Antioxidant status in patients with psoriasis

Psoriasis is a chronic inflammatory skin disease with an unknown aetiology that has been associated with abnormal plasma lipid metabolism and oxidative stress. There are controversial results in the previous studies investigating oxidant/antioxidant systems in psoriasis. The aim of this work was to evaluate the plasma levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), total bilirubin (T. Bili), direct bilirubin (D. Bili), uric acid (UA), apolipoproteins (ApoA1 and ApoB), Lp(a) and activities of paraxonase 1 (PON1) in 100 patients with psoriasis and 100 controls, and to look for a correlation between these parameters in psoriasis. PON1, bilirubin and UA were measured spectrophotometrically, MDA by the high‐performance liquid chromatography method, apolipoproteins and Lp(a) by immunoprecipitation assays, and lipid and other biochemical parameters were determined by routine laboratory methods. In patients with psoriasis, there was a significant decrease in PON1, SOD and CAT activities (P < 0.05) and an increase in MDA levels (P < 0.01). Also, the levels of bilirubin (total and direct) and UA were decreased in patients with psoriasis but were not significant (P > 0.05). These results suggest that psoriasis was in a state of oxidative stress and that the protective effects of high‐density lipoprotein against atherosclerosis may be dependent on PON1 activity. Moreover, there is a negative correlation between antioxidant with Lp(a), apoB and MDA levels, suggesting that subjects with higher levels of Lp(a) and apoB and lower levels of antioxidant are more exposed to oxidative damage. These findings may explain in part the reported increase in cardiovascular mortality in psoriasis. Copyright © 2013 John Wiley & Sons, Ltd.     

The effect of hemolysis on plasma oxidation and nitration in patients with sickle cell disease

Abstract

This study aimed to determine the effect of haemolysis on plasma oxidation and nitration in sickle cell disease (SCD) patients. Blood was collected from haemoglobin (Hb)A volunteers and homozygous HbSS patients who had not received blood transfusions in the last 3 months. Haemolysis was characterised by low levels of haemoglobin and haptoglobin and high levels of reticulocyte, mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), plasma cell-free haemoglobin, bilirubin, total lactate dehydrogenase (LDH) and dominance of LDH-1 isoenzyme. Plasma 8-isoprostane, protein carbonyl and nitrotyrosine levels were measured to evaluate oxidised lipids, oxidised and nitrated proteins, respectively. Plasma nitrite–nitrate levels were also determined to assess nitric oxide (NO) production in both SCD patients and controls. Markers of haemolysis were significantly evident in SCD patients compared to controls. Plasma 8-isoprostane, protein carbonyl and nitrotyrosine levels were markedly elevated in SCD patients compared to controls. Linear regression analysis revealed a significant inverse correlation between haemoglobin and reticulocyte counts and a significant positive correlation of plasma cell-free haemoglobin with protein carbonyl and nitrotyrosine levels. The obtained data shows that increased haemolysis in SCD increases plasma protein oxidation and nitration.     

Consequences of haemolysis without haptoglobin

Abstract

Haptoglobin (Hp), a conserved plasma glycoprotein, forms very stable soluble complexes with free plasma haemoglobin. Haemoglobin binding by haptoglobin is thought to be important in the rapid hepatic clearance of haemoglobin from the plasma and in the inhibition of glomerular filtration of haemoglobin. It is thought to reduce haemoglobin-induced renal damage during haemolysis. To evaluate these functions, Hp knockout (Hp^-/-) mice were created. The Hp^-/- mouse was generated by a standard gene replacement technique in mouse embryonic stem cells. These mice were evaluated with and without haemolysis using several parameters: mortality, haemoglobin clearance, renal tissue damage and function.

Hp^-/- mice were viable but had a small, significant reduction in postnatal viability. The lack of Hp did not impair clearance of free plasma haemoglobin. Induction of severe haemolysis by phenylhydrazine caused extensive haemoglobin precipitation in the renal tubular cells. However, haemoglobin precipitation in the kidney was not increased in Hp^-/- mice. Nevertheless, Hp^-/- mice were more susceptible to phenylhydrazine with a mortality rate of 55% in Hp^-/- mice versus 18% in Hp^+/+ mice. In general, phenylhydrazine-treated Hp^-/- mice suffered greater tissue damage, as evidenced by the induction of a hepatic acute phase response, resulting in increased plasma₁-acidic glycoprotein (AGP) levels and higher plasma malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (HNE) levels. Gross pathological analysis indicated that the kidney was the most affected tissue in phenylhydrazine-treated Hp^-/- and Hp^+/+ mice, and Hp^-/- mice were more severely affected. They had lower mitotic indices in their kidneys, higher basal levels of renal lipid peroxidation, as evidenced by levels of malonaldehyde and 4-hydroxy-2(E)-nonenal (MDA/HNE) and elevated levels of 8-hydroxyguanine (but not other products of oxidative DNA damage). There also was increased induction of haem oxygenase-1. The more severe renal damage in Hp^-/- mice was also evident in the delayed erythropoietin gene expression and poorer renal clearance of [³H]-inulin. The reduction in glomerular filtration function in Hp ^+/+ and Hp^-/- mice could be restored to baseline by vasodilators (prazosin or diazoxide), implicating renal vasoconstriction as a major mechanism of acute renal failure during induced haemolysis.

These data suggest that Hp plays a pivotal role in reducing renal oxidative damage during haemolysis.     

Cytoprotective effects of the antioxidant phytochemical indicaxanthin in β-thalassemia red blood cells

Antioxidant phytochemicals are investigated as novel treatments for supportive therapy in β-thalassemia. The dietary indicaxanthin was assessed for its protective effects on human β-thalassemic RBCs submitted in vitro to oxidative haemolysis by cumene hydroperoxide. Indicaxanthin at 1.0–10 μM enhanced the resistance to haemolysis dose-dependently. In addition, it prevented lipid and haemoglobin (Hb) oxidation, and retarded vitamin E and GSH depletion. After ex vivo spiking of blood from thalassemia patients with indicaxanthin, the phytochemical was recovered in the soluble cell compartment of the RBCs. A spectrophotometric study showed that indicaxanthin can reduce perferryl-Hb generated in solution from met-Hb and hydrogen peroxide (H₂O₂), more effectively than either Trolox or vitamin C.

Collectively our results demonstrate that indicaxanthin can be incorporated into the redox machinery of β-thalassemic RBC and defend the cell from oxidation, possibly interfering with perferryl-Hb, a reactive intermediate in the hydroperoxide-dependent Hb degradation. Opportunities of therapeutic interest for β-thalassemia may be considered.     

Haptoglobin in lung defence

Abstract

Haptoglobin (Hp) has been known to be associated with the host defence response to infection and inflammation. The biological functions of Hp can be related to its ability to bind haemoglobin or to modulate immune response. Hp is expressed at a high level in lung cells, yet its protective role (s) in the lung is not known. Using transgenic mice overexpressing Hp, we demonstrated that Hp can reduce blood-induced lung injury. Hp-mediated haemoglobin catabolism in lung cells appears to be linked to iron mobilization, and may be an efficient mechanism to reduce oxidative damage associated with haemolysis.     

Bilirubin Toxicity in Hepatoma Cells

BILIRUBIN is present in toxic concentrations in foetuses and premature infants with haemolysis due to blood group incompatibility¹. Hyperbilirubinaemia in the neonate has been associated with irreversible nuclear damage in the brain and other tissues^2,3 and experimental evidence suggests that bilirubin interferes with oxidative phosphorylation^4,5. We have shown that bilirubin inhibits the growth of cells which share with developing tissues the ability to derive an appreciable part of their energy from extramitochondrial processes.     

Uric acid correlates to oxidation and inflammation in opposite directions in women

Abstract

Objective: To evaluate the association of uric acid (UA) levels with a panel of markers of oxidative stress and inflammation.

Methods: Plasma UA levels, along with a panel of oxidative stress and inflammatory markers, were measured in 755 Chinese women.

Results: Plasma UA levels were inversely associated with urinary levels of the oxidative stress marker F₂-isoprostanes and positively correlated to levels of inflammatory markers, such as C-reactive protein and some proinflammatory cytokines (tumor necrosis factor-α and interleukin-6) in blood as well as prostaglandin E₂ metabolites in urine.

Conclusions: Plasma UA levels correlate to oxidation and inflammation biomarkers in opposite directions in women.     

Bilirubin and oxidative stress in term and preterm infants

Hyperbilirubinemia is the most frequent clinical problem neonatologists must deal with during the newborn period. It has been suggested that bilirubin is involved in the balance between antioxidant and pro-oxidant agents due to its antioxidant properties. However, the relevance of these effects in vivo in term and preterm infants is still debated. We performed a literature review of studies that investigated the association between total serum bilirubin (TSB) and oxidative stress in newborn infants. We found that studies in term infants give contradictory results, while studies in preterm infants suggest that the TSB increase is associated with an oxidative stress increase due to concurrent factors other than bilirubin level, such as heme oxygenase (HO) activity. Moreover, it could be speculated that low physiologic TSB values are associated with antioxidant effects, while high pathologic TSB values are associated with pro-oxidant effects. Literature data do not allow the establishment of whether if the antioxidant properties of bilirubin are important from a clinical point of view and can affect the outcome in ill infants.     

Urinary oxidative stress markers in children with autism

Abstract

Oxidative stress caused by increased production of free radicals and impaired functions of antioxidants remains as the major factor associated with the pathophysiology of many neuropsychiatric diseases.

Objective

The objective of the present study was to analyze the oxidative stress markers in urine sample since the collection of blood from these children is highly meticulous and also to evaluate whether these urinary markers can be correlated with the severity of autism.

Methods

The subjects of the study were 45 autistic children with different grades of severity (low functioning autism (LFA), medium functioning autism (MFA), and high functioning autism (HFA) according to Childhood Autism Rating Scale (CARS), n = 15 children in each group and 50 healthy children (age and sex matched). The boys and girls ratio involved in this study was 4:1, and they were of age 4–12 years. We determined the urinary levels of oxidative stress markers like thiobarbituric acid-reacting substances, lipid hydroperoxides, 4-hydroxy nonenal, protein carbonyls, sulfhydryl groups, total antioxidant capacity, total peroxide content, oxidative stress index, and also UA/Cr ratio in autistic children.

Results

The study observed a significant elevation in the level of oxidative stress markers in autistic children when compared with normal children. The level of antioxidants excreted in urine was found to be significantly low in autistic children. These findings when correlated with the degrees of severity, oxidative stress markers showed positive correlation with increasing order of severity (LFA > MFA > HFA), whereas antioxidants showed negative correlation.

Discussion

The study reveals that the urinary levels of oxidative stress markers can be considered as the measure of oxidative stress index in autistic children. The significant correlation between the severity of autism with urinary lipid peroxidation products also support the use of oxidative stress markers and antioxidants as biomarkers of autism.     

Cross-training effect of chronic whole-body vibration exercise: a randomized controlled study

Abstract

Purpose: To determine whether unilateral leg whole-body vibration (WBV) strength training induces strength gain in the untrained contralateral leg muscle. The secondary aim was to determine the potential role of spinal neurological mechanisms regarding the effect of WBV exercise on contralateral strength training.

Materials and Methods: Forty-two young adult healthy volunteers were randomized into two groups: WBV exercise and Sham control. An isometric semi-squat exercise during WBV was applied regularly through 20 sessions. WBV training was applied to the right leg in the WBV group and the left leg was isolated from vibration. Sham WBV was applied to the right leg of participants in the Control group. Pre- and post-training isokinetic torque and reflex latency of both quadricepses were evaluated.

Results: The increase in the strength of right (vibrated) knee extensors was 9.4?±?10.7% in the WBV group (p?=?.001) and was 1.2?±?6.6% in the Control group (p?=?.724). The left (non-vibrated) extensorsvibrated) knee extensors w4?±?8.4% in the WBV group (p?=?.038), whereas it decreased by 1.4?±?7.0% in the Control (p?=?.294). The strength gains were significant between the two groups. WBV induced the reflex response of the quadriceps muscle in the vibrated ipsilateral leg and also in the non-vibrated contralateral leg, though with a definite delay. The WBV-induced muscle reflex (WBV-IMR) latency was 22.5?±?7.7?ms for the vibrated leg and 39.3?±?14.6?ms for the non-vibrated leg.

Conclusions: Chronic WBV training has an effect of the cross-transfer of strength to contralateral homologous muscles. The WBV-induced muscular reflex may have a role in the mechanism of cross-transfer strength.     

Attenuation of oxidative stress and alteration of hepatic tissue ultrastructure by D-pinitol in streptozotocin-induced diabetic rats

Abstract

The present study was aimed to investigate the effect of D-pinitol on hyperglycaemia mediated oxidative stress by analysing the hepatic antioxidant competence, pro-inflammatory cytokines and ultrastructural changes in liver tissues of streptozotocin-induced diabetic rats. Oral administration of D-pinitol (50 mg/kg b.w.) resulted in significant (p < 0.05) attenuation in blood glucose, glycosylated haemoglobin and pro-inflammatory markers such as TNF-α, IL-1β, IL-6, NF-κB p65 unit and NO and significant (p < 0.05) elevation in the plasma insulin level. In addition, D-pinitol instigated a significant escalation in the levels of hepatic tissue non-enzymatic antioxidants and the activities enzymatic antioxidants of diabetic rats with significant (p < 0.05) decrease in lipid peroxides and hydroperoxides formation, thus demonstrating the protective role of D-pinitol on the hepatic tissues from oxidative stress-induced liver damage. These biochemical observations were complemented by histological and ultrastructural examination of liver section. Thus, the present study demonstrates the hepatoprotective nature of D-pinitol by attenuating hyperglycaemia-mediated pro-inflammatory cytokines and oxidative stress.     

Alterations in neuromuscular junctions and oxidative stress of the soleus muscle of obese Wistar rats caused by vibratory platform training

Objectives:evaluate the effects that whole-body vibration (WBV) causes on the neuromuscular junctions and oxidative stress of the soleus muscle of obese Wistar rats.Methods:32 male Wistar rats were used, 16 of which were obesity induced by monosodium glutamate, randomized into four groups: control (GC), control with WBV (GCP), obese (GO) and obese with WBV (GOP). At the 70 days old, the training on WBV was started, performed 3 times a week, during 8 consecutive weeks. At the 130 days old, the animals were euthanized and the soleus muscles were collected.Results:Regarding the analysis of the neuromuscular junctions, the obese groups had lower mean size when compared to the control groups. On the other hand, the WBV presented higher averages when compared to the groups that did not perform the training. Regarding the oxidative stress, for the lipid peroxidation there was a significant difference between obese and non-obese animals, however, there was no difference between the animals WBV and those who did not.Conclusion:WBV promotes beneficial changes such as increased measurements of the structures of the neuromuscular junctions, but is not able to promote changes in the concentration of the cholinesterase enzyme in the synaptic cleft.     

The effect of hemolysis on plasma oxidation and nitration in patients with sickle cell disease

This study aimed to determine the effect of haemolysis on plasma oxidation and nitration in sickle cell disease (SCD) patients. Blood was collected from haemoglobin (Hb)A volunteers and homozygous HbSS patients who had not received blood transfusions in the last 3 months. Haemolysis was characterised by low levels of haemoglobin and haptoglobin and high levels of reticulocyte, mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), plasma cell-free haemoglobin, bilirubin, total lactate dehydrogenase (LDH) and dominance of LDH-1 isoenzyme. Plasma 8-isoprostane, protein carbonyl and nitrotyrosine levels were measured to evaluate oxidised lipids, oxidised and nitrated proteins, respectively. Plasma nitrite-nitrate levels were also determined to assess nitric oxide (NO) production in both SCD patients and controls. Markers of haemolysis were significantly evident in SCD patients compared to controls. Plasma 8-isoprostane, protein carbonyl and nitrotyrosine levels were markedly elevated in SCD patients compared to controls. Linear regression analysis revealed a significant inverse correlation between haemoglobin and reticulocyte counts and a significant positive correlation of plasma cell-free haemoglobin with protein carbonyl and nitrotyrosine levels. The obtained data shows that increased haemolysis in SCD increases plasma protein oxidation and nitration.     

Urinary heme oxygenase-1 in children with congenital hydronephrosis due to ureteropelvic junction obstruction

Context: Heme oxygenase-1 (HO-1) is implicated to be correlated with renal function in oxidative stress.

Objective: To determine whether urinary (u) HO-1 is associated with the progression of congenital obstructive hydronephrosis (HN).

Methods: A total 50 children with HN (study group and control 1) and 30 healthy children were enrolled in this study.

Results: The uHO-1/cr levels increased significantly and negatively correlated with split renal function in study group before and during surgery. One month after surgery, it decreased significantly.

Conclusion: Increased uHO-1 levels could be a potential biomarker for evaluating the progression of obstructive nephropathy.     

The common variant in the <Emphasis Type="Italic">GSTM1</Emphasis> and <Emphasis Type="Italic">GSTT1</Emphasis> genes is related to markers of oxidative stress and inflammation in patients with coronary artery disease: a case-only study

Recent studies suggest that the common variant in the GSTM1 and GSTT1 genes modifies the risk of coronary artery disease (CAD), however, it is unclear whether the risk of CAD modulated by variants in the GSTM1 and GSTT1 genes was associated with alterations of indices of oxidative stress and inflammation. Our study is an attempt to provide insight into the role of GST genetic variant and markers of oxidative stress and inflammation in CAD patients. A total of 719 Chinese CAD patients were successfully genotyped. Plasma total antioxidant status (TAOS), glutathione(GSH), C-reactive protein (CRP), fibrinogen (FIB) and white blood cell count (WBC) were determined to evaluate the oxidative stress and inflammatory response. The correlations between GSTM1/GSTT1 genotypes and alterations of indices of oxidative stress and inflammation were analyzed. We found GSTM1-0/GSTT1-0 subjects had higher CRP and FIB and lower TAOS compared to patients with wild-type GSTM1/GSTT1 genes. A stepwise elevations in age, the incidences of hypertension and diabetes mellitus, levels of FIB and the number of WBC were associated with increased number of stenosed vessels. Reductions of plasma TAOS and GSH were associated with increased number of stenosed vessels. Our results suggest that GST polymorphisms maybe modify the effect on markers of oxidative stress and inflammation in Chinese CAD patients.     

脉冲电场和磁场对高血粘和高凝血影响的比较研究

比较研究脉冲电场和脉冲磁场对高血粘和高凝血的影响,探寻降低血液粘度,抑制凝血过快、过强的物理方法.每份血样等分9份,1份作对照,对另外8份分别作不同的脉冲电场或磁场处理.结果显示不同上升沿速率的脉冲电场和磁场对高血粘和高凝血的影响程度不同,上升沿速率为2.5 × 105T s-1的脉冲磁场使全血表观粘度η降低(P＜0.01)、复钙凝血时间tr变长(P＜0.01),血块的最大剪切应力τax变小(P＜0.01).脉冲磁场作用能改善高血粘和高凝血状况.     

延髓头端腹外侧区血管升压素能机制在应激性高血粘度中的作用

观察延髓头端腹外侧区（ｒＶＬＭ）微量注射血管升压素（ＡＶＰ）能否影响正常大鼠的血压和血粘度,并分析ｒＶＬＭ内ＡＶＰ能机制在清醒大鼠经悬吊加束缚引起应激性升压反应和高血粘度中的影响。结果如下：⑴正常大鼠双侧ｒＶＬＭ微量注射ＡＶＰ（每侧０．５μｇ／０．５μｌ）,可引起血压和血粘度升高;此作用可被事先在同一位置微量注射ＡＶＰ－Ｖ１受体拮抗剂ｄ（ＣＨ２）５「Ｔｙｒ（Ｍｅ）＾２」ＡＶＰ（每侧０．１μｇ／０．     

A biomarker of tissue damage,lactate dehydrogenase,is associated with fibulin-1 and oxidative stress in blacks: the SAfrEIC study

Context: Extracellular matrix (ECM) remodeling and oxidative stress is present in hypertension and associated arterial stiffness, but little is known on the physiological link among lactate dehydrogenase (LDH), fibulin-1, and reactive oxygen species (ROS).

Objective: The objective of this study is to explore the link among a marker of tissue damage (LDH), fibulin-1 (as ECM biomarker), and ROS.

Methods: We included 316 black and 305 white South Africans and determined the above-mentioned biomarkers along with additional cardiometabolic risk factors.

Results: LDH associated positively with fibulin-1 (β?=?0.23; p?<?0.001) and ROS (β?=?0.11; p?=?0.30) in blacks only.

Conclusion: Our finding suggests that increased circulating levels of LDH may be due to early ECM remodeling and oxidative stress in blacks that are subjected to detrimental and uncontrolled lifestyle risk factors.     

Caffeic Acid Derivatives: In Vitro and In Vivo Anti-inflammatory Properties

Objective: This study examined whether, daily fruit (blueberries) consumption (250 g) for three weeks or acute fruit ingestion (250 g) would attenuate angiotensin converting enzyme (ACE) activity and reduce oxidative stress in chronic cigarette smokers.

Methods: Twenty subjects were recruited and randomized into fruit or control groups. Blood samples and blood pressure were obtained at baseline and then pre and one hour post when subjects returned to the lab three weeks later. To examine acute effects, the fruit group immediately ingested 250 g of blueberries after returning and at least one hour prior to the post blood draw. Plasma samples were analyzed for ACE activity, F₂- isoprostanes and lipid hydroperoxides (LH) as measures of oxidative stress, and ferric reducing ability of plasma (FRAP) as a measure of antioxidant potential. A 2 (treatment) × 3 (time) repeated measures ANOVA was used for statistical analysis. If interaction was significant, then Student's t-tests were used to further examine this relationship. For these comparisons, a Bonferroni adjustment was made with statistical significance set at P < 0.025.

Results: The pattern of change between treatments was not significant for any variable except LH (P < 0.001).

Conclusion: This study indicates that LH are significantly reduced by daily fruit consumption, but not affected by acute ingestion. This finding could be one way in which fruit consumption contributes to prevention of cardiovascular disease.     

Iron-deficiency anaemia enhances red blood cell oxidative stress

Oxidative stress associated with iron deficiency anaemia in a murine model was studied feeding an iron-deficient diet. Anaemia was monitored by a decrease in hematocrit and haemoglobin. For the 9 week study an increase in total iron binding capacity was also demonstrated. Anaemia resulted in an increase in red blood cells (RBC) oxidative stress as indicated by increased levels of fluorescent heme degradation products (1.24-fold after 5 weeks; 2.1-fold after 9 weeks). The increase in oxidative stress was further confirmed by elevated levels of methemoglobin for mice fed an iron-deficient diet. Increased haemoglobin autoxidation and subsequent generation of ROS can account for the shorter RBC lifespan and other pathological changes associated with iron-deficiency anaemia.