Septic Shock: A Prospective Study

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Giusy Tiseo ◽  
Elena Cavarretta ◽  
Arianna Forniti ◽  
Cristina Nocella ◽  
Sebastiano Sciarretta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Septic Shock ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Healthy Controls ◽  
Sample Collection ◽  
Oxidative Stress Status ◽  
Sepsis And Septic Shock ◽  
A Prospective Study

Background. Although preclinical studies highlighted the potential role of NADPH oxidase (NOX) in sepsis, only few studies evaluated the oxidative stress in patients with sepsis and septic shock. The objective of the study is to appraise the oxidative stress status and platelet function in patients with sepsis and septic shock compared to healthy controls. Methods and Results. Patients with sepsis or septic shock admitted to the hospital Policlinico Umberto I (Sapienza University, Rome) underwent a blood sample collection within 1 hour from admission. Platelet aggregation, serum thromboxane B2 (TxB2), soluble NOX2-derived peptides (sNox2-dp), and hydrogen peroxide breakdown activity (HBA) were measured and compared to those of healthy volunteers. Overall, 33 patients were enrolled; of these, 20 (60.6%) had sepsis and 13 (39.4%) septic shock. Compared to healthy controls ( n = 10 , age 67.8 ± 3.2 , male 50%), patients with sepsis and septic shock had higher platelet aggregation (49% (IQR 45-55), 60% (55.75-67.25), and 73% (IQR 69-80), respectively, p < 0.001 ), higher serum TxB2 (77.5 (56.5-86.25), 122.5 (114-131.5), and 210 (195-230) pmol/L, respectively, p < 0.001 ), higher sNox2-dp (10 (7.75-12), 19.5 (17.25-21), and 33 (29.5-39) pg/mL, respectively, p < 0.001 ), and lower HBA (75% (67.25-81.5), 50% (45-54.75), and 27% (21.5-32.5), respectively, p < 0.001 ). Although not statistically significant, a trend in higher levels of serum TxB2 and sNox2-dp in patients who died was observed. Conclusions. Patients with septic shock exhibit higher Nox2 activity and platelet activation than patients with sepsis. These insights joined to better knowledge of these mechanisms could guide the identification of future prognostic biomarkers and new therapeutic strategies in the scenario of septic shock.

scholarly journals Curcuma oil ameliorates hyperlipidaemia and associated deleterious effects in golden Syrian hamsters

2013 ◽  
Vol 110 (3) ◽  
pp. 437-446 ◽  
Author(s):  
Vishal Singh ◽  
Manish Jain ◽  
Ankita Misra ◽  
Vivek Khanna ◽  
Minakshi Rana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Activation ◽  
Vascular Dysfunction ◽  
Curcuma Longa ◽  
Hdl Cholesterol ◽  
Transcript Level ◽  
Chow Diet ◽  
Standard Drug ◽  
Syrian Hamsters ◽  
Hepatic Expression

Essential oil components from turmeric (Curcuma longa L.) are documented for neuroprotective, anti-cancer, anti-thrombotic and antioxidant effects. The present study aimed to investigate the disease-modifying potential of curcuma oil (C. oil), a lipophilic component from C. longa L., in hyperlipidaemic hamsters. Male golden Syrian hamsters were fed a chow or high-cholesterol (HC) and fat-rich diet with or without C. oil (30, 100 and 300 mg/kg) for 28 d. In HC diet-fed hamsters, C. oil significantly reduced plasma total cholesterol, LDL-cholesterol and TAG, and increased HDL-cholesterol when compared with the HC group. Similar group comparisons showed that C. oil treatment reduced hepatic cholesterol and oxidative stress, and improved liver function. Hyperlipidaemia-induced platelet activation, vascular dysfunction and repressed eNOS mRNA expression were restored by the C. oil treatment. Furthermore, aortic cholesterol accumulation and CD68 expression were also reduced in the C. oil-treated group. The effect of C. oil at 300 mg/kg was comparable with the standard drug ezetimibe. Delving into the probable anti-hyperlipidaemic mechanism at the transcript level, the C. oil-treated groups fed the chow and HC diets were compared with the chow diet-fed group. The C. oil treatment significantly increased the hepatic expression of PPARα, LXRα, CYP7A1, ABCA1, ABCG5, ABCG8 and LPL accompanied by reduced SREBP-2 and HMGCR expression. C. oil also enhanced ABCA1, ABCG5 and ABCG8 expression and suppressed NPC1L1 expression in the jejunum. In the present study, C. oil demonstrated an anti-hyperlipidaemic effect and reduced lipid-induced oxidative stress, platelet activation and vascular dysfunction. The anti-hyperlipidaemic effect exhibited by C. oil seems to be mediated by the modulation of PPARα, LXRα and associated genes involved in lipid metabolism and transport.

Oxidative Status of Platelets in Normal and Thalassemic Blood.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3765-3765
Author(s):  
Johnny Amer ◽  
Eitan Fibach
Keyword(s):  
Oxidative Stress ◽  
Platelet Activation ◽  
Specific Antigen ◽  
Calcium Ionophore ◽  
Iron Chelator ◽  
Oxidative Status ◽  
Beta Thalassemia ◽  
Ros Generation ◽  
Continuous Exposure ◽  
Light Scatter

Abstract Thromboembolic complications, possibly involving chronic platelet activation, are an important cause of morbidity and mortality in beta-thalassemia. Oxidative stress, with the generation of reactive oxygen species (ROS), has been suspected to play a role in the pathophysiology of thalassemia and cardiovascular disorders. Previous investigations demonstrated that ROS profoundly affect platelet function and promote platelet activation. Other studies have shown that platelets themselves produce ROS upon activation. In the present study, we adapted flow cytometric techniques to measure oxidative-state markers, ROS generation and reduced glutathione (GSH), using 2′-7′-dichlorofluorescin diacetate and mercury orange, respectively, in platelets. GSH is the major intracellular antioxidant - an important scavenger of ROS. To exclude non-platelets from analysis, a two-parameter (side light scatter and forward light scatter) gate was set. The identity of the gated cells was verified by immunofluorescence staining for CD41 - a platelet-specific antigen. Using these techniques, the average Mean Fluorescence Channel (MFC) values of platelets from 46 normal donors and 22 beta-thalassemic donors were 176 ± 99 vs. 314 ± 81, respectively, for ROS and 319 ± 87 vs. 113 ± 47, respectively, for GSH. These results show that thalassemic platelets contain higher ROS and lower GSH levels than do normal platelets, indicating a state of oxidative stress. The relationship between platelet activation and oxidative status was determined by treating platelets with thrombin (0.1 U/ml), calcium ionophore (5 μM) or phorbol myristate acetate (400 ng/ml). All these treatments caused platelet activation as well as ROS generation; thalassemic platelets were more responsive than platelets from normal controls. In the absence of any known inherent abnormality in thalassemic platelets, the increased oxidative status was attributable to continuous exposure to oxidative insults from extra-platelet sources. Indeed, further investigation indicated that the oxidative status of normal platelets was increased by thalassemic plasma and was inhibited by the iron-chelator Desferoxamin. Iron and hemin, whose levels are increased in thalassemic plasma, stimulated the platelets’ oxidative stress. This was also affected by RBC: it was higher in normal platelets incubated with thalassemic RBC than when incubated with normal RBC. Normal RBC stimulated with hydrogen peroxide, a treatment which results in an elevated oxidative status, increased platelet ROS to a greater extent (3.3-fold) than did unstimulated RBC. These results suggest that thalassemic RBC, having higher than normal ROS, mediate oxidative stress in platelets directly, probably by contact or close proximity. Platelet oxidative stress was ameliorated by antioxidants such as N-acetyl-L-cysteine and vitamin C. Treatment with these agents of oxidant-stimulated platelets reduced ROS and enhanced the GSH level. The present results indicate that in thalassemia, platelets are in a state of oxidative stress, causing their chronic activation and possibly thromboembolic consequences. This situation may also prevail in other RBC anomalies, such as sickle cell anemia, Polycythemia Vera and Paroxysmal Nocturnal Hemoglobinuria, which are also associated with thromboembolic phenomena. Our findings raise the possibility of using antioxidants in addition to antithrombotic drugs as prophylactic treatment in these diseases.

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