OBJECTIVETo examine changes of blood oxidative-antiovidative level in schizophrenic patients and its relationship with clinical symptoms.

METHODSForty-six Chinese patients met DSM-IV (Diagnostic and Statistical Manual of Mental Disorders-IV) criteria for schizophrenia and fifty age- and sex-matched healthy controls were enrolled in the present study. Baseline psychiatric symptom severity was assessed with brief psychiatric rating scale, positive and negative syndrome scale on the blood draw day. Fresh blood samples were collected to measure levels of nitric oxide and lipid peroxide in plasma as well as activities of superoxide dismutase, catalase and glutathione peroxidase in red blood cells by spectrophotometric assays simultaneously.

RESULTSComparison of the biochemical parameters indicated that the level of nitric oxide and lipid peroxide increased in patient group, which represented a positive correlation with positive scale scores; while the activities of three critical enzymes decreased and showed a negative linear correlation.

CONCLUSIONThis study showed that there are dysregulation of free radical metabolism and poor activities of the antioxidant defense systems in schizophrenic patients. Excess free radicals formation may play a critical role in the etiology of schizophrenia. Using antioxidants might be an effective therapeutic approach to partially alleviate or prevent the symptoms of schizophrenia.

Adolescent ; Adult ; Antioxidants ; metabolism ; Female ; Free Radicals ; Humans ; Lipid Peroxides ; metabolism ; Male ; Middle Aged ; Nitric Oxide ; metabolism ; Schizophrenia ; etiology ; metabolism

OBJECTIVETo observe effects of ginsenoside-Rb (G-Rb) on total cholesterol, lipoprotein cholesterol metabolism and anti-oxidation in experimental hyperlipidemia rats.

METHODHyperlipidemia rats were respectively given G-Rb 50, 100, 200 mg x kg(-1) x d(-1) ig for twelve days. Total cholesterol, lipoprotein cholesterol and lipid peroxidation (LPO) contents, prostacycline (PGI2), thromboxane (TXA2), superoxide dismutase (SOD) and blood viscosity were measured. Fat accumulation in liver was also observed.

RESULTTriglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-c) in serum, TXA2 in plasma, LPO in serum and liver, and blood viscosity were decreased significantly. High density lipoprotein cholesterol (HDLc) in serum, PGI2 in plasma and SOD in serum and liver were significantly increased by G-Rb (100, 200 mg x kg(-1)) in experimental hyperlipidemia rats. In addition, G-Rb could decrease TC/HDL-c, LDLc/HDL-c ratio, increase PGI2/TXA2 ratio and inhibit fat accumulation in liver.

CONCLUSIONG-Rb could have anti-arteriosclerosis effect by improving cholesterol and lipoprotein-cholesterol metabolism, suppressing lipid peroxidation, increasing anti-oxidase activity and PGI2/TXA2 ratio.

Animals ; Antioxidants ; pharmacology ; Female ; Ginsenosides ; pharmacology ; Hyperlipidemias ; metabolism ; Lipid Peroxides ; metabolism ; Liver ; metabolism ; Male ; Rats ; Rats, Wistar

Using lipid bilayer reconstitution technique, we investigated the oxidation effect of t-butyl hydrogen peroxide (tBHP) on the single channel activity of the sarcoplasmic reticulum (SR) calcium release channels isolated from canine latissimus dorsi muscles. When 0.7% tBHP was added in the cytosolic side, the channel activity became suppressed (n = 7), and it was recovered by changing the solution to the control solution. The suppression was due to the change in the gating mode of the channel: before tBHP the channel opened to four sub-conductance levels, but it opened to only one level after tBHP. These effects by tBHP were different from the previous finding using hydrogen peroxide (H2O2), which may be explained by different oxidation patterns between the two oxidants.
Animal ; Calcium Channels/drug effects* ; Dogs ; Hydrogen Peroxide/pharmacology ; Peroxides/pharmacology* ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum/drug effects* ; tert-Butylhydroperoxide

The Protective effect of vitamin E and selenium against peroxidative damage in white blood cells was studied. Forty-eight male rats (~100g BW) were divided into four groups and were fed with a torula yeast based diet deficient in Vit.E and Se. Vit.E (100IU/Kg diet) and Se (0.3ppm) supplementation increased the total peritoneal cell (P.C) population and cell survival rate. Selenium supplementation decreased the hydrogen peroxide generation (half of the control) significantly and Vit.E supplementation reduced the malonaldehyde production during phagocytosis in vitro. However, superoxide generation was not affected by the supplementation of Vit.E or Se. There were no significant differences in catalase activity between groups but glutathione peroxidase activity was increased about twofold by Se supplementation with no effect of Vit.E. In a separate experiment, activated alveolar macrophages were obtained from BCG infected rabbits fed a diet supplemented with Vit.E (100 IU/Kg diet) or Se (0.3 ppm). Se supplementation increased glutathione peroxidase in cells, and both Vit.E and Se increased the cell survival rate during phagocytosis as compared to the control. Both Vit.E and Se are necessary to protect host cells from peroxidative damage during phagocytosis.
Animal ; Macrophages/drug effects ; Macrophages/physiology* ; Male ; Peroxides/metabolism* ; Phagocytosis/drug effects* ; Rats ; Selenium/pharmacology* ; Vitamin E/pharmacology*

OBJECTIVETo observe clinical therapeutic effect of head point-through-point electroacupuncture on Parkinson's disease and the mechanism.

METHODSSeventy-six cases of Parkinson's disease were randomly divided into a treatment group (n=37) treated with head point-through-point electroacupuncture and oral administration of madopa, and a control group (n=39) with only oral administration of madopa. Superoxide dismutase (SOD) and lipids peroxides (LPO) were determined before and after treatment.

RESULTSThe effective rate was 97.3% in the treatment group and 61.5% in the control group with a very significant difference between the two groups (P < 0.01). SOD activity and LPO content were significantly improved after treatment in the treatment group (P < 0.01), with a significant difference between the two groups (P < 0.01).

CONCLUSIONHead point-through-point electroacupuncture can improve SOD activity and LPO content in the body so as to cure Parkinson's disease.

Acupuncture Points ; Adult ; Aged ; Electroacupuncture ; methods ; Female ; Head ; Humans ; Lipid Peroxides ; analysis ; Male ; Middle Aged ; Parkinson Disease ; metabolism ; therapy ; Superoxide Dismutase ; metabolism

Aging ; physiology ; Animals ; Catalase ; metabolism ; Circadian Rhythm ; Free Radicals ; metabolism ; Lipid Peroxides ; metabolism ; Male ; Melatonin ; metabolism ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Thymus Hormones ; pharmacology

PURPOSE: Apoptosis is known to be induced either by direct oxidative damage from oxygen free radicals or hydrogen peroxide, or from their generation in cells by injurious agents. Peroxiredoxin plays an important role in eliminating peroxides generated during metabolism. The aim of this study is to elucidate the role of Prx (peroxiredoxin) enzymes during the cellular response to oxidative stress. METHODS: The presence of Prx isoforms was demonstrated by immunoblot analysis using Prx isoforms-specific antibodies, and RT-PCR using Prx isozyme coding sequences. Annexin V-FITO apoptosis detection method was used to measure the cell death following exposure to H2O2. RESULTS: Treatment of MCF7 cell lines with H2O2 resulted in the dose-dependent expression of Prx I and II. Observed decreases in the mRNA expressions of Prx I and II, analyzed by RT-PCR, correlated well with the results of immunoblot analysis. The treatment of normal breast cell line, MCF10A, with H2O2 resulted in rapid cell death, while the breast cancer cell line, MCF7, was resistant. In addition, we confirmed that Prx I and II transfected MCF10A cells were more prone to cell death than MCF10A transfected with vector alone, after H2O2 treatment. CONCLUSION: These findings suggest that Prx I and II have an important function as inhibitors of cell death during the cellular response to oxidative stress.
Antibodies ; Apoptosis* ; Breast ; Breast Neoplasms ; Cell Death ; Cell Line ; Clinical Coding ; Free Radicals ; Hydrogen Peroxide ; MCF-7 Cells* ; Metabolism ; Oxidative Stress ; Oxygen ; Peroxides ; Peroxiredoxins ; Protein Isoforms ; RNA, Messenger

This study was performed to investigate the age-related changes of the lipid metabolism and thrombogenic capacity in Sprague-Dawley (SD) rats at the ages of 4, 8, 12, 16, 20 and 24 months old. Total lipid, triglyceride (TG) and total cholesterol in plasma and liver, HDL-cholesterol concentration, and eicosanoid contents in plasma were measured. Lipid peroxides were determined by the levels of thiobarbituric acid reactive substance (TBARS) in LDL fraction. Body weight was increased continuous until 16 months and decreased after 20 months. Epididymal fat pad (EFP) weight was increased continuously until 20 months and decreased at 24 months. Total lipid and TG concentrations in plasma were increased until 20 months and then rapidly decreased at 24 months but plasma cholesterol was increased continuously with aging. HDL-cholesterol level was increased continuously until 12 months, but decreased at 16 months and maintained there after. The TBARS levels in LDL fraction were the highest level at 24 months. Liver total lipid, TG, and total cholesterol concentrations were shown a tendency to increase with aging, and especially TG concentration was increased rapidly from 12 months to 16 months. Plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 (6-keto-PGF1) contents did not change with aging, but the ratio of TXB2/6-keto-PGF1 was increased with aging, especially from 8 to 12 months. These results showed that lipid levels in plasma and liver, TBARS levels in LDL fraction, and TXB2/6-keto- PGF1 ratio were increased with aging.
Adipose Tissue ; Aging ; Animals ; Body Weight ; Child, Preschool ; Cholesterol ; Humans ; Lipid Metabolism* ; Lipid Peroxides ; Liver ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Thiobarbituric Acid Reactive Substances ; Thromboxane B2 ; Triglycerides

OBJECTIVETo investigate the plasma levels of ascorbic acid and vitamin E in patients with liver cirrhosis and to explore their significance.

METHODSThe plasma levels of ascorbic acid,vitamin E and lipoperoxides in patients with liver cirrhosis were measured, and the results were compared with those of sex-and age-matched healthy subjects.

RESULTThe plasma levels of ascorbic acid, vitamin E and lipoperoxides in the patients group were (42.94 +/-6.99)micromol/L, (17.99 +/-3.51)micromol/L and (14.09 +/-1.28)micromol/L, respectively, while those in the control group were (53.30 +/-9.45)micromol/L (t=9.50, P=0.000), (24.59 +/-7.22)micromol/L (t=7.94, P=0.000) and (12.11 +/-1.20)micromol/L (t=17.21, P=0.000), respectively.

CONCLUSIONThe levels of ascorbic acid and vitamin E in patients with liver cirrhosis decrease significantly,which may indicates the disturbance of balance between oxidation and antioxidation.

Adult ; Aged ; Aged, 80 and over ; Ascorbic Acid ; blood ; Female ; Humans ; Lipid Peroxides ; blood ; Liver Cirrhosis ; blood ; metabolism ; Male ; Middle Aged ; Vitamin E ; blood

Heme oxygenase-1 (HO-1) has been described as an inducible protein that is capable of cytoprotection via radical scavenging and the prevention of apoptosis. Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, and this process has been termed glucose toxicity. Yet little is known about the relation between glucose toxicity and HO-1 in the islets. The purposes of the present study were to determine whether prolonged exposure of pancreatic islets to a supraphysiologic glucose concentration disrupts the intracellular balance between reactive oxygen species (ROS) and HO-1, and so this causes defective insulin secretion; we also wanted to evaluate a protective role for HO-1 in pancreatic islets against high glucose levels. The intracellular peroxide levels of the pancreatic islets (INS-1 cell, rat islet) were increased in the high glucose media (30 mM glucose or 50 mM ribose). The HO-1 expression was induced in the INS-1 cells by the high glucose levels. Both the HO-1 expression and glucose stimulated insulin secretion (GSIS) was decreased simultaneously in the islets by treatment of the HO-1 antisense. The HO-1 was upregulated in the INS-1 cells by hemin, an inducer of HO-1. And, HO-1 upregulation induced by hemin reversed the GSIS in the islets at a high glucose condition. These results suggest HO-1 seems to mediate the protective response of pancreatic islets against the oxidative stress that is due to high glucose conditions.
Reactive Oxygen Species ; Rats, Wistar ; Rats ; Peroxides/metabolism ; Oxidative Stress ; Male ; Islets of Langerhans/*metabolism ; Insulin/secretion ; Hemin/metabolism ; Heme Oxygenase-1/metabolism/*physiology ; Glucose/metabolism/*pharmacology ; *Gene Expression Regulation ; Flow Cytometry ; Animals