Mean Malondialdehyde Concentration Research Articles

Attenuation of oxidative injury after induction of experimental intracerebral hemorrhage in heme oxygenase–2 knockout mice

Experimental evidence suggests that hemoglobin degradation products contribute to cellular injury after intracerebal hemorrhage (ICH). Hemoglobin breakdown is catalyzed in part by the heme oxygenase (HO) enzymes. In the present study, the authors tested the hypothesis that HO-2 gene deletion is cytoprotective in an experimental ICH model. After anesthesia was induced with isoflurane, 3- to 6-month-old HO-2 knockout and wild-type mice were stereotactically injected with 15 microl autologous blood and a group of control mice were injected with an equal volume of sterile saline. Striatal protein and lipid oxidation were quantified 72 hours later using carbonyl and malondialdehyde assays. Cell viability was determined by performing a 3(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) assay. Following blood injection, the investigators found a 3.4-fold increase in protein carbonylation compared with that in the contralateral striatum in wild-type mice; in knockout mice, the investigators found a twofold increase. The mean malondialdehyde concentration in injected striata was increased twofold in wild-type mice at this time, compared with 1.5-fold in knockout mice. Cell viability, as determined by MTT reduction, was reduced in injected striata to 38 +/- 4% of that in the contralateral striata in wild-type mice, compared with 66 +/- 5% in HO-2 knockout mice. Baseline striatal HO-1 protein expression was similar in wild-type and HO-2 knockout mice, but was induced more rapidly in the former after blood injection. Deletion of HO-2 attenuates oxidative cell injury after whole-blood injection into the mouse striatum. Therapies that specifically target HO-2 may improve outcome after ICH.

Effects of Nasal Positive Airway Pressure Treatment on Oxidative Stress in Patients With Sleep Apnea-Hypopnea Syndrome

To analyze whether nasal continuous positive airway pressure (CPAP) reduces oxidative stress in patients with sleep apnea-hypopnea syndrome (SAHS). Thirty-six patients with SAHS requiring nasal CPAP treatment and 10 controls in whom SAHS was ruled out were enrolled. Oxidative stress was evaluated by measuring plasma malondialdehyde (MDA) concentrations to assess lipid peroxidation at the beginning of the study and then again after a mean (SD) of 2.9 (0.6) months of nasal CPAP. Plasma MDA concentrations were determined by measuring thiobarbituric acid reactive substances. We controlled for the following factors known to influence oxidative stress: age, sex, use of vitamin supplements, smoking habit, body mass index (kg/m2), ischemic cardiopathy, hypertension, diabetes, and hypercholesterolemia. The mean age of patients with SAHS was 51.4 (9.9) years and the mean body mass index was 32.9 (5.3) kg/m2. Nasal CPAP was titrated to a mean pressure of 8.9 (3.4) cm H2O. The mean score on the Epworth sleepiness scale was 10.2 (4.3) before treatment and 4.2 (2.8) after treatment (P<.001). The apnea-hypopnea index decreased from 43.7 (22.6) before treatment to 4 (3.5) after treatment (P<.001). Mean MDA concentrations in patients with SAHS were 2.0 (1.1) micromol/mL before treatment and decreased significantly to 1.6 (.07) micromol/mL after treatment, whereas MDA concentrations remained unchanged in control subjects. Nasal CPAP treatment significantly reduced oxidative stress in patients with SAHS in our study.

Control of Oxidant-Stress and Inflammation by Iron Chelators Deferasirox (ICL670) or Deferoxamine in β-Thalassemia: An Ancillary Study of the Novartis CICL670A0107 Trial.

Objective: We examined whether oxidant-stress and inflammation in β-thalassemia can be controlled by deferasirox as effectively as by deferoxamine (DFO) through analysis of body iron burden and biomarkers of lipid peroxidation and inflammation.Methods: Thalassemia Clinical Research Network patients participating in the Novartis CICL670A0107 trial (a randomized comparison of deferasirox, an oral iron chelator, vs. DFO) were eligible and 44 (25 male, 21.8±11.1 yrs) were enrolled in the study. Blood samples were obtainedfasting after a 5-day washout of DFO prior to commencing treatment with study drug, and24 hours post-chelator and antioxidant supplementation at 1, 6, and 12 months on study. Thirty healthy untreated controls matched for age, sex, and race (15 male, 24.5±9 yrs) were also studied.Plasma levels of malondialdehyde (MDA), a marker of lipid peroxidation, were determined by GC-MS; vitamin C by spectrophotometry; α-tocopherol by HPLC; and high-sensitivity C-reactive protein (hsCRP), a marker of inflammation, by nephelometry. In patients with thal, liver iron concentration (LIC) was analyzed by atomic absorption spectrometry and ferritin by immuno-assay. MDA, α-tocopherol, and hsCRP were log-transformed prior to analysis. Back-transformed means are reported.Results: Mean MDA concentrations (nmol/L) at 0, 1, 6, and 12 months were as follows: deferasirox: 78, 77, 46, 48; DFO: 40, 44, 37, 33. Mean MDA concentration in control subjects was 19 nmol/L (range 2–76 nmol/L). MDA was elevated in both treatment groups as compared to controls (p<.05). Mean MDA was highest prior to commencing study treatment and after 1 mo of study treatment with a significant decrease noted in both treatment groups over the course of treatment (deferasirox −27 nmol/L, DFO −12 nmol/L, p<.001 for average decline, p=.34 for difference in rate of decline). This parallels significant declines in both groups in LIC (mean 2.0 mg/g dry/yr, p=.01) and ferritin (mean 444 ng/mL/yr, p<.001). In cross-sectional analysis, MDA was positively correlated with ferritin (r2=.21, p=.06) and LIC (r2=.42, p<.001) and negatively correlated with Vitamin C (r2= −.37, p<.001) and α-tocopherol (r2= −.38, p<.001). Mean hsCRP (mg/L) at months 0, 1, 6, and 12 were as follows: deferasirox: 1.4, 2.1, 0.9, 0.6; DFO: 0.8, 1.1, 0.9, 1.2. Mean hsCRP concentration in control subjects was 0.66 mg/L (range 0.2–5.1 mg/L). In contrast with MDA trajectories, hsCRP showed significant decrease only in the group receiving deferasirox (deferasirox −1.0 mg/L, DFO +0.37 mg/L, p<.001).Conclusions: These results demonstrated a correlation of iron burden with elevated biomarkers of oxidant-stress and inflammation. Iron chelation therapy with DFO or with deferasirox showed equal effectiveness in decreasing MDA. In contrast, only therapy with deferasirox produced a significant decline in hsCRP.

Lipid Peroxidation at Various Estradiol Concentrations in Human Circulation during Ovarian Stimulation with Exogenous Gonadotropins

The aim of our study was to investigate the correlation between serum malondialdehyde levels and serum estradiol concentrations in healthy human female subjects. Nine hundred and fifty-five blood samples, from infertile women undergoing controlled ovarian hyperstimulation treatment with recombinant follicle-stimulating hormone, were collected for estradiol and malondialdehyde measurements. Five groups were formed according to serum estradiol levels: Group I (< 50 pg/ml), group II (50 - 299 pg/ml), group III (300-999 pg/ml), group IV (1000-1999 pg/ml) and group V (> or = 2000 pg/ml). One-way analysis of variance was used for comparisons. Mean malondialdehyde concentrations were 1.74 +/- 0.24 mmol/ml (group I), 1.53 +/- 0.20 mmol/ml (group II), 1.69 +/- 0.24 mmol/ml (group III), 1.77 +/- 0.21 mmol/ml (group IV) and 1.86 +/- 0.20 mmol/ml (group V), respectively. Mean serum malondialdehyde level at physiological estradiol concentrations (50-199 pg/ml, group II) was significantly (p < 0.01) lower than the mean malondialdehyde levels in other groups. Mean malondialdehyde concentrations among the remaining groups did not significantly differ. Our findings suggest that in vivo lipid peroxidation might be increased when circulating estradiol concentrations are below (< 50 pg/ml) or above (> 300 pg/ml) the physiological limits. High blood estradiol levels in human female subjects during ovarian stimulation with exogenous gonadotropins could be associated with increased serum malondialdehyde concentrations.

Comparison of malondialdehyde concentrations in different muscle areas of tench Tinca tinca L

The concentration of malondialdehyde (MDA), a marker of lipid peroxidation changes, was measured in the muscles of male and female common tench (Tinca tinca L.). Differences in MDA concentrations were determined in samples in cranio-caudal and dorso-ventral directions and in surface and deep muscle layers. Mean MDA concentration in both sexes (n=27) was 0.037 μmol g-1 tissue (wet weight), with the highest levels in the cranial segment. The difference between the cranial and other segments was significant (p < 0.05 in males andp < 0.01 in females). HigherMDAvalues were found in the cranial segment (malesp < 0.05, femalesp < 0.01), in females in ventral part of the cranio-medial segment, in males in the ventral part of the medio-caudal and dorsal parts of the caudal segment (p < 0.05). Both sexes had higher MDA levels in the ventral parts of the first three segments and in the dorsal part of the caudal segment. The results show lipid peroxidation products that may constitute a potential risk for consumers. We found that the content of these substances in tench varies with body topography. The malondialdehyde content of fresh muscle tissue in tench correlated with its content on a fat weight basis. The highest correlation was found for the dorsal part of segments in females (r = 0.9964), the lowest for ventral parts of segments in males. Quantitative distribution of MDA in body segments of the examined tench population was used as a criterion for creating types and subtypes of lipid peroxidation. Samples for hygienic analysis should include musculature from the site least stable in terms of lipid peroxidation, i.e. the cranial segment.

Solid-Phase Extraction in Malondialdehyde Analysis

Malondialdehyde (MDA) has been widely used as an index of lipoperoxidation in biological and medical sciences as well as in the food industry. A solid-phase extraction (SPE) of the condensation product of the MDA with 2-thiobarbituric acid (TBA) was developed using LiChrolut C18ec, 200 mg (Merck, Darmstadt, Germany), as a SPE cartridge and methanol as an eluent for sample pretreatment before HPLC analysis. The samples of blood plasma, platelet concentrates, or erythrocyte membranes (ghosts) were deproteinized by acetonitrile in the presence of sodium hydroxide prior to the reaction with TBA. The reaction mixture was processed using SPE. The SPE extracts (800 μL of methanol) were put to dryness and after dissolution with 100 μl of mobile phase, 50 μl was analyzed by RP-HPLC with fluorescence detection (excitation at 514 nm, emission at 556 nm). The mean MDA concentration in plasmas of 32 healthy donors was 0.37 ± 0.25 μmol/L and the mean MDA concentration in normal ghosts was 8.3 ± 4.1 pmol/μg of protein content. In the case of a patient with a severe form of β-thalassemia, the concentration of plasma MDA was raised to 1.22 μmol/L and the amount of MDA in erythrocytal ghosts was raised to 21.05 pmol/μg of protein content. MDA concentration in platelet concentrates (six bags) in the first day of storage was 0.46 ± 0.18 μmol/L and in the fifth day of storage was 0.55 ± 0.44 μmol/L.

Increased malondialdehyde in peripheral blood of patients with congestive heart failure

Malondialdehyde (MDA), a marker of lipid peroxidation, was measured in the plasma of patients with congestive heart failure (CHF) having varying degrees of clinical symptoms and in control subjects. The 53 patients studied were divided in two groups based on their left ventricular ejection fraction (LVEF). Group A consisted of 30 symptomatic patients with chronic CHF (NYHA classes II and III) and LVEF <40%. Group B consisted of 23 asymptomatic patients with LVEF >40%. Patients in group A (mean LVEF = 28) had a significantly greater history of myocardial infarction (88% vs 48%; p = 0.002) than those in group B. Group B patients and the controls had similar LVEFs (58.0 vs 62.1; p = 0.14). Neither patients in the CHF group nor group B patients showed correlation between MDA values and LVEF, unless controls were included. Mean MDA concentrations in groups A (2.65 ± 1.03 μmol/L) and B (2.1 ± 0.7 μmol/L) were significantly higher than those in the control group (1.45 ± 0.77 μmol/L; p < 0.05), supporting the hypothesis that the CHF state and underlying risk conditions appear to be associated with abnormal oxidative stress. Moreover, a significant correlation ( r = 0.74; p = 0.0001) was found in group A patients between the MDA values and the duration in years (chronicity) of the CHF state.

Serum Lipoperoxides in Induced and Spontaneous Abortions

Abortion, primarily as a measure of population control, certainly continues to be an emotional, frustrating and stressful event. In continuation of our work on stressful situations in the female life span and biochemical parameters, serum lipid peroxide levels in terms of malondialdehyde (nmol/ml) have been determined in females undergoing abortion [suction curettage (n = 30), Emcredil-induced abortion (n = 30) and spontaneous abortion (n = 40)] and were compared with appropriate gestational controls. Irrespective of the type of abortion, the serum lipid peroxide levels before abortion [mean malondialdehyde concentrations (nmol/ml): suction curettage 2.67, Emcredil-induced abortion 3.22, and spontaneous abortion 3.49] were found to be significantly elevated in comparison with those after abortion (suction curettage 1.91, Emcredil 1.97 and spontaneous abortion 1.95), indicating a maximum at peak time of stress and a minimum at the end of stress. The levels of serum lipid peroxide encountered before abortion were found to be significantly elevated in case of Emcredil-induced abortion and spontaneous abortion when compared with controls (second trimester mean levels 1.82 and first trimester 2.4) whereas the levels before suction curettage were found to be nonsignificant in comparison with controls, indicating a lesser degree of stress. It is felt that monitoring of serum lipid peroxide levels in serum and tissues (placenta), backed by scavenging enzyme superoxide dismutase, can be more helpful for corroborating safety and the risk of free radical toxicity in pregnancy and abortion.