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Sacha Sorrentino, Tonino Bucciarelli,
Alessandro Corsaro,
Alessio Tosatto,
Stefano Thellung,
Valentina Villa,
M Eugenia Schininà,
Bruno Maras,
Roberta Galeno,
Luca Scotti,
Francesco Creati,
Alessandro Marrone,
Nazzareno Re,
Antonio Aceto,
Tullio Florio,
Michele Mazzanti
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Sacha Sorrentino, Tonino Bucciarelli,
Alessandro Corsaro,
Alessio Tosatto,
Stefano Thellung,
Valentina Villa,
M Eugenia Schininà,
Bruno Maras,
Roberta Galeno,
Luca Scotti,
Francesco Creati,
Alessandro Marrone,
Nazzareno Re,
Antonio Aceto,
Tullio Florio,
Michele Mazzanti
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ABSTRACT: The aim of this study was to investigate the effects of acute pharmacological treatment on the plasma levels of l-arginine, asymmetrical dimethylarginine (ADMA), and symmetrical dimethylarginine (SDMA). We also investigated the related effects on endothelial nitric oxide synthase (eNOS) expression and activity and cytochrome c oxidase activity in the primary blood mononuclear cells (PBMCs) isolated from patients with acute congestive heart failure (ACHF). Compared to pre-treatment values, ADMA, SDMA, and l-arginine plasma levels were significantly higher after pharmacological treatment (ADMA, 0.82 versus 0.43 µM; SDMA, 1.52 versus 1.12 µM; l-arginine, 1.78 versus 1.29 µM; p < 0.01. In addition, the levels of eNOS expression and activity were decreased after pharmacological treatment, while cytochrome c oxidase activity resulted in higher O2-production. In the PBMCs isolated from patients with acute congestive heart failure (ACHF) and impaired renal function, higher SDMA and ADMA levels were more evident after therapy, as were reduced expression and activity of eNOS. Increased O2- produced after treatment may be involved in impaired recovery of cardiac function associated with higher plasma levels of SDMA.
Frontiers in bioscience (Elite edition) 01/2013; E5:551-557.
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ABSTRACT: The benefits of cardiovascular therapies such as statins for the treatment of atherosclerosis have been well documented. Many studies have demonstrated important benefits in patients with asymptomatic carotid atherosclerosis. We have evaluated the effect of low dose of rosuvastatin on asymptomatic carotid atherosclerosis in elderly versus adult subjects. Among 640 participants in the Asymptomatic Carotid Atherosclerotic Disease In Manfredonia Study (ACADIM Study) forty-five patients (21 adults, 24 elderly) with hypercholesterolemia and asymptomatic carotid atherosclerosis on baseline carotid ultrasound investigation (CUI) were examined with repeat CUI after one treatment year with rosuvastatin (ROS) (10 mg/day). Total and low density lipoprotein cholesterol decreased significantly (p<0.001) while high density lipoprotein cholesterol increased significantly (p<0.001) during the intervention. Mean decrease in carotid intima media thickness (CIMT) of the right and left common carotid arteries were higher in adult versus elderly subjects (p<0.04 for each), even if in both group there was a significant regression in carotid atherosclerosis respect to baseline values (P<0.001). These results confirm the reduction in IMT of the CCAs in response to ROS at a low dose in a one-year treatment period, even if in elderly subjects this effect is lower respect to adult. The treatment of asymptomatic carotid atherosclerosis defined by CIMT started in the adult age is more effective.
Frontiers in bioscience (Elite edition) 01/2012; 4:2718-21.
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Sacha Sorrentino, Tonino Bucciarelli,
Alessandro Corsaro,
Alessio Tosatto,
Stefano Thellung,
Valentina Villa,
M Eugenia Schininà,
Bruno Maras,
Roberta Galeno,
Luca Scotti,
Francesco Creati,
Alessandro Marrone,
Nazzareno Re,
Antonio Aceto,
Tullio Florio,
Michele Mazzanti
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ABSTRACT: The pathological form of prion protein (PrP(Sc)), as other amyloidogenic proteins, causes a marked increase of membrane permeability. PrP(Sc) extracted from infected Syrian hamster brains induces a considerable change in membrane ionic conductance, although the contribution of this interaction to the molecular mechanism of neurodegeneration process is still controversial. We previously showed that the human PrP fragment 90-231 (hPrP₉₀₋₂₃₁) increases ionic conductance across artificial lipid bilayer, in a calcium-dependent manner, producing an alteration similar to that observed for PrP(Sc). In the present study we demonstrate that hPrP₉₀₋₂₃₁, pre-incubated with 10 mM Ca⁺⁺ and then re-suspended in physiological external solution increases not only membrane conductance but neurotoxicity as well. Furthermore we show the existence of a direct link between these two effects as demonstrated by a highly statistically significant correlation in several experimental conditions. A similar correlation between increased membrane conductance and cell degeneration has been observed assaying hPrP₉₀₋₂₃₁ bearing pathogenic mutations (D202N and E200K). We also report that Ca⁺⁺ binding to hPrP₉₀₋₂₃₁ induces a conformational change based on an alteration of secondary structure characterized by loss of alpha-helix content causing hydrophobic amino acid exposure and proteinase K resistance. These features, either acquired after controlled thermal denaturation or induced by D202N and E200K mutations were previously identified as responsible for hPrP₉₀₋₂₃₁ cytotoxicity. Finally, by in silico structural analysis, we propose that Ca⁺⁺ binding to hPrP₉₀₋₂₃₁ modifies amino acid orientation, in the same way induced by E200K mutation, thus suggesting a pathway for the structural alterations responsible of PrP neurotoxicity.
PLoS ONE 01/2012; 7(7):e38314. · 4.09 Impact Factor
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ABSTRACT: The widely observed between-subject variability in cardiovascular responses to coffee may have a genetic basis.
We evaluated acute blood pressure (BP) responses to caffeine and explored whether they are influenced by candidate gene variants affecting caffeine metabolism (for cytochrome P450 1A2), adenosine metabolism (for adenosine receptor and AMP deaminase), or catecholamine receptors.
We recruited 110 healthy male habitual moderate coffee drinkers who refrained from drinking coffee on the day preceding the study. Each subject underwent ambulatory BP monitoring at 6-min intervals for 2 h. Each participant was administered, in a double-blind design, 40 mL of either a decaffeinated coffee preparation plus 3 mg caffeine/kg (caf) or the corresponding vehicle (decaf). The protocol was repeated 24 h later with the alternative preparation. Blood samples were collected for genetic and plasma caffeine and catecholamine evaluations.
Compared with decaf, caf was associated with a mean (± SD) significant increase in systolic BP of 4 ± 12 mm Hg and in diastolic BP of 3 ± 10 mm Hg (P < 0.001 for both). Plasma caffeine and adrenaline increased after caf, but not after decaf. Of 11 gene polymorphisms analyzed, a relation was observed between the ADORA2A TT variant and the change in SBP peak and between the ADRA2B I variant and the changes in both SBP mean and peak; mean peak change in SBP; these variants were associated with increased SBP responses to caf.
Variability in the acute BP response to coffee may be partly explained by genetic polymorphisms of the adenosine A2A receptors and α(2)-adrenergic receptors. This trial is registered at clinicaltrials.gov as NCT01330680.
American Journal of Clinical Nutrition 12/2011; 95(1):241-8. · 6.67 Impact Factor
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ABSTRACT: Recent evidence indicates that rosuvastatin 40 mg may exert a beneficial effect in both carotid and coronary atherosclerosis progression. In particular, 2-year rosuvastatin treatment reduced the progression of carotid intima-media thickness (cIMT) in patients with low cardiovascular risk. However, despite the fact that in clinical practice lower doses of rosuvastatin are usually administered at this time, there are no clear data about its effect on cIMT. Thus, the aim of this study was to evaluate the effect of rosuvastatin 10 mg/day on cIMT over a 2-year follow-up.
Forty-five patients with hypercholesterolemia and asymptomatic carotid atherosclerosis on baseline carotid ultrasound investigation were treated with rosuvastatin 10 mg/day for 24 months. cIMT and lipid profile were assessed after 12 months and at the end of the study (24 months).
After 24 months, the treatment showed a 35.67% reduction in low-density lipoprotein cholesterol concentration (171 vs 110 mg/dl; p < 0.001), a 32.27% reduction in total cholesterol (251 vs 170 mg/dl; p < 0.001), a 19.67% increase in high-density lipoprotein cholesterol concentration (49 vs 61 mg/dl; p < 0.001), and a 10% reduction in triglycerides (120 vs 108 mg/dl; p < 0.01). Rosuvastatin treatment was associated with a 26.6% reduction in left cIMT (1.20 vs 0.90 mm; p < 0.001) and a 22.2% reduction in right cIMT (1.22 vs 0.95 mm; p < 0.001).
Two-year treatment with rosuvastatin 10 mg/day in hypercholesterolemic adults with evidence of subclinical atherosclerosis establishes a significant reduction in cIMT and improves lipid and lipoprotein levels, with a good tolerability profile.
Expert Opinion on Pharmacotherapy 12/2011; 12(17):2599-604. · 3.20 Impact Factor
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ABSTRACT: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) which plays an important role in controlling vascular tone and regulates the contractile properties of cardiac myocytes. The aim of this study was to investigate the effect of pharmacological treatment on symmetric dimethylarginine (SDMA), ADMA and arginine plasma concentrations in patients with acute congestive heart failure (ACHF) through the evaluation of type-1 system cationic amino acid transporter-1/type 1 dimethylarginine dimethylaminohydrolases-1 (CAT-1/DDAH-1).
25 hospitalized cardiology patients with symptomatic acute congestive HF (NYHA Class III-IV) and impaired left ventricular (LV) function (ejection fraction<35%) were included in the study. ADMA, SDMA, and arginine plasma concentrations were assessed before and after pharmacological treatment by high performance liquid chromatography. All patients received an adequate pharmacological treatment for ACHF. ADMA and SDMA plasma levels were significantly higher after pharmacological treatment respect to baseline values (pre-treatment) (0.75 vs 0.48; 1.31 vs 1.03; p<0.01). Arginine plasma concentration was significantly lower after therapy respect to baseline values (0.78 vs 0.99; p<0.01). This is associated more with the modulation of DDAH-1 protein than with of CAT-1 system transport.
In patients with ACHF, acute renal impairment function and the modulation of metabolism and extracellular transport by the DDAH-1/CAT-1 system determine high ADMA and SDMA levels after therapy for acute congestive heart failure.
Microvascular Research 06/2011; 82(3):391-6. · 2.83 Impact Factor
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ABSTRACT: Mutations in prion protein are thought to be causative of inherited prion diseases favoring the spontaneous conversion of the normal prion protein into the scrapie-like pathological prion protein. We previously reported that, by controlled thermal denaturation, human prion protein fragment 90-231 acquires neurotoxic properties when transformed in a β-rich conformation, resembling the scrapie-like conformation. In this study we generated prion protein fragment 90-231 bearing mutations identified in familial prion diseases (D202N and E200K), to analyze their role in the induction of a neurotoxic conformation. Prion protein fragment 90-231(wild type) and the D202N mutant were not toxic in native conformation but induced cell death only after thermal denaturation. Conversely, prion protein fragment 90-231(E200K) was highly toxic in its native structure, suggesting that E200K mutation per se favors the acquisition of a peptide neurotoxic conformation. To identify the structural determinants of prion protein fragment 90-231 toxicity, we show that while the wild type peptide is structured in α-helix, hPrP90-231 E200K is spontaneously refolded in a β-structured conformer characterized by increased proteinase K resistance and propensity to generate fibrils. However, the most significant difference induced by E200K mutation in prion protein fragment 90-231 structure in native conformation we observed, was an increase in the exposure of hydrophobic amino-acids on protein surface that was detected in wild type and D202N proteins only after thermal denaturation. In conclusion, we propose that increased hydrophobicity is one of the main determinants of toxicity induced by different mutations in prion protein-derived peptides.
The international journal of biochemistry & cell biology 03/2011; 43(3):372-82. · 4.89 Impact Factor
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Graziano Riccioni,
Lorenza Speranza,
Luca Scotti,
Valentina Bucciarelli,
Emanuela Di Ilio,
Nicolantonio D'Orazio,
Mirko Pesce,
Antonio Aceto,
Valeria Sorrenti,
Alessandro Frigiola, Tonino Bucciarelli
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ABSTRACT: Asymmetric dimethylarginine (ADMA) plays a crucial role in the arginine-nitric oxide (NO) pathway. NO plays an important role in controlling vascular tone and regulates the contractile properties of cardiac myocytes. The purpose of this study was to investigate the effect of pharmacological treatment on asymmetrical dimethylarginine (ADMA) plasma levels in patients with acute congestive heart failure (HF). Patients with symptomatic acute congestive HF (NYHA Class III-IV) and impaired left ventricular (LV) function (ejection fraction less than 40 percent) were included in the study. ADMA and SDMA concentrations were assessed before and after pharmacological treatment in 18 critically ill patients on the intensive care unit by high performance liquid chromatography. All patients received a complete pharmacological treatment (diuretics, digoxin, ACE-inhibitors or angiotensin receptor blockers, and nitroglicerin) for the treatment of acute congestive HF. ADMA plasma levels of critically ill patients were significantly higher after pharmacological treatment respect baseline values (pre-treatment). In critically ill patients with acute congestive HF acute renal impairment function and the modulation of NOS determine plasma ADMA/SDMA levels after therapy.
Frontiers in bioscience (Elite edition) 01/2011; 3:1310-4.
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ABSTRACT: Depending on the absolute altitude and the duration of exposure, a high altitude environment induces various cellular effects that are strictly related to changes in oxidative balance. In this study, we used in vitro isolated peripheral blood lymphocytes as biosensors to test the effect of hypobaric hypoxia on seven climbers by measuring the functional activity of these cells. Our data revealed that a 21-day exposure to high altitude (5000 m) (1) increased intracellular Ca(2+) concentration, (2) caused a significant decrease in mitochondrial membrane potential, and (3) despite possible transient increases in intracellular levels of reactive oxygen species, did not significantly change the antioxidant and/or oxidative damage-related status in lymphocytes and serum, assessed by measuring Trolox-equivalent antioxidant capacity, glutathione peroxidase activity, vitamin levels, and oxidatively modified proteins and lipids. Overall, these results suggest that high altitude might cause an impairment in adaptive antioxidant responses. This, in turn, could increase the risk of oxidative-stress-induced cellular damage. In addition, this study corroborates the use of peripheral blood lymphocytes as an easily handled model for monitoring adaptive response to environmental challenge.
High altitude medicine & biology 01/2010; 11(4):333-42. · 1.58 Impact Factor
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ABSTRACT: Few studies have examined the relationship among carotid atherosclerosis, vascular risk factors, and antioxidant plasma concentrations, and those that have reported conflicting results. The aim of this study was to assess the relationship between asymptomatic carotid atherosclerosis, as defined by carotid intima-media thickness (CIMT), and inflammatory markers, plasma lipids and serum antioxidant vitamins.
We examined baseline characteristics of the 640 participants in the Asymptomatic Carotid Atherosclerotic Disease In Manfredonia Study. All participants were asymptomatic with respect to carotid artery disease in 2006-2007 and underwent physical examination with carotid ultrasound investigation, the collection of medical history and laboratory data. Analysis of variance methods were used to examine differences between participants by category of CIMT. Of the 640 participants, 291 did not have evidence of carotid atherosclerosis (CIMT<0.8 mm), 232 were found to have some atherosclerosis (0.8 mm< or =CIMT<1.2 mm), and 117 were found to have extensive atherosclerosis (CIMT>1.2 mm). Among participants with CIMT> or =0.8 mm, body mass index, blood pressures, total cholesterol, LDL cholesterol, triglycerides, uric acid, C-reactive protein, and fibrinogen were significantly higher, whereas concentrations of vitamin A, vitamin E, lycopene, and beta-carotene were all significantly lower when compared with participants who did not show evidence of carotid atherosclerosis (P<0.001).
The optimal control of hypertension, diabetes, and dyslipidemia, in addition to smoking cessation and an adequate intake of antioxidant micronutrients from foods represent a key for the prevention of atherosclerotic disease.
European journal of cardiovascular prevention and rehabilitation: official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology 05/2009; 16(3):351-7. · 2.51 Impact Factor
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ABSTRACT: The inactivation of the homotetrameric cytosolic alcohol dehydrogenase I from Kluyveromyces lactis (KlADH I) by naturally occurring disulfides, oxidized glutathione, cystine and cystamine, was studied. The inactivation was fully reversed by dithiothreitol. The nicotinamide coenzyme, but not the substrate ethanol, protected KlADH I from inactivation. Gel filtration experiments and SDS-PAGE analysis, also, revealed that enzyme inactivation coincides with inter-subunits disulfide bond formation which are noticeably enhanced after prolonged oxidation with GSSG. Moreover, oxidized KlADH I, as its reduced state, retained the tetrameric stucture and appears mainly as a dimer under non-reducing SDS-PAGE. Conversely, KlADH I Cys278Ile mutant is unaffected by disulfides treatment. Therefore, in vitro, KlADH I wild-type could exist in two reversible forms: reduced (active) and oxidized (inactive), in which the Cys278 residues of each tetramer are linked by disulfide bonds. The redox state of KlADH I could represent the path for modulating its activity and then a regulatory step of glycolysis under hypoxic conditions. It might be hypothesized that KlADH I could represent an important target in redox signaling of Kluyveromyces lactis cell by inhibiting, under oxidative stress, the glycolytic pathway in favor of the pentose-phosphate shunt to restore its reducing potential.
Biochimica et Biophysica Acta 01/2009; 1794(3):563-8. · 4.66 Impact Factor
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ABSTRACT: Cysteinyl-leukotrienes (Cys-LTs) and LTB4 are potent proinflammatory mediators derived from arachidonic acid through the 5-lipoxygenase (5-LO) pathway, which exerts important pharmacological effects through their interaction with specific receptors: Cys-LT receptors (CysLT1 and CysLT2) and LTB4 receptors (BLT1 and BLT2). Published evidence justifies a broader role for LT receptor antagonists (LTRAs), in particular, montelukast, in the treatment of bronchial asthma, allergic rhinitis, and recently, in cardiocerebrovascular disease. The actions of Cys-LTs on the cardiovascular (CV) system are well-documented and include a broad array of activities with promising therapeutic targets in animal models exploring the use of selective 5-LO (or 5-LO-activating protein) inhibitors or dual LO-cycloxygenase-blocking agents in experimentally induced acute myocardial infarction. The picture that emerges from studies with LTRAs is more controversial at the moment, and some findings suggest a role for Cys-LTs in the extension of ischemic damage and in cardiac dysfunction during reperfusion; others do not. The aim of this short review is to summarize the state of present research about LT modifier treatment in CV disease.
Journal of Leukocyte Biology 10/2008; 84(6):1374-8. · 4.99 Impact Factor
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ABSTRACT: Atherosclerosis remains clinically mute for a long time and frequently manifests itself with an acute cardiovascular event. The possibility of detecting this disease in a subclinical phase and reducing or reversing its progression is an issue of relevance. Published studies on the association between antioxidant vitamins and carotenoids and carotid intima-media thickness (CIMT) have been inconclusive.
We enrolled 220 consecutive, asymptomatic participants. After carotid ultrasound investigation, a medical history was taken, a physical examination was performed and venous blood samples were collected. Venous blood samples were analyzed for concentrations of antioxidant vitamins and carotenoids.
Low concentrations of vitamin A (p < 0.01), vitamin E (p < 0.001), lycopene (p < 0.01) and beta-carotene (p < 0.001) were significantly associated with carotid atherosclerosis (CIMT > or = 0.8 mm). In addition, marginally higher body mass index, plasma haemoglobin and high-density lipoprotein cholesterol were also associated with carotid atherosclerosis, while other laboratory parameters considered in this study (total cholesterol, low-density lipoprotein cholesterol, triglycerides and C-reactive protein) were not significantly associated with carotid atherosclerosis.
Low plasma concentrations of antioxidant vitamins (A, E, beta-carotene) and lycopene were associated with early carotid atherosclerotic lesions as measured by CIMT. Regular intake of foods rich in lycopene and antioxidant vitamins may slow the progression of atherosclerosis.
Annals of Nutrition and Metabolism 10/2008; 53(2):86-90. · 2.26 Impact Factor
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ABSTRACT: An increase in carotid intima-media thickness (CIMT) represents an early phase of the atherosclerotic process. The aim of this study was to evaluate whether a reduction in CIMT could be seen with only 16 weeks of treatment with rosuvastatin (10 mg/day).
Sixty-six participants of the ACADIM Study with hypercholesterolemia and carotid atherosclerosis at baseline carotid ultrasound investigation (CUI) were examined, with repeat CUI after 16 weeks of treatment. Demographic and lifestyle data were collected, as well as physical examination and fasting venous blood samples. Total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglycerides decreased significantly (p < 0.0001), while high density lipoprotein cholesterol (HDL-C) increased significantly (p < 0.0001) during the intervention. The mean decrease in IMT of the right and left common carotid arteries (CCAs) was 0.35 and 0.38 mm, respectively (p < 0.05 for each). Age and lipid profile parameters were significant predictors of change in CIMT in linear regression analyses after adjustment for established atherosclerosis risk factors.
Treatment with rosuvastatin in adults with evidence of subclinical atherosclerosis significantly reduced the CIMT of both CCAs, as well as improving lipid and lipoprotein levels.
Expert Opinion on Pharmacotherapy 10/2008; 9(14):2403-8. · 3.20 Impact Factor
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ABSTRACT: Glutathione transferases (GSTs) constitute a class of detoxifying enzymes involved in Phase II metabolism. Using GSH-affinity chromatografy followed by HPLC analysis, two GST isoforms were isolated from the Anguilla anguilla liver cytosol. The major GST belongs to the piscine-specific rho class and accounted for about 59% of total GST affinity eluted fraction, while the remaining 41% was represented by a Pi class GST. Both isoforms were cloned, heterologously expressed in Escherichia coli and their enzyme activities were characterized with respect to a broad spectrum of well-known GST substrates. Our data indicate that only a fraction of prototypical GST substrates are conjugated by these enzymes and that Pi class GST has higher specific activity than rho class GST against 1-chloro-2,4-dinitrobenzene (CDNB), ethracrynic acid, 4-nitroquinoline-1-oxide and p-nitrophenyl acetate while trans-2-nonenal is detoxified more efficiently by rho class GST. Analysis of the kinetics parameters of the conjugation against CDNB indicated that the utilization ratio K(cat)/K(m) is slightly higher for rho class GST with respect to pi class GSTs. Finally, to determine the potential for environmental inhibition of the GST isoforms, we examined the effect of the widely used herbicide atrazine as an inhibitor of catalytic activity. The inhibition studies revealed that atrazine was an effective inhibitor of GST-CDNB catalytic activities of both isoforms at micromolar concentrations, suggesting the sensitivity of these isoforms to pesticide inhibition at environmentally relevant concentrations.
Aquatic toxicology (Amsterdam, Netherlands) 09/2008; 90(1):48-57. · 3.12 Impact Factor
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ABSTRACT: Low birth weight is associated with an increased risk of metabolic and cardiovascular diseases in adulthood. The development of insulin resistance (IR) seems to play a pivotal role; no data on the oxidant-antioxidant status are available in this risk group.
This study is an assessment of oxidant-antioxidant status in prepubertal children born small for gestational age (SGA) in comparison to healthy controls and the relationship to IR.
This cross-sectional study compares indexes of IR and oxidant-antioxidant status in three different groups (SGA+, SGA-, controls), with analysis by post hoc and Pearson correlation.
The study was conducted in the Academic Department of Pediatrics.
A total of 19 SGA+ and 16 SGA- children were compared with 13 controls.
No intervention was used.
Indexes of IR (glucose to insulin ratio, homeostasis model assessment of IR) were evaluated, and markers of oxidative stress (lag phase, malonildialdehyde, vitamin E) were measured.
Homeostasis model assessment of IR was significantly higher in SGA+ than SGA- children (1.32+/-0.9 vs. 0.69+/-0.47; P=0.03) and controls (0.71+/-0.37; P=0.04). Glucose to insulin ratio was significantly lower in SGA+ than SGA- children (12.41+/-5.01 vs. 26.54+/-17.18; P=0.02) and controls (26.96+/-20.70; P=0.04). Lag phase was significantly shorter in SGA+ than SGA- children (24.3+/-4.38 vs. 35.59+/-11.29 min; P=0.003) and controls (45.28+/-7.69 min; P=0.0001) and in SGA- than controls (P=0.01). Malonildialdehyde was significantly higher in SGA+ than SGA- children (0.79+/-0.3 vs. 0.6+/-0.1 nmol/mg; P=0.03) and controls (0.36+/-0.04 nmol/mg; P=0.0001) and in SGA- children than controls (P=0.02). Vitamin E was significantly reduced in SGA+ children than controls (27.54+/-7.9 vs. 43.23+/-11.32 micromol/liter; P=0.002).
Oxidative stress is present in both SGA+ and SGA- children, with a continuous alteration in relation to IR. Therefore, catch-up growth might exert the greatest influence in the development of future diseases.
Journal of Clinical Endocrinology & Metabolism 05/2007; 92(4):1372-8. · 6.50 Impact Factor
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Giovanni Ciabattoni,
Ettore Porreca,
Concetta Di Febbo,
Angelo Di Iorio,
Roberto Paganelli, Tonino Bucciarelli,
Lea Pescara,
Letizia Del Re,
Cinzia Giusti,
Angela Falco,
Antonella Sau,
Carlo Patrono,
Giovanni Davì
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ABSTRACT: To investigate the rate of platelet thromboxane (TX) biosynthesis and its determinants in Alzheimer's disease.
A cross-sectional comparison of urinary 11-dehydro-TXB(2) and 8-iso-prostaglandin (PG)F(2alpha) (markers of in vivo platelet activation and lipid peroxidation, respectively), plasma Vitamin E, C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, was carried-out in 44 Alzheimer patients and 44 matched controls. To investigate the cyclooxygenase (COX)-isoform involved in TXA(2) biosynthesis, nine Alzheimer patients were treated with low-dose aspirin (100mg/d) or rofecoxib (25mg/d) for 4 days. Urinary 11-dehydro-TXB(2) and 8-iso-PGF(2alpha) were significantly higher in Alzheimer patients than in controls (Median: 1983.5 versus 517.5pg/mg creatinine and 938.5 versus 304.0pg/mg creatinine, p<0.0001, respectively), with a significant correlation between the two metabolites (rho=0.75, p<0.0001). An inverse correlation was observed between Vitamin E and both urinary metabolites (8-iso-PGF(2alpha): R(s)=-0.51, p=0.0004; 11-dehydro-TXB(2): R(s)=-0.44, p=0.0026) in Alzheimer patients. No difference was found in CRP, TNF-alpha and IL-6 levels between the two groups. Urinary 11-dehydro-TXB(2) was significantly reduced by aspirin, but not by rofecoxib, consistently with a COX-1-mediated TXA(2) biosynthesis. 8-iso-PGF(2alpha) excretion was not modified by either COX-inhibitor, consistently with its oxygen radical-catalyzed formation.
Platelet activation is persistently enhanced in Alzheimer's disease. This is related, at least in part, to increased lipid peroxidation associated with inadequate levels of Vitamin E.
Neurobiology of aging 03/2007; 28(3):336-42. · 5.94 Impact Factor
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ABSTRACT: The influence of nutrition on chronic bronchial asthma has an important place in the management of this disease. Evidence suggests that specific inflammatory abnormalities exist in the airways of subjects suffering from mild-to-moderate persistent asthma, in whom an inflammatory state is often associated with increased generation of reactive oxygen species and the damaging effects of free radicals. For this reason oxidant stress may be an important pathogenic factor in the progress of the disease. The role of nutrition in bronchial asthma is related to antioxidant vitamins A, C, and E. By counteracting oxidants and reducing external attacks (bacteria, virus, toxins, xenobiotics) in the lung, antioxidant vitamins modulate the development of asthma and the impairment of pulmonary function. Dietary studies suggest relations between oxidative stress, bronchial inflammation, development of asthmatic symptoms, and reduction of cellular functions. Dietary interventions may reduce oxidant stress and prevent or minimize asthmatic symptoms. Such interventions may provide a cost-effective approach to asthma management that may supplement current pharmacological strategies, although this conclusion is not supported by many randomized, placebo-controlled studies. The aim of this short review is to summarize current knowledge regarding the relations between antioxidant vitamins and the treatment of bronchial asthma.
Annals of clinical and laboratory science 02/2007; 37(1):96-101. · 0.96 Impact Factor
