Effects of Dietary Carbohydrate Concentration and Glycemic Index on Blood Glucose Variability and Free Fatty Acids in Individuals with Type 1 Diabetes.

Monitoring glycemic control status is the cornerstone of diabetes management. This study aimed to reveal whether moderate-carbohydrate (CHO) diets increase the risk of free fatty acid (FFA) levels, and it presents the short-term effects of four different diet models on blood sugar, glycemic variability (GV), and FFA levels. This crossover study included 17 patients with type 1 diabetes mellitus to identify the effects of four diets with different CHO contents and glycemic index (GI) on GV and plasma FFA levels. Diet 1 (D1) contained 40% CHO with a low GI, diet 2 (D2) contained 40% CHO with a high GI, diet 3 (D3) contained 60% CHO with a low GI, and diet 4 (D4) contained 60% CHO with a high GI. Interventions were performed with sensor monitoring in four-day periods and completed in four weeks. No statistical difference was observed among the groups in terms of blood glucose area under the curve (p = 0.78), mean blood glucose levels (p = 0.28), GV (p = 0.59), and time in range (p = 0.567). FFA and total triglyceride levels were higher in the D1 group (p < 0.014 and p = 0.002, respectively). Different diets may increase the risk of cardiovascular diseases by affecting GI, FFA, and blood glucose levels.

Effect of octreotide on oxidative stress in the erythrocyte and kidney tissue in adriamycin-induced experimental nephrotic syndrome model / Efeito do octreotide no estresse oxidativo em eritrócitos e no tecido renal no modelo de síndrome nefrótica experimental induzida por adriamicina

Abstract Introduction: Nephrotic syndrome (NS) is one of the reasons of end-stage kidney disease, and elucidating the pathogenesis and offer new treatment options is important. Oxidative stress might trigger pathogenesis systemically or isolated in the kidneys. Octreotide (OCT) has beneficial antioxidant effects. We aimed to investigate the source of oxidative stress and the effect of OCT on experimental NS model. Methods: Twenty-four non-uremic Wistar albino rats were divided into 3 groups. Control group, 2 mL saline intramuscular (im); NS group, adriamycin 5 mg/kg intravenous (iv); NS treatment group, adriamycin 5 mg/kg (iv) and OCT 200 mcg/kg (im) were administered at baseline (Day 0). At the end of 21 days, creatinine and protein levels were measured in 24-hour urine samples. Erythrocyte and renal catalase (CAT) and thiobarbituric acid reactive substance (TBARS) were measured. Renal histology was also evaluated. Results: There was no significant difference among the 3 groups in terms of CAT and TBARS in erythrocytes. Renal CAT level was lowest in NS group, and significantly lower than the control group. In treatment group, CAT level significantly increased compared with NS group. In terms of renal histology, tubular and interstitial evaluations were similar in all groups. Glomerular score was significantly higher in NS group compared with control group and it was significantly decreased in treatment group compared to NS group. Conclusions: Oxidative stress in NS might be due to the decrease in antioxidant protection mechanism in kidney. Octreotide improves antioxidant levels and histology in renal tissue and might be a treatment option.

Resumo Introdução: Síndrome nefrótica (SN) é uma das causas de doença renal em estágio terminal. É importante elucidar a patogênese e oferecer novas opções de tratamento. Estresse oxidativo pode desencadear a patogênese sistemicamente ou isoladamente nos rins. O octreotide (OCT) tem efeitos antioxidantes benéficos. Nosso objetivo foi investigar a fonte de estresse oxidativo e efeito do OCT no modelo experimental de SN. Métodos: Dividimos 24 ratos albinos Wistar não urêmicos em 3 grupos. Grupo controle, 2 mL de solução salina intramuscular (im); grupo SN, adriamicina 5 mg/kg intravenosa (iv); grupo tratamento SN, adriamicina 5 mg/kg (iv) e OCT 200 mcg/kg (im) foram administrados no início do estudo (Dia 0). Aos 21 dias, mediram-se os níveis de creatinina e proteína em amostras de urina de 24 horas. Mediu-se a catalase (CAT) eritrocitária e renal e a substância reativa ao ácido tiobarbitúrico (TBARS). Avaliou-se também histologia renal. Resultados: Não houve diferença significativa entre os três grupos em termos de CAT e TBARS em eritrócitos. O nível de CAT renal foi menor no grupo SN e significativamente menor que no grupo controle. No grupo tratamento, o nível de CAT aumentou significativamente em comparação com o grupo SN. Quanto à histologia renal, as avaliações tubular e intersticial foram semelhantes em todos os grupos. O escore glomerular foi significativamente maior no grupo SN em comparação com o grupo controle e diminuiu significativamente no grupo de tratamento em comparação com o grupo SN. Conclusões: Estresse oxidativo na SN pode ser devido à diminuição do mecanismo de proteção antioxidante nos rins. O octreotide melhora níveis de antioxidantes e histologia do tecido renal e pode ser uma opção de tratamento.

Effect of octreotide on oxidative stress in the erythrocyte and kidney tissue in adriamycin-induced experimental nephrotic syndrome model.

INTRODUCTION: Nephrotic syndrome (NS) is one of the reasons of end-stage kidney disease, and elucidating the pathogenesis and offer new treatment options is important. Oxidative stress might trigger pathogenesis systemically or isolated in the kidneys. Octreotide (OCT) has beneficial antioxidant effects. We aimed to investigate the source of oxidative stress and the effect of OCT on experimental NS model. METHODS: Twenty-four non-uremic Wistar albino rats were divided into 3 groups. Control group, 2 mL saline intramuscular (im); NS group, adriamycin 5 mg/kg intravenous (iv); NS treatment group, adriamycin 5 mg/kg (iv) and OCT 200 mcg/kg (im) were administered at baseline (Day 0). At the end of 21 days, creatinine and protein levels were measured in 24-hour urine samples. Erythrocyte and renal catalase (CAT) and thiobarbituric acid reactive substance (TBARS) were measured. Renal histology was also evaluated. RESULTS: There was no significant difference among the 3 groups in terms of CAT and TBARS in erythrocytes. Renal CAT level was lowest in NS group, and significantly lower than the control group. In treatment group, CAT level significantly increased compared with NS group. In terms of renal histology, tubular and interstitial evaluations were similar in all groups. Glomerular score was significantly higher in NS group compared with control group and it was significantly decreased in treatment group compared to NS group. CONCLUSIONS: Oxidative stress in NS might be due to the decrease in antioxidant protection mechanism in kidney. Octreotide improves antioxidant levels and histology in renal tissue and might be a treatment option.

Effects of ozone treatment to the levels of neurodegeneration biomarkers after rotenone induced rat model of Parkinson's disease.

The study investigated the effects of ozone treatment on the neurodegeneration of stereotaxic rotenone-induced parkinson's disease (PD) model. The model was confirmed using the apomorphine rotation test. α-synuclein, amyloid-ß, Tau, phosphorylated Tau, as well as tyrosine hydroxylase(+), nNOS(+), and glial cell counts were used to evaluate neurodegeneration in the substantia nigra pars compacta and ventral tegmental area. The experiment involved 48 Sprague-Dawley rats divided into four groups: dimethyl sulfoxide (DMSO), DMSO with ozone (O), DMSO/rotenone (R), and D/R/O. Ozone treatment significantly improved tissue α-synuclein level and TH+, nNOS+, and glial cell counts compared to the rotenone-only group. The study suggests that ozone treatment may have beneficial effects on PD biomarkers in the rotenone model. Further studies on ozone dosage, duration, and administration methods in humans could provide more evidence for its potential use in Parkinson's disease treatment.

A novel biorecognition receptor Citropin-A modified impedimetric biosensor for detection of LNCaP prostate cancer cells.

In this study, Citropin-A (Cit-A) as a biorecognition receptor was used for the first time to develop electrochemical impedance spectroscopy (EIS) based biosensor for the detection of Lymph Node Carcinoma of the Prostate (LNCaP) cancer cells. The biosensor was engineered by modification of a gold electrode (AuE) with cysteamine (Cys), Poliamidoamin (PAMAM (G4)) dendrimers, avidin, and biotinylated Cit-A, respectively. The detection time of the LNCaP cells was determined as 300 s by chronoimpedance (CI). Chronoimpedance also provided an exact detection time to avoid non-specific adsorptions. The biosensor showed good linearity between 1500 cells/L and 12000 cells/L, limit of detection (LOD), and limit of quantification (LOQ) values were 518 cells/L and 1570 cells/L, respectively.

The Relationship Between Blood Hypoxia-Inducible Factor-1α, Fetuin-A, Fibrinogen, Homocysteine, and Amputation Level.

Reduced life expectancy has resulted from an increased incidence of chronic complications in patients with diabetes. The diabetic foot is one of these complications and generally presents together with diabetic neuropathy and vascular insufficiency. Hypoxia-inducible factor-1α (HIF-1α) is important in developing the adaptation response to hypoxia and facilitates healing through regulation of keratinocyte migration and epithelium restoration in wounds. Fetuin-A is a transporter protein that is synthesized in the liver and inhibits vascular and ectopic calcifications. It has been observed that altered fetuin-A is associated with peripheral artery disease through vascular calcification and is associated with inflammation and metabolic syndrome occurrence in diabetic patients. Fibrinogen is an acute-phase reactant and has a major role in homeostasis, tissue repair, and wound healing. Increased fibrinogen blood level is one of the factors that facilitates the hypercoagulability in diabetics. Homocysteine has atherogenic features and causes vascular toxicity by enhancing low-density lipoprotein oxidation. We evaluated the association of serum HIF-1α, fetuin-A, fibrinogen, and homocysteine levels with amputation in 31 patients diagnosed with diabetes mellitus. According to our evaluation, a negative correlation was determined between fetuin-A and amputation level (P = .012, r = -0.450), which was statistically significant. Unfortunately, there was no significant correlation between HIF-1α, fibrinogen, homocysteine, and amputation level (P > .05). As a result, it was suggested that vascular calcification due to fetuin-A deficiency may be important in the diabetic foot pathogenesis and that fetuin-A levels may be a predictor for amputation level.

Using dynein heavy chain 5 and creatine kinase levels in cervical fluid and blood for early diagnosing of ectopic pregnancy.

AIM: Ectopic pregnancy is a life-threatening problem in reproductive ages. Diagnosing ectopic pregnancy in the early period provides to reducing mortality and morbidity and gives an opportunity for medical treatment to preserve fallopian tubes. Evaluation of cervical fluid for determining ectopic pregnancy with new promising markers provided different aspects for diagnosing ectopic pregnancy in the present study. METHODS: In this prospective clinical study, ectopic pregnant patients as ectopic pregnancy group (n = 46), intrauterine pregnant patients as intrauterine pregnancy group (n = 29) and not-pregnant patients as nonpregnancy group (n = 10) participated to study. Cervical fluid samples were collected with using merocel sponge. In addition, serum samples were obtained from patients. Dynein heavy chain 5 (DNAH5) and creatine kinase (CK) levels were determined by enzyme-linked immunosorbent assay kits in samples. RESULTS: Reduced cervical fluid DNAH5 levels was diagnosed in ectopic pregnancy group compared to intrauterine pregnancy group (median 3.42 ng/mL; 25-75% percentile 0-9.56 ng/mL vs median 6.14 ng/mL; 1.40-8.31 ng/mL; P < 0.001). On the other hand, DNAH5 protein was not detected in nonpregnant patients' samples. In addition, statistical significant increased cervical fluid CK levels were diagnosed in ectopic pregnancy group compared to intrauterine pregnancy group (median 4477.61 IU/L; 0-64 925.37 IU/L vs 0 IU/L; 0-6832.30 IU/L; P = 0.006). CONCLUSION: Measuring of CK and DNAH5 in cervical fluid could be promising markers for early diagnosing of ectopic pregnancy. Decreased DNAH5 levels in cervical fluid might be result from abnormal cilia function in ectopic pregnant patients. ClinicalTrials.gov ID. NCT02995356.

Fullerene-PAMAM(G5) composite modified impedimetric biosensor to detect Fetuin-A in real blood samples.

The aim of this study is to develop a nanomaterial-dendrimer composite modified biosensor to detect Fetuin-A (HFA) in real blood samples. For this purpose, we designed an Electrochemical Impedance Spectroscopy (EIS) based anti-Fetuin-A (Anti-HFA) modified biosensor system and tested in real blood samples. Chronoimpedance was also employed. The same samples were analyzed with ELISA and the results were compared for validation of the new system. Gold screen printed electrodes (AuSPE) were used as transducer. Firstly, a self-assembly monolayer (SAM) was formed on gold surface by 4-aminothiophenol (4-ATP), Fullerene and PAMAM-NH2 (G5), layers were formed, consecutively. Then Anti-HFA was immobilized on Au/4-ATP/Fullerene/PAMAM electrode via glutaraldehyde. The chronoimpedance test was employed to investigate the optimum analysis duration. According to the data of chronoimpedance, the total analysis time for EIS was chosen as 3 min. The new biosensor was compared with the ELISA method which required 150 min. The calibration curve was prepared electron transfer resistance of the electrode (ΔRet) per minute as ohm and 1.66-134 ng/mL.min with a R2 = 0.9912. The LOD and LOQ of the biosensor was calculated as 0.48 ng/mL.min, 1.46 ng/mL.min, respectively. Linear regression analysis indicated that the novel developed biosensor results agreed well with that of the conventional ELISA assay.

Monocyte chemotactic protein-1, RANTES and macrophage migration inhibitory factor levels in gingival crevicular fluid of metabolic syndrome patients with gingivitis.

OBJECTIVE: The aim of the present study was to determine gingival crevicular fluid (GCF) levels of monocyte chemotactic protein-1 (MCP-1), regulated on activation, normal T-cell expressed and secreted protein (RANTES) and macrophage migration inhibitory factor (MIF) in metabolic syndrome patients with gingivitis. DESIGN: Twenty metabolic syndrome patients with gingivitis (MSG), 20 MetS patients with clinically healthy periodontium (MSH), 20 systemically healthy subjects with gingivitis and 20 subjects who were both systemically and periodontally healthy were included. Periodontal and systemical parameters were recorded. GCF MCP-1, RANTES and MIF levels were assayed by enzyme-linked immunosorbent assay method. RESULTS: MSG and MSH groups had elevated blood pressure, triglyceride, waist circumference and fasting glucose values in comparison to gingivitis and healthy groups (P<0.0001). Clinical periodontal parameters were higher in MSG and gingivitis groups when compared to those of the MSH and healthy groups (P<0.0001). MCP-1 and RANTES levels (ng/mg total protein) of MSG group were higher than those of the MSH groups (P=0.005, P=0.0001, respectively). Also gingivitis group had higher MCP-1, RANTES and MIF levels compared to the healthy group (P=0.011, P=0.0001, P=0.011 respectively). The RANTES level of MSG group was significantly higher than those of the gingivitis group (P=0.01), but MCP-1 and MIF levels were similar in the MSG and gingivitis groups (P>0.05). CONCLUSION: Elevated levels of GCF RANTES in MetS patients with gingivitis might associate with the presence of increased gingival inflammation by MetS. Low-grade systemic inflammation associated with MetS and adipose tissue-derived RANTES might lead to altered GCF RANTES levels in the presence of gingival inflammation.

Chitotriosidase as a possible marker of clinically evidenced atherosclerosis in dyslipidemic children.

A correlation has been clearly shown between inflammation markers and subclinical atherosclerosis markers in the early stages of atherogenesis in subjects with familial hypercholesterolemia (FH). The aim of this study was to investigate potential inflammation markers in the diagnosis of atherosclerosis in children with FH. A total of 48 dyslipidemic children and 24 healthy age-matched control subjects were taken into study. Inflammation and macrophage activation markers (hsCRP, myeloperoxidase, chitotriosidase, YKL-40, TNF-α, IL-6, IL-18, MMP-1 and MMP-9) and lipid parameters of all patients were measured. Carotid intima-media thickness (cIMT) and flow-mediated dilation (FMD) levels were determined. Our data suggested that clinically evidenced (by cIMT and FMD levels) atherosclerosis starts in the early ages in hypercholesterolemic children. Higher cholesterol levels strongly correlated with macrophage activation markers (ChT, YKL-40 and myeloperoxidase). ChT and YKL-40 seem to be the more predictable markers of atherosclerosis even in early ages (<6 years old) than other classical inflammation markers such as hs-CRP, IL-6 and TNF-α.

Low-dose fluvastatin prevents the functional alterations of endothelium induced by short-term cholesterol feeding in rabbit carotid artery.

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, commonly known as statins, are the medical treatment of choice for hypercholesterolemia. In addition to lowering serum-cholesterol levels, statins appear to promote pleiotropic effects that are independent of changes in serum cholesterol. In this study, we investigated the effects of low-dose fluvastatin on antioxidant enzyme activities (superoxide dismutase, SOD; catalase), total nitrite/nitrate levels, and vascular reactivity in 2% cholesterol-fed rabbits. This diet did not generate any fatty streak lesions on carotid artery wall. However, SOD activity significantly increased with cholesterol feeding whereas the catalase activities decreased. The levels of nitrite/nitrate, stable products of NO degradation, diminished. Moreover, dietary cholesterol reduced vascular responses to acetylcholine, but contractions to serotonin were augmented. Fluvastatin treatment abrogated the cholesterol-induced increase in SOD, increased the levels of nitric oxide metabolites in tissue, and restored both the impaired vascular responses to acetylcholine and the augmented contractile responses to serotonin without affecting plasma-cholesterol levels. Phenylephrine contractions and nitroglycerine vasodilatations did not change in all groups. This study indicated that fluvastatin treatment performed early enough to improve impaired vascular responses may delay cardiovascular complications associated with several cardiovascular diseases.

A panel of oxidative stress assays does not provide supplementary diagnostic information in Behcet's disease patients.

BACKGROUND: Recent findings suggest a role of oxidative stress in the pathogenesis of Behcet's disease (BD), but the utility of oxidative stress-associated assays in offering diagnostic information or in the monitoring of disease activity is largely unassessed. OBJECTIVE AND METHODS: We aimed to measure oxidative and inflammatory markers, along with the markers of reactive nitrogen species, S-nitrosothiols and 3-nitrotyrosine, in BD patients (n = 100) and healthy volunteers (n = 50). These markers were evaluated in regard to their role in the pathogenesis of BD as well as their relation to clinical presentation, disease activity and duration. RESULTS: Median values for erythrocyte sedimentation rate (ESR), C-reactive protein, leukocyte count, and IL-18 levels, as well as myeloperoxidase (MPO) activity, were statistically higher in the patient group compared to controls. Some inflammation markers (ESR, neutrophil and leukocyte counts) were statistically higher (p < 0.05) in the active period. In contrast, oxidative stress-associated measures (erythrocyte lipid peroxidation, antioxidant enzymes and measures of serum antioxidant capacity), revealed no statistically significant differences between the median values in BD patients versus healthy control subjects (p > 0.05 in all statistical comparisons), nor was there any difference in median levels of these oxidative stress markers in active disease versus disease remission. S-nitrosothiols and 3-nitrotyrosine were undetectable in BD plasma. CONCLUSIONS: The application of oxidative stress-associated measures to BD blood samples offered no supplemental diagnostic or disease activity information to that provided by standard laboratory measures of inflammation. S-nitrosothiols and 3-nitrotyrosine appeared not to be markers for active BD; thus the search for biochemical markers that will indicate the active period should be continued with larger studies.

Pomegranate wine has greater protection capacity than red wine on low-density lipoprotein oxidation.

Although there is a large body of evidence on the main role of red wine in protection of low-density lipoprotein (LDL) against oxidation, there are few data on the role of pomegranate juice, which has high phenolic content. We conducted this study considering the possible importance of pomegranate wine as an antioxidant and in order to make a comparison between red and pomegranate wines. The phenol levels of pomegranate and red wines (4,850 mg/L gallic acid equivalents and 815 mg/L gallic acid equivalents, respectively) were in accordance with their total antioxidant activity (39.5% and 33.7%, respectively). Both wines decreased LDL-diene levels following a 30-minute incubation period compared with controls (145 +/- 3.2 micromol/mg of LDL protein). However, pure pomegranate wine demonstrated a greater antioxidant effect (P < .01) on diene level (110 +/- 4.6 micromol/mg of LDL protein) than pure red wine (124 +/- 3.2 micromol/mg of LDL protein). In conclusion, we suggest that pomegranate wine has potential protective effects toward LDL oxidation, and it may be a dietary choice for people who prefer fruit wines.

Effects of estrogen-only therapy on LDL oxidation in women with hysterectomy: does paraoxonase genotype play a role?

OBJECTIVES: This study investigated the effects of estrogen-only therapy on lipid profile (through susceptibility of low density lipoproteins to oxidation) and on oxidant-antioxidant parameters in surgical menopausal women. PON genotypes are also evaluated considering that they may be associated with the personal differences observed in antioxidant effects induced by estrogen. METHODS: Thirty women who had undergone hysterectomy+bilateral ovariectomy in the last 3 years, with causes other than malignancy were included and given estrogen-only (Premarin-Wyeth Inc. 0.625 mg/day/6 months, equine conjugated estrogen). Blood samples were collected at baseline, first and sixth month of treatment. Serum (total antioxidant activity-TAO and PON activity), erythrocyte (TBARS and catalase activity), LDL and Cu2+ induced ox-LDL (TBARS and diene levels) samples were evaluated and PON1 192 polymorphisms were determined by PCR amplification & restriction enzyme digestion. RESULTS: At the sixth month, a higher TAO activity (p=0.016) and a lower eTBARS (p=0.028) were detected compared to the basal values. LDL and Cu induced ox-LDL TBARS levels at the sixth month of treatment were significantly (p=0.012 and 0.026, respectively) lower compared to the pretreatment values. Baseline eTBARS (p=0.007), LDL TBARS (p=0.044) and eCAT (p=0.033) activities were significantly higher in homozygote Q allele carriers compared to subjects with R allele. LDL TBARS and Cu2+ induced ox-LDLTBARS of QQ subjects (p=0.018 and 0.050) as well as LDL TBARS of QR subjects (p=0.044) showed a significant decrease with estrogen-only treatment. CONCLUSIONS: Our study drives the attention to PON polymorphism in postmenopausal women who have risk for atherosclerosis. Although our data is limited, this study is the first that focuses on the role of PON genotypes in antiatherosclerotic effects of estrogen-only and provides important points for further studies.

The effect of melatonin on lipid peroxidation and nitrite/nitrate levels, and on superoxide dismutase and catalase activities in kainic acid-induced injury.

Kainic acid (KA) initiates neuronal injury and death by inducing oxidative stress and nitric oxide release from various regions of the brain. It was recently shown that melatonin has free radical-scavenging action and may protect against kainate-induced toxicity. In order to assess the possible supportive effect of melatonin treatment in KA-induced injury in the rat brain cortex, we determined malondialdehyde (MDA) levels as an index of lipid peroxidation, and assessed the activities of catalase (CAT) and superoxide dismutase (SOD) and the levels of nitrite/nitrate 35 male rats were divided into five groups, each receiving a different intraperitoneal treatment: saline solution (0.2 ml), kainic acid (15 mg/kg), melatonin (20 mg/kg), KA then melatonin (each as above, 15 min apart), or melatonin then KA (each as above, 30 min apart). Administration of KA caused an about five-fold increase in the catalase activity and an increase in the SOD activity in the cortex relative to the activities for the controls. Treatment with melatonin 15 min after KA injection kept malondialdehyde levels and catalase and superoxide dismutase activities at the normal levels, and led to an increase in the levels of nitrite/nitrate. Our data suggests that melatonin treatment following KA administration has a protective effect on antioxidant enzyme activities and thus supports the role of melatonin and oxidative stress in the regulation of antioxidative enzyme activity.

Protection capacity against low-density lipoprotein oxidation and antioxidant potential of some organic and non-organic wines.

Current research suggests that phenolics from wine may play a positive role against oxidation of low-density lipoprotein (LDL), which is a key step in the development of atherosclerosis. Considering the effects of different wine-making techniques on phenols and the wine consumption preference influencing the benefical effects of the product, organically and non-organically produced wines were obtained from the grapes of Vitis vinifera origin var: Carignan, Cabernet Sauvignon, Merlot, Grenache, Columbard and Semillon. Levels of total phenols [mg/l gallic acid equivalents (GAE)], antioxidant activity (%) and inhibition of LDL oxidation [%, inhibition of diene and malondialdehyde (MDA) formation] were determined. Some phenolic acids (gallic acid, p-hydroxybenzoic acid, syringic acid, 2,3-dihydroxybenzoic acid, ferulic acid, p-coumaric acid and vanillic acid) were quantified by high-performance liquid chromatography equipped with an electrochemical detection carried at +0.65 V (versus Ag/AgCl, 0.5 microA full scale). The highest concentrations of gallic, syringic and ferulic acids were found in organic Cabernet Sauvignon; 2,3-dihydroxybenzoic acid in organic Carignan and p-coumaric and vanillic acids in non-organic Merlot wine. High levels of antioxidant activity (AOA), inhibition of LDL oxidation and total phenol levels were found in non-organic Merlot (101.950% AOA; 88.570% LDL-diene; 41.000% LDL-MDA; 4700.000 mg/l GAE total phenol) and non-organic Cabernet Sauvignon (92.420% AOA; 91.430% LDL-diene; 67.000% LDL-MDA; 3500.000 mg/l GAE total phenol) grape varieties. Concentrations of some individual phenolic constituents (ferulic, p-coumaric, vanillic) are correlated with high antioxidant activity and inhibition of LDL oxidation. The best r value for all examined characteristics was determined for gallic acid, followed by 2,3-dihydroxybenzoic, syringic, ferulic and p-coumaric acids. Negative correlation of vanillic with MDA and p-hydroxybenzoic acid with LDL were confirmed by principal component analysis (PCA) analyses. Red wines display a higher antioxidant activity (81.110% AOA) than white ones (19.512% AOA). The average level of LDL inhibition capacity in red wine was determined as 87.072% and for the white as 54.867%.

A modified method for preparing platelet-rich plasma: an experimental study.

PURPOSE: In this study, our aim was to prepare low-cost autogenous platelet-rich plasma (PRP) for use in minor bone grafting procedures. This was the preliminary study of an experimental study concerning augmentation of bony defects with a mixture of PRP and beta-tricalcium phosphate. MATERIALS AND METHODS: Venous blood was collected from marginal ear veins of New Zealand White rabbits in EDTA (K3) vacutainer tubes. Blood samples were divided into 2 groups, and PRP was prepared through 2 methods, 1 of which is a variant of the other. The 2 PRP preparation methods described in this study were modified from Landesberg et al (J Oral Maxillofac Surg 58:297, 2000) after several trials, because the platelet enrichment percentages we obtained using their method were very low. Complete blood counts of venous blood samples, PRP, and platelet poor plasma (PPP) were made. Statistical analyses were performed using SPSS for Windows (SPSS, Chicago, IL). RESULTS: It took approximately 30 minutes to prepare PRP with both methods. Platelet counts in PRP were increased with respect to venous blood platelet counts. The differences between the experimental groups and genders were evaluated statistically with Mann-Whitney U tests (P < .05). Correlations between the groups and genders were also evaluated (P < .05). CONCLUSION: It was experimentally shown that PRP with high platelet counts can be prepared using this modified method without the need for costly autotransfusion systems.

Effects of iron(II) salts and iron(III) complexes on trace element status in children with iron-deficiency anemia.

Iron-deficiency anemia (IDA) is the most common nutritional deficiency in childhood throughout the world. Although it has been shown that IRA is associated with elevated plasma copper and depleted zinc levels in children, there are conflicting results on the effect of iron supplementation on the absorption of these elements. The aim of this study was to investigate the effects of ferrous and ferric iron supplementation on the trace element status in children (n=25, aged 8-168 mo) with IDA. Fourteen of them were treated with ferric hydroxide-polymaltose complex (Ferrum, Vifor, Switzerland) (6 mg/d in the first 3 mo for initial therapy and 3 mg/kg for 3 mo as maintenance); the others were treated with a ferrous sulfate complex (FerroSanol, Schwarz, Germany) (6 mg/d in the first 3 mo for initial therapy and 3 mg/kg for 3 mo as maintenance). Plasma copper, zinc, and ceruloplasmin levels as well as hematological parameters were determined at baseline and the first, third, and sixth month of the treatment period. The hemoglobin and iron levels of patients in both groups were higher in the first and sixth months compared to baseline. Although the ceruloplasmin levels were depleted (48.9 mg/dL vs 41.4 mg/dL, p=0.035) during ferrous iron treatment, the copper and zinc levels remained unchanged. On the other hand, ferric iron supplementation led to an increase in zinc levels in the sixth month of treatment (0.77 mg/L vs 1.0 mg/L, p=0.021). The plasma copper levels were lower in the ferrous iron-treated group at the end of the first month of treatment than in the ferric irontreated group (1.06 mg/L vs 1.29 mg/L, p=0.008). In conclusion, our data showed that copper and ceruloplasmin metabolisms were affected by ferrous iron supplementation, whereas ferric iron kept them to normal levels of zinc, possibly by affecting their absorption. We conclude that the copper and zinc status of patients with IDA should be taken into consideration before and after iron therapy.

Contradictory effects of chlorpromazine on endothelial cells in a rat model of endotoxic shock in association with its actions on serum TNF-alpha levels and antioxidant enzyme activities.

We examined the effects of the phenothiazine derivative, chlorpromazine on thoracic aortic endothelial cell histology (14 h after LPS challenge) in a model of endotoxic shock in rats. Since excessive formation of tumor necrosis factor-alpha (TNF-alpha) and oxygen-derived free radicals contribute to endothelial injury in endotoxemia, we also evaluated the effect of the drug on the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase in liver tissue in this model and tried to find out whether this possible effect was associated with a change in serum TNF-alpha levels (measured 90 min after chlorpromazine administration). Endotoxemia was induced by a single i.p. injection of lipopolysaccharide (LPS) (5 mg kg(-1) in 1.5 ml of saline; LPS from Escherichia coli serotype 055:B5, L-2880, Sigma Chemical Company). Electron microscopic evaluation of the aortas revealed that chlorpromazine (administered 30 min prior to LPS challenge), in smaller doses (3 mg kg(-1)) ameliorated the endothelial cell injury caused by LPS, whereas it caused deterioration of endothelial cell morphology in higher doses (10 and 25 mg kg(-1)). Chlorpromazine administration caused a significant reduction in serum TNF-alpha levels, which was correlated well with an increase in SOD activity in all drug doses (3, 10 and 25 mg kg(-1)). Catalase activity was increased only in the 25 mg kg(-1) chlorpromazine group.