Consumption of Mercury-contaminated Rice Induces Oxidative Stress and Free Radical Aggravation in Rats

Objective To study the oxidative stress induced by consumption of mercury-contaminated rice in rats, and to assess the possible public health risk of mercury contamination in Wanshan mining area. Methods Sprague Dawley rats were fed the mercury-contaminated rice produced from Wanshan area for 90 days. The antioxidant status and the free radicals in rat serum were evaluated. Results High mercury accumulation in organs of rats fed the mercury-contaminated rice confirmed the server pollution of mercury in Wanshan mining area. The intensity of electron spin resonance （ESR） signal increased by 87.38% in rats fed the rice from Wanshan compared with that in the control rats fed the rice from Shanghai, suggesting that chronic dietary consumption of rice from mercury mining area could induce an aggravation of free radicals. Feeding the mercury-contaminated rice was associated with significant decreases in the antioxidant enzymatic activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） and concentration of serum nitric oxide （NO）, but it had no effect on serum nitric oxide synthase （NOS） activity. Feeding the mercury-contaminated rice raised the level of serum malonyldialdehyde （MDA）, indicating the occurrence of oxidative stress. Conclusion The long-term dietary consumption of mercury-contaminated rice induces the aggravation of free radicals and exerts oxidative stress.

Oxidative Stress and Free Radical Damage in Patients With Acute Dipterex Poisoning

Objective To investigate whether acute dipterex poisoning (ADP) may cause oxidative stress and free radical damage in the bodies of acute dipterex poisoning patients (ADPPs), and to explore the mechanisms by which ADP may cause oxidative stress and free radical damage. Methods Fifty ADPPs and fifty healthy adult volunteers (HAVs) whose ages, gender and others were matched with the ADPPs were enrolled in a randomized controlled study, in which concentrations of nitric oxide (NO), vitamin C (VC), vitamin E (VE) and P-carotene (P-CAR) in plasma as well as concentration of lipoperoxide (LPO), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric analytical methods. Results Compared with the average values of experimental parameters in the HAVs group, the average values of plasma NO and erythrocyte LPO in the ADPPs group were significantly increased (P<0.0001), while those of plasma VC, VE and P-CAR as well as erythrocyte SOD, CAT, GPX and AChE in the ADPPs group were significantly decreased (P<0.0001). Bivariate correlation analysis and partial correlation analysis suggested that when NO and LPO values were increased, and VC, VE, β-CAR, SOD, CAT and GPX values were decreased in the ADPPs, AChE value was decreased gradually in the ADPPs (P<0.001-0.0001). Reliability analysis of experimental parameters reflecting oxidative stress and free radical damage in the ADPPs showed that the reliability coefficient (8 items) alpha=0.6909, and the standardized item alpha=0.8574. Conclusion The findings in the present study suggest that ADP can cause oxidative stress and free radical damage, and inhibit markedly erythrocyte acetylcholinesterase activity in ADPPs.

May Chronic Childhood Constipation Cause Oxidative Stress and Potential Free Radical Damage to Children?

Objective To investigate whether chronic childhood constipation (CCC) may cause oxidative stress and potential free radical damage to children, and to explore the mechanisms by which CCC may cause oxidative stress and potential free radical damage to chronic constipation patients (CCPs). Methods Sixty CCPs and sixty healthy child volunteers (HCVs) whose ages, gender and others were matched for the CCPs were enrolled in a randomized controlled study, in which levels of vitamin C (VC) and vitamin E (VE) in plasma as well as activities of superoxide dismutase (SOD) and catalase (CAT) in erythrocytes were determined by spectrophotometric analytical methods. Results Compared with average values of the above biochemical parameters in the HCVs group, the average values of VC and VE in plasma as well as those of SOD and CAT in erythrocytes in the CCPs group were significantly decreased (P<0.0001). Linear regression and bivariate correlation analysis showed that with prolonged course of the CCPs, the levels of VC and VE in plasma as well as the activities of SOD and CAT in erythrocytes in the CCPs were decreased gradually (P<0.0001). Conclusion The findings in the present study suggest that chronic childhood constipation causes oxidative stress and potential free radical damage to children with chronic constipation.

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy

Objective: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies. Methods: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and β-carotene (β-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric mothods. Results: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P＜0.0001), while those ofVC, VE and β-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgANP group were significantly decreased (P＜0.0001). Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those ofVC, VE, β-CAR,SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually (P＜0.0001); and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, β-CAR, SOD, CAT and GPX were decreased gradually (P＜0.005). The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgAN patients were 73.8%-92.5%, and the correct rates for the HAV were 70.0%-91.3% when independent discriminant analysis was used; and the correct rate for the IgAN patients was increased to 98.8%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. The above biochemical parameters' reliability coefficient (alpha) were used to estimate the oxidative damage of the IgAN patients as 0.8145, the standardized item alpha=0.9730, F=53273.5681, P＜0.0001. Conclusions: A series of free radical chain reactions caused serious pathological aggravation in the IgANP' bodies, thus resulting in oxidative damage in their bodies. In treating IgANP, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Oxidative stress and free radicals related diseases of the newborn

Free radicals (FRs) generation is an unavoidable consequence of the life in an oxygen-rich atmosphere. FRs can be considered a double-edged sword. Beneficial effects of FRs occur at moderate concentrations and involve physiological roles in cellular responses to noxia, as in defense against infectious agents, in the function of a number of cellular signaling pathways and the induction of a mitogenic response. The over-production of FRs and the insufficiency of an antioxidant mechanism result in oxidative stress (OS), a deleterious process and important mediator of damage to cell structures and tissues. It occurs at birth in all newborns as a consequence of the hyperoxic challenge after the transition from the hypoxic intrauterine environment to extrauterine life. During the perinatal period, OS can be magnified by others predisposing conditions such as hyperoxia, hypoxia, ischemia, hypoxia-reperfusion, inflammation and high levels of non-protein bound iron. Epidemiological studies linked OS occurring during fetal stages and early infancy with adverse health outcomes later in life, indicating that OS is an early event in the etiology of these chronic diseases. Newborns, especially if preterm, are particularly susceptible to OS and damage due to the increased generation of FRs, the lack of adequate antioxidant protection, and the inability to induce antioxidant defenses during the hyperoxic challenge at birth. This impairment of the oxidative balance has been thought to be the common factor of pathologies grouped together as “free radical disease in the neonate” that include retinopathy of prematurity (which may lead to blindness in severe cases), bronchopulmonary dysplasia (a particularly debilitating pulmonary lesion of the preterm infant), periventricular leukomalacia (an important cause of severe neurodisability) and necrotizing enterocolitis. In this review we discuss in detail these perinatal diseases. Particularly, we analyze the current knowledge about the role of OS in their pathogenesis.

Abnormal Reactions of Free Radicals and Oxidative Damages in the Bodies of Patients With Chronic Glomerulonephritis

Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.

Increased Oxidative Stress in Women With Pregnancy-induced Hypertension

Objective To investigate whether pregnancy-induced hypertension （PIH） may increase oxidative stress in women with PIH, and to explore the mechanisms by which PIH may increase oxidative stress and potential free radical damage. Methods Seventy women with PIH and seventy women with uncomplicated normotensive pregnancy （UNP） whose age, nutritional conditions, levels of hemoglobin and albumin were all matched, were enrolled in a randomized controlled trial. Their plasma concentrations of nitric oxide （NO）, vitamin C （VC）, vitamin E （VE）, and β-carotene （β-CAR） as well as their erythrocyte malondialdehyde （MDA）, and activities of superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） were determined by spcctrophotometry. Results Compared with average values of the above experimental parameters in the women with UNP, the average value of erythrocyte MDA in the women with PIH significantly increased （P〈0.0001）, while the average values of plasma NO, VC, VE, and β-CAR as well as those of erythrocyte SOD, CAT, and GPX in the women with PIH significantly decreased （P〈0.0005-0.0001）. The findings from partial correlation analysis （controlling for age） for 70 women with PIH showed that with elevated systolic blood pressure （SBP） and diastolic blood pressure （DBP）, MDA value gradually increased （P〈0.001）, and NO, VC, VE, β-CAR, SOD, CAT, and GPX values gradually decreased （P〈0.02-0.001）. The findings from reliability analysis for NO, VC, VE, β-CAR, SOD, CAT, GPX, and MDA values used to reflect increased oxidative stress and potential free radical damage in women with PIH showed that the reliability coefficients （alpha, 8 items） = 0.7062, P〈 0.0001, and the standardized item alpha = 0.9116, P〈 0.0001. Conclusion The findings in the present research suggest that pregnancy-induced hypertension can increase oxidative stress and potential free radical damage in women with pregnancy-induced hypertension.

The Effect of Mild-Pressure Hyperbaric Therapy (Oasis O₂) on Fatigue and Oxidative Stress

Mild-pressure hyperbaric therapy (mHBT) has become increasingly popular among elite athletes and most recently among the general public yet there is very little scientific underpinnings on its therapeutic use. In this study, fifteen healthy volunteers (8 men, 7 women, mean age 29.7 ± 8.1 years) were exposed to 1.3 atmospheres absolute (ATA) for 40 minutes in a mild hyperbaric chamber called “Oasis O2” to determine the effect of ambient air at 1.3 ATA on oxidative stress, antioxidant potential, fatigue, and blood chemistry. Reactive oxygen metabolites (ROMs), an index of oxidative stress, significantly reduced by 11% (p = 0.006), while biological antioxidant potential (BAP), an index of antioxidant capacity, did not show a significant change (p = 0.749). WBC count significantly reduced by 10.4% (p = 0.005) whereas WBC differential did not show a marked change. The mean visual analog scale (VAS) score for fatigue significantly decreased from 5.0 to 2.1 (p < 0.001). Our findings suggest that mild-pressure hyperbaric therapy reduces oxidative stress as indicated by a significant decrease in serum ROM, and also helps improve fatigue as seen by a significant decrease in VAS fatigue scores.

Overweight and Obesity-Induced Oxidative Stress in Children

Objective To investigate whether overweight and obesity might cause oxidative stress and potential oxidative damage in overweight and obese children, and to explore its possible mechanism. Methods Eighty-five overweight and obese children （OOC）, and eighty-five age-matched healthy children （HC） were recruited in this case-control study. The present study analyzed spectrophotometrically vitamin C （VC）, vitamin E （VE）, and β-carotene （β-CAR） in plasma, as well as the activities of superoxide dismutase （SOD）, catalase （CAT）, and the level of malondialdehyde （MDA） in erythrocytes. Results Compared with those of VC, VE, β-CAR, SOD, CAT and MDA in the HC group, the average values of VC, VE, β-CAR, SOD, and CAT in the OOC group were significantly decreased （P〈0.001）, while the average value of MDA in the OOC group was significantly increased （P〈0.001）. The regression analysis demonstrated that VC, VE, β-CAR, SOD, and CAT were negatively correlated （P〈0.05-0.01）, and MDA was positively correlated with BMI （P〈0.05）. Fitting to the model of multiple stepwise regression of BMI on VC, VE, β-CAR, SOD, CAT, and MDA in 85 OOC was Y = 27.0041 ＋ 0,2541MDA - 2.1448β-CAR -- 0.0090CAr, where F = 43.8088, P〈0.001, r = 0.7866, r^2= 0.6187, adjusted r^2= 0.6046. The findings from the reliability analysis for VC, VE, β-CAR, SOD, CAT, and MDA used to reflect increased oxidative stress and potential oxidative damage in the OOC showed that the reliability coefficients （alpha, 6 items） = 0.7231, P〈0.0001, and that the standardized item alpha = 0.9207, P〈0.0001, Conclusion The present study suggests that there exists an increased oxidative stress in overweight and obese children.

N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat

AIM: There is increasing evidence that alcohol-induced liverdamage may be associated with increased oxidative stress.We aimed to investigate free-radical scavenger effect of n-acetylcysteine in rats intragastrically fed with ethanol.METHODS: Twenty-four rats divided into three groups werefed with ethanol (6 g/kg/day, Group 1), ethanol and n-acetylcysteine (1 g/kg, Group 2), or isocaloric dextrose(control group, Group 3) for 4 weeks. Then animals weresacrificed under ether anesthesia, intracardiac blood andliver tissues were obtained. Measurements were performedboth in serum and in homogenized liver tissues.Malondialdehyde (MDA) level was measured by TBARSmethod. Glutathione peroxidase (GSH-Px) and superoxidedismutase (SOD) levels were studied by commercial kits.Kruskal-Wallis test was used for statistical analysis.RESULTS: ALT and AST in Group 1 (154 U/Land 302 U/L,respectively) were higher than those in Group 2 (94 U/L and155 U/L) and Group 3 (99 U/L and 168 U/L) (P＝0.001 forboth). Serum and tissue levels of MDA in Group 1 (1.84 nmol/mL and 96 nmol/100 mg-protein) were higher than Group 2(0.91 nmol/mL and 64 nmol/100 mg-protein) and Group 3(0.94 nmol/mL and 49 nmol/100 mg-protein) (P＜0.001 forboth). On the other hand, serum GSH-Px level in Group 1(8.21 U/g-Hb) was lower than Group 2 (16 U/g-Hb) andGroup 3 (16 U/g-Hb) (P＜0.001). Serum and liver tissue levelsof SOD in Group 1 (11 U/mL and 26 U/100 mg-protein)were lower than Group 2 (18 U/mL and 60 U/100 mg-protein)and Group 3 (20 U/mL and 60 U/100 mg-protein) (P＜0.001for both).CONCLUSION: This study demonstrated that ethanol-induced liver damage is associated with oxidative stress,and co-administration of n-acetylcysteine attenuates thisdamage effectively in rat model.

Overexpression of heme oxygenase-1 protects smooth muscle cells against oxidative injury and inhibits cell proliferation

To investigate whether the expression of exogenous heme oxygenase-1 (HO-1) gene within vascular smooth muscle cells (VSMC) could protect the cells from free radical attack and inhibit cell proliferation, we established an in vitro transfection of human HO-1 gene into rat VSMC mediated by a retroviral vector. The results showed that the profound expression of HO-1 protein as well as HO activity was 1.8- and 2.0-fold increased respectively in the transfected cells compared to the non-transfected ones. The treatment of VSMC with different concentrations of H2O2 led to the remarkable cell damage as indicated by survival rate and LDH leakage. However, the resistance of the HO-1 transfected VSMC against H2O2 was significantly raised. This protective effect was dramatically diminished when the transfected VSMC were pretreated with ZnPP-IX, a specific inhibitor of HO, for 24 h. In addition, we found that the growth potential of the transfected cells was significantly inhibited directly by increased activity of HO-1, and this effect might be related to decreased phosphorylation of MAPK. These results suggest that the overexpression of introduced hHO-1 is potentially able to reduce the risk factors of atherosclerosis, partially due to its cellular protection against oxidative injury and to its inhibitory effect on cellular proliferation.

Acute effect of aspartame-induced oxidative stress in Wistar albino rat brain

The present study was carried out to investigate the acute effect of aspartame on oxidative stress in the Wistar albino rat brain. We sought to investigate whether acute administration of aspartame （75 mg/kg） could release methanol and induce oxidative stress in the rat brain 24 hours after administration. To mimic human methanol metabolism, methotrexate treated rats were used to study aspartame effects. Wistar strain male albino rats were administered with aspartame orally as a single dose and studied along with controls and methotrexate treated controls. Blood methanol and formate level were estimated after 24 hours and rats were sacrificed and free radical changes were observed in discrete regions by assessing the scavenging enzymes, reduce dglutathione （GSH）, lipid peroxidation and protein thiol levels. There was a significant increase in lipid peroxidation levels, superoxide dismutase activity （SOD）, glutathione peroxidase levels （GPx）, and catalase activity （CAT） with a significant decrease in GSH and protein thiol. Aspartame exposure resulted in detectable methanol even after 24 hours. Methanol and its metabolites may be responsible for the generation of oxidative stress in brain regions. The observed alteration in aspartame fed animals may be due to its metabolite methanol and elevated formate. The elevated free radicals due to methanol induced oxidative stress.

Protective role of buffalo pineal proteins on arsenic-induced oxidative stress in blood and kidney of rats

Objective: Exposure to various toxic metals has become an increasingly recognized source of ill- ness in human and animals, worldwide. Arsenic (As) and its compounds cause adverse health effects in animals and humans. Recently, it has been suggested that the pineal gland may also have antioxidants role due to secretary product other than melatonin. With keeping this view, pre-sent investigation tested effect of buffalo (Bubalus bubalis) pineal proteins (PP) on arsenic-induced oxidative stress in RBCs (Red blood cells) and kidney of rats. Methods: Eighteen adult female Wistar rats were grouped into group-I (Control), group-II (Arsenic control), and group-III (Arsenic + Pineal proteins). Experimental rats were given 100 ppm arsenic (p.o.) for 4 weeks alone or along with pineal proteins at a dose of 100 μg/kg body weight (i.p.). Results: Interestingly, arsenic ex-posure led to the stimulation of kidney catalase (CAT) activity, but inhibition of RBCs CAT activ-ity and significantly (P<0.05) increased the RBCs and kidney lipid peroxidation level (LPO). How-ever, arsenic treatment caused depletion of glu- tathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) in kidney tissues. In RBCs, only GR and CAT activity were significantly (P<0.05) declined. These changes were significantly (P<0.05) reversed by PP treatment in arsenic exposed animals. Conclusion: Therefore, present study indicated the significant protecting effect of buf-falo (Bubalus bubalis) PP against arsenic in-duced-oxidative stress through antioxidant de-fense systems in rats.

Influence of 10-(6-plastoquinonyl) decyltriphenylphosphonium on free-radical homeostasis in the heart and blood serum of rats with streptozotocin-induced hyperglycemia

BACKGROUND It is known that under conditions of tissue tolerance to insulin,observed during type 2 diabetes mellitus(DM2),there is an increased production of reactive oxygen species.Moreover,the free radicals can initiate lipid peroxidation(LPO)in lipoprotein particles.The concentration of LPO products can influence the state of insulin receptors,repressing their hormone connection activity,which is expressed as a reduction of the glucose consumption by cells.It is possible that reduction in glucose concentration during administration of 10-(6-plastoquinonyl)decyltriphenylphosphonium(SkQ1)to rats with DM2 may be related to the antioxidant properties of this substance.AIM To establish the influence of SkQ1 on free-radical homeostasis in the heart and blood serum of rats with streptozotocin-induced hyperglycemia.METHODS To induce hyperglycemia,rats were fed a high-fat diet for 1 mo and then administered two intra-abdominal injections of streptozotocin with a 7-d interval at a 30 mg/kg of animal weight dose with citrate buffer equal to pH 4.4.SkQ1 solution was administered intraperitoneally at a 1250 nmol/kg dose per day.Tissue samples were taken from control animals,animals with experimental hyperglycemia,rats with streptozotocin-induced glycemia that were administered SkQ1 solution,animals housed under standard vivarium conditions that were administered SkQ1,rats that were administered intraperitoneally citrate buffer equal to pH 4.4 once a week during 2 wk after 1-mo high-fat diet,and animals that were administered intraperitoneally with appropriate amount of solution without SkQ1(98%ethanol diluted eight times with normal saline solution).To determine the intensity of free radical oxidation and total antioxidant activity,we used the biochemiluminescence method.Aconitate hydratase(AH),superoxide dismutase,and catalase activities were estimated using the Hitachi U-1900 spectrophotometer supplied with software.The amount of citrate was determined by means of the Natelson method.Real-time polymerase chain reaction was carried out using an amplifier ANK-32.RESULTS It was found that the mitochondrial-directed antioxidant elicits decrease of biochemiluminescence parameter values that increase by pathology as well as the levels of primary products of LPO,such as diene conjugates and carbonyl compounds,which indicate intensity of free radical oxidation.At the same time,the activity of AH,considered a crucial target of free radicals,which decreased during experimental hyperglycemia,increased.Apparently,increasing activity of AH influenced the speed of citrate utilization,whose concentration decreased after administering SkQ1 by pathology.Moreover,the previously applied antioxidant during hyperglycemia influenced the rate of antioxidant system mobilization.Thus,superoxide dismutase and catalase activity,as well as the level of gene transcript under influence of SkQ1 at pathology,were changing to the direction of control groups values.CONCLUSION According to the results of performed research,SkQ1 can be considered a promising addition to be included in antioxidant therapy of DM2.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.

Oxidative Stress in Patients With Acute Coxsackie Virus Myocarditis

Objective To study the state of oxidative stress in patients with acute coxsackie virusmyocarditis (ACM), and to investigate the pathological chain reactions of a series of freeradicals and oxidative and lipoperoxidative damages in their bodies. Methods Eighty ACMpatients and 80 healthy adult volunteers (HAV) were enrolled in a case-control study, inwhich concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma andLPO in erythrocytes (RBC), vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) inplasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathioneperoxidase (GSH-Px) in RBC were determined by using spectrophotometric assays. ResultsCompared with the average values (AV) of the above biochemical parameters (BP) in theHAV group, the AV of NO in plasma, and LPO in plasma and RBC in the ACM group weresignificantly increased (P=0.0001), while the AV of VC, VE, b-CAR, SOD, CAT and GSH-Px in the ACM group were significantly decreased (P=0.0001). The values of the above BPwere used to estimate the relative risk ratio (RR) between the ACM group and the HAVgroup; the RR and its 95 % confidence interval were 12.467 (5.745~27.051), 4.333(2.126~8.834), 6.517 (3.225~13.618), 3.310 (1.598~6.858), 31.000 (12.611~76.201),4.663 (2.228~9.759), 11.769 (5.440~25.462), 3.043 (1.486~6.229) and 6.594 (3.045~14.281)respectively, and their P levels ranged from 0.002 to 0.0001. The results were asfollows: D = 22.143 - 0.017SOD + 0.008NO + 0.244LPO in RBC, Eigenvalue = 13.659,Canonical correlation = 0.965, Wilks’λ= 0.068, c2 = 420.212, P = 0.0001. The correct rateof discrimination to the ACM group and to the HAV group was 87.5% and 95.0 %, respectively,and 91.3 % of originally grouped cases was correctly classified. Conclusion The findingsin this study suggested that the oxidative stress in bodies of ACM patients was severelyaggravated, and marked high oxidative constituents and low antioxidants and antioxidasesin the human body might increase the relative risk of inducing acute coxsackie virusmyocarditis, and measuring the values of NO in plasma, SOD and LPO in RBC mightincrease the correct rates of discriminatory analysis of the ACM.

3,4-Methylenedioxymethamphetamine(MDMA)Abuse Markedly Inhibits Acetylcholinesterase Activity and Induces Severe Oxidative Damage and Liperoxidative Damage

Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. Methods 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. Results Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P<0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P<0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P<0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P<0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453. Conclusion The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.

Increased Oxidative Stress and Damage in Patients With Chronic Bacterial Prostatitis

Objective To investigate whether chronic bacterial prostatitis （CBP） increases oxidative stress and damage in patients with CBP, and to explore its possible mechanism. Methods Eighty patients with CBP and 80 healthy adults as controls were enrolled in a case-control study, in which levels of nitric oxide （NO）, vitamin C （VC）, and vitamin E （VE） in plasma, as well as malondialdehyde （MDA）, activities of superoxide dismutase （SOD）, and eatalase （CAT） in erythrocytes were determined by spectrophotometry. Results Compared with the average values of NO, VC, VE, MDA, SOD, and CAT in the healthy control group, those of plasma N O and erythrocyte MDA in the CBP group were significantly increased （P〈0.00 1）, and those of plasma VC and VE as well as erythrocyte SOD and CAT in the CBP group were significantly decreased （P〈0.001）. Findings from partial correlation analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in 80 patients with CBP, adjusted for age, suggested that with prolonged course of the disease, values of NO and MDA were gradually increased （P〈0.001）, and those of VC, VE, SOD, and CAT were gradually decreased （P〈0.05-0.001）. The findings from stepwise regression analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in CBP group suggested that the model of stepwise regression was Y = -19.1160 ＋0.3112MDA ＋ 0.0337NO, F = 22.1734, P〈0.001, r = 0.6045, P〈0.001. The findings from the reliability analysis for VC, VE, SOD, CAT, NO, and MDA in the CBP group showed that the reliability coefficients＇ alpha （6 items） was 0.7195, P〈0.0001, and the standardized item alpha was 0.9307, P〈0.0001. Conclusion There exist increased oxidative stress and damage induced by chronic bacterial prostatitis in patients, and such a phenomenon is closely related to the course of disease.

Reduced antioxidant level and increased oxidative damage in intact liver lobes during ischaemia-reperfusion

AIM： To determine whether increased blood flow of the liver can cause oxidative stress and hepatocyte damage, and to elaborate methods suitable for measuring the antioxidant defence during hepatic surgery on rat model.METHODS： In nembutal narcosis, the left lateral and the medial lobes of the liver were clipped for 45 rain to make the total blood supply flow through the other lobes. Total antioxidant status, glutathione peroxidase and superoxide dysmutase activity, as well as the concentrations of diene conjugates and free sulphydril groups, H-donating ability and reducing power of the liver samples were determined. Chemiluminescent intensity of the liver was also measured. Metal ions （Al, Ca, Cu, Fe, Mg, Mn, Zn） and P and S concentrations of the liver were determined with an inductively coupled plasma optical emission spectrometer and Se content was measured by cathodic stripping voltammetry.RESULTS： Glutathione peroxidase and superoxide dysmutase activities of the liver decreased significantly in the hyperemia group compared to those observed in the sham operated group. The level of total antioxidant status was also significantly lower in the hyperemia group. H-donating ability, reducing power and free sulphydril group concentration showed the same tendency. A significant correlation （P〈0.05） was found between the changes in non-specific antioxidant activities. This pointed to simultaneous activity of the antioxidant defence system. Al, Cu, Mn, Zn, and S were lower in the hyperemia group than in the sham operated group when the levels of Ca, Fe, Mg, Se and P ions were higher during hyperemia.CONCLUSION： Oxidative stress is one of the main factors for the injury of intact liver lobes during ischaemia-reperfusion.

Protective effect of low dose of melatonin against cholestatic oxidative stress after common bile duct ligation in rats

AIM: To investigate the role of oxidative injury and the effect of exogenous melatonin administration on liver damage induced by bile duct ligation (BDL), and second, to evaluate the role of nitric oxide (NO), a free oxygen radical, in oxidative injury. METHODS: Thirty-two Sprague-Dawley rats were assigned to four groups: sham operation (SO), BDL, BDL+melatonin, and BDL+vehicle. Cholestasis was achieved by double ligature of the common bile duct. Melatonin was injected intraperitoneally 500 μg/(kg·d) for 8 d. Hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA), and reduced GSH. Total nitrite (NOx) concentrations were determined in hepatic homogenates. Histopathological examination was performed using a histological scoring system. RESULTS: The histopathological changes including portal inflammation, necrosis,apoptosis, focal inflammation and fibrosis were severe in the BDL and BDL+vehicle groups. There were numerous large areas of coagulation necrosis. Histological Activity Index scores of these groups were significantly higher than that of the SO group. Treatment with melatonin reduced these alterations significantly. The degree of necro-inflammation and fibrosis showed significant difference between the BDL and BDL+melatonin groups. BDL was accompanied by a significant increase in MDA and NOx, and a significant decrease in GSH levels. Mean±SE values of MDA, GSH and NOx levels of SO group were 147.47±6.69, 0.88±0.33 μmol/g and 180.70±6.58 nm/g, respectively. The values of BDL group were 200.14±21.30, 0.65±0.02 μmol/g, and 400.46±48.89 nm/g, respectively, whereas the values of BDL+melatonin group were 115.93±6.8,0.74±0.02 μmol/g, and 290.38±32.32 nm/g, respectively. Melatonin treatment was associated with a significant recovery of MDA, GSH and NOx levels. CONCLUSION: We have concluded that oxidative stress is associated with the pathogenesis of cholestatic liver damage and NO contributes to oxidative damage. Melatonin, even at low dose, is an efficient agent in reducing negative parameters of cholestasis.