Oxidative damage of dust storm fine particles instillation on lungs,hearts and livers of rats

The purpose of this study was to investigate the effects of dust storm fine particles (PM_2.5) on oxidative damage in lungs, hearts and livers of rats. Wistar rats were randomly divided into treated groups using PM_2.5 at different concentration (1.5, 7.5, 37.5 mg/kg) and control groups using saline. After a single intratracheal instillation 24 h, rats were sacrificed and activities of Cu,Zn-superoxide dismutase (SOD), levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) were investigated in these three organs of rats. Results show that dust storm PM_2.5 and normal weather PM_2.5 from both Baotou city and Wuwei city caused a dose-dependent decrease of SOD activities and GSH contents in lungs and livers, and a dose-dependent increase of TBARS levels in lungs, hearts and livers of rats as compared to their respective controls. Though the effects induced by normal weather PM_2.5 slightly heavier than dust storm PM_2.5 in both Baotou city and Wuwei city on each examined index, no significant difference was found. Furthermore, no significant difference was observed between the effects induced by dust storm PM_2.5 from Baotou city and that from Wuwei city, or between the effects induced by normal weather PM_2.5 from Baotou city and that from Wuwei city. These results lead to conclusions that both dust storm PM_2.5 and normal weather PM_2.5 could lead to oxidative damage of different disagrees in lungs, hearts and livers, suggesting that the dust storm PM_2.5 whose airborne mass concentrations were much higher should be more harmful. Its toxic effects might be attributed to oxidative damage mediated by pro-oxidant/antioxidant imbalance or excess free radicals. Further work is required to understand the toxicological role of dust storm PM_2.5 on multiple or even all organs in mammals.     

Evaluation of micronucleus induction of sand dust storm fine particles (PM(2.5)) in human blood lymphocytes

Sand dust storms are common phenomena in the arid and semi-arid regions. Previous studies have demonstrated that the airborne air fine particulate matter (PM_2.5, particulates with an aerodynamic diameter ≤2.5 μm) and its extracts can induce human genetic damage of lymphocytes such as micronucleus formation, chromosomal aberration and so on. However, little is known about the health risks associated with sand dust storm PM_2.5 and its extracts. The aim of the present study is to investigate the micronucleus induction of sand dust storm PM_2.5 (include its organic and inorganic extract) from two different towns on human lymphocytes. The samples of normal PM_2.5 and sand dust storm PM_2.5 were collected in Wuwei (Gansu Province) and Baotou (Inner Mongolia), China. The cytochalasin-B cytokinesis-block test was employed and the cells were treated with 0, 33, 100, 300 μg ml⁻¹ sand dust storm PM_2.5 or normal ambient air PM_2.5 suspension (physiological saline as solvent control), or inorganic extract (0, 75, 150, 300 μg ml⁻¹, physiological saline as solvent control) or organic extract (0, 20, 40, 80 μg ml⁻¹, DMSO as solvent control) at the beginning of the cell culture. Both sand dust storm and normal PM_2.5 and their extract treatment cultures revealed an increase in the frequency of micronucleus. With the increase of treatment concentrations the frequency of micronucleus increased and the nuclear division index (NDI) values declined in a dose–response manner (P < 0.01). In the same concentrates, the frequency of micronucleus of normal ambient air PM_2.5 and its extract were significant higher than those of sand dust storm PM_2.5 (P < 0.01) except the treatment of Wuwei sample at higher doses, the treatment of inorganic extract of PM_2.5 at the highest dose (300 μg ml⁻¹) and the treatment of organic extract of PM_2.5 at the higher dose (40 and 80 μg ml⁻¹) either in Baotou or in Wuwei (P > 0.05). The toxicity of sand dust storm PM_2.5 and its extract at high dose is very potent. The frequency of micronucleus of normal PM_2.5 (include its organic extract) from Baotou were higher than those of Wuwei especially in low and middle dose (P < 0.05), but the treatment results of sand dust storm PM_2.5 (include its all extract) was not significantly different between the towns (P > 0.05).     

Damage effects of dust storm PM2.5 on DNA in alveolar macrophages and lung cells of rats.

The aim of the present study was to investigate in vitro toxicological effects of PM2.5 suspensions, their water-soluble fraction and solvent-extractable organics from dust storm on the viability and DNA of rat alveolar macrophages and in vivo toxicological effects of PM2.5 suspensions on DNA of lung cells of rats. PM2.5 samples from dust storm and normal weather were collected in Baotou city, Inner Mongolia Autonomous Region, and Wuwei city, Gansu Province, China, in March, 2004. DNA damage was detected with single cell gel electrophoresis technique and cytotoxicity was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay. The results showed that: (1) In vitro, PM2.5 suspensions, their water-soluble fraction and solvent-extractable organics from both dust storm and normal weather caused a decrease of the cell viability and an increase of DNA damage of rat alveolar macrophages in a dose-response manner; for both Baotou city and Wuwei city, the samples of normal weather showed higher DNA damage than those of dust storm at the highest treated dosage; for both normal weather PM2.5 and dust storm PM2.5, their solvent-extractable organics showed higher DNA damage than the water-soluble fraction. (2) In vivo, PM2.5 from both dust storm and normal weather caused an increase of DNA damage of rat lung cells in a dose-response manner. (3) Baotou city is one of the heavy industrial cities, while Wuwei is one of agricultural cities in Northwest region of China. The effects induced by normal weather samples in Baotou city slightly higher than those in Wuwei city on DNA damage, though there was no significant difference was found between two cities. These results lead to conclusions that dust storm PM2.5 as well as normal weather PM2.5 could lead to DNA damage and the organic compounds and the insoluble particle-core might be the main contributors to DNA damage. Our results suggest that the risk of health effects may be greater during dust storms because dust storm PM2.5 whose airborne mass were much higher. Further studies are needed to determine the components of dust storm particles that may contribute to the particle toxicity.     

Oxidative DNA damage in vitamin C-supplemented guinea pigs after intratracheal instillation of diesel exhaust particles

The health effects of diesel exhaust particles (DEP) are thought to involve oxidative damage. We have investigated the effect of intratracheal DEP instillation to guinea pigs in three groups of 12 animals each given 0, 0.7, or 2.1 mg. Five days later guinea pigs exposed to DEP had increased levels of oxidized amino acids (gamma-glutamyl semialdehyde), DNA strand breaks, and 7-hydro-8-oxo-2'-deoxyguanosine (8-oxodG) in the lung. Bulky DNA ad- ducts were not significantly elevated in the lung. The antioxidant enzyme activity of glutathione reductase was increased in the lung of DEP-exposed guinea pigs, whereas glutathione peroxidase and superoxide dismutase enzyme activities were unaltered. There was no difference in DNA strand breaks in lymphocytes or urinary excretion of 8-oxodG at the two doses tested. Protein oxidations in plasma and in erythrocytes were not altered by DEP exposure. The concentrations of ascorbate in liver, lung, and plasma were unaltered by the DEP exposure. The results indicate that in guinea pigs DEP causes oxidative DNA damage rather than bulky DNA adducts in the lung. Guinea pigs, which are similar to humans with respect to vitamin C metabolism, may serve as a new model for the study of oxidative damage induced by particulate matter.     

Oxidative stress and NFkappaB activation in the lungs of rats: a synergistic interaction between soot and iron particles

Particulate matter (PM) has been associated with a variety of adverse health effects primarily involving the cardiopulmonary system. However, the precise biological mechanisms to explain how exposure to PM exacerbates or directly causes adverse effects are unknown. Particles of varying composition may play a critical role in these effects. To study such a phenomenon, a simple, laminar diffusion flame was used to generate aerosols of soot and iron particles in the ultrafine size range. Exposures of healthy adult rats were for 6 h/day for 3 days. Conditions used included exposure to soot only, iron only, or a combination of soot and iron. We found animals exposed to soot particles at 250 microg/m3 had no adverse respiratory effects. Exposure to iron alone at a concentration of 57 microg/m3 also had no respiratory effects. However, the addition of 45 microg/m3 of iron to soot with a combined total mass concentration of 250 microg/m3 demonstrated significant pulmonary ferritin induction, oxidative stress, elevation of IL-1beta, and cytochrome P450s, as well as activation of NFkappaB. These findings suggest that a synergistic interaction between soot and iron particles account for biological responses not found with exposure to iron alone or to soot alone.     

Oxidative stress, antioxidants, and vascular damage

Oxidative stress has been recognized as a key mechanism in the development of vascular damage, particularly atherosclerosis. In spite of substantial experimental evidence demonstrating reversal of endothelial dysfunction and prevention of atherosclerosis in experimental settings, no benefits have been observed in large clinical trials in which antioxidants have been given in high-risk patients for the prevention of cardiovascular events. Evaluation of the clinical relevance of the oxidative modification hypothesis requires identification of potential molecular targets of antioxidant interventions and effective antioxidant agents. Future research should necessarily consider quantification of interindividual variations in oxidative stress using appropriate biomarkers.     

大气细颗粒物浓度与儿童咳嗽变异性哮喘的相关性

目的 探讨大气细颗粒物（PM2.5）浓度与儿童咳嗽变异性哮喘的关系。方法 选择2015年4月至2016年4月南京医科大学附属淮安第一人民医院诊断为咳嗽变异性哮喘儿童48例（咳嗽变异性哮喘组）和典型哮喘儿童50例（典型哮喘组）,同期选择慢性肺炎儿童50例（肺炎组）和健康儿童50例（对照组）,比较发病1个月内环境中平均PM2.5浓度,检测血清淋巴细胞比率、CD⁺₄/CD⁺₈、IgE、肺通气指标水平。结果 ①咳嗽变异性哮喘组和典型哮喘组的平均PM2.5浓度高于肺炎组和对照组[（85.6±10.3）、（76.4±11.4）μg/m³ vs（41.3±12.5）、（25.9±10.5）μg/m³],差异有统计学意义（P<0.05）;②咳嗽变异性哮喘组和典型哮喘组的淋巴细胞比率和IgE水平高于其他两组,CD₄⁺/CD₈⁺低于其他两组,差异均有统计学意义（P<0.05）;③咳嗽变异性哮喘组的FEV₁% Pred、FEV₁/FVC和MMEF% Pred分别为（88.7±13.5）%、（80.2±7.8）%、（78.6±15.4）%,典型哮喘组分别为（85.4±14.6）%、（76.3±7.6）%、（72.5±16.3）%,均分别低于其他两组（P<0.05）,而咳嗽变异性哮喘组相关数据与典型哮喘组则基本一致（P>0.05）。结论 PM2.5与儿童咳嗽变异性哮喘发作有关,免疫调节和通气功能降低与典型哮喘改变可能一致。     

重组人生长激素对败血症大鼠氧化损伤和抗氧化损伤的影响

目的观察重组人生长激素(rhGH)对败血症大鼠氧化损伤和抗氧化损伤的影响。方法采用ipE.coli复制大鼠败血症模型。42只♀SD大鼠随机分为正常对照组(C组)、败血症组(S组)及rhGH治疗组(T组),S组、T组依观察时点再分为S1d、S3d和T1d、T3d两个亚组。观测3组的血浆硫代巴比妥酸反应物(TBARS)水平及超氧化物歧化酶(SOD)活力。结果S组大鼠血浆TBARS水平在各时点均明显高于C组和T组;T组各时点与C组无明显差异;S组大鼠血浆SOD活力在各时点均明显低于C组;T1d组与C组相比虽无显著差异,但却明显高于S1d组,T3d组明显高于C组及S3d组。结论rhGH能明显提高机体的抗氧化损伤能力。     

Effects of Resveratrol Supplementation on Oxidative Damage and Lipid Peroxidation Induced by Strenuous Exercise in Rats

The purpose of the present study was to investigate the effects of resveratrol supplementation on oxidative damage and lipid peroxidation induced by strenuous exercise in rats. The rats were randomly divided into five groups: a sedentary control group, an exercise control group, and three treatment exercise groups administered increasing doses of resveratrol (25, 50, and 100 mg/kg body weight). Resveratrol was administered by oral gavage once daily for four weeks. At the end of the four-week period, the rats performed a strenuous exercise on the treadmill, and the levels of lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured. The results showed that resveratrol supplementation had protective effects against strenuous exercise-induced oxidative damage and lipid peroxidation by lowering the levels of LDH, CK, MDA, 4-HNE, and 8-OHdG in the serum or muscle of rats. These beneficial effects are probably owing to the inherent antioxidant activities of resveratrol.     

Comparative effects of inhaled diesel exhaust and ambient fine particles on inflammation,atherosclerosis, and vascular dysfunction

Ambient air PM_2.5 (particulate matter less than 2.5 μm in diameter) has been associated with cardiovascular diseases (CVDs), but the underlying mechanisms affecting CVDs are unknown. The authors investigated whether subchronic inhalation of concentrated ambient PM_2.5 (CAPs), whole diesel exhaust (WDE), or diesel exhaust gases (DEGs) led to exacerbation of atherosclerosis, pulmonary and systemic inflammation, and vascular dysfunction; and whether DEG interactions with CAPs alter cardiovascular effects. ApoE^?/? mice were simultaneously exposed via inhalation for 5 hours/day, 4 days/week, for up to 5 months to one of five different exposure atmospheres: (1) filtered air (FA); (2) CAPs (105 μg/m³); (3) WDE (DEP = 436 μg/m³); (4) DEG (equivalent to gas levels in WDE group); and (5) CAPs+DEG (PM_2.5: 113 μg/m³; with DEG equivalent to WDE group). After 3 and 5 months, lung lavage fluid and blood sera were analyzed, and atherosclerotic plaques were quantified by ultrasound imaging, hematoxylin and eosin (H&E stain), and en face Sudan IV stain. Vascular functions were assessed after 5 months of exposure. The authors showed that (1) subchronic CAPs, WDE, and DEG inhalations increased serum vascular cell adhesion molecule (VCAM)-1 levels and enhanced phenylephrine (PE)-induced vasoconstriction; (2) for plaque exacerbation, CAPs > WDE > DEG?=?FA, thus PM components (not present in WDE) were responsible for plaque development; (3) atherosclerosis can exacerbated through mechanistic pathways other than inflammation and vascular dysfunction; and (4) although there were no significant interactions between CAPs and DEG on plaque exacerbation, it is less clear whether the effects of CAPs on vasomotor dysfunction and pulmonary/systemic inflammation were enhanced by the DEG coexposure.     

The effect of antioxidative vitamins A and E and coenzyme Q on the morphological picture of the lungs and pancreata of rats intoxicated with sodium fluoride

Fluorides, when taken in amounts exceeding the standard therapeutic dosage, are regarded as toxic substances. Recent studies show that fluorides may affect the oxidoreductive processes of cells.The aim of the following study is to investigate the effect of antioxidative vitamins A and E and coenzyme Q on the morphological picture of the lungs and pancreata of rats exposed to high doses of sodium fluoride. The study was performed on 18 female rats, which were divided into 3 groups: a control group and 2 experimental groups. The control group received distilled water and standard fodder. Experimental groups I and II both received sodium fluoride (2.5 mg/rat/24 h). In addition, animals in group II received vitamin A (250 IU/rat/24 h), vitamin E (3 mg/rat/24 h), and coenzyme Q (200 μg/rat/24 h). The experiment was conducted for a period of 35 days. Upon dissection, lungs and pancreata were taken for histopathological examination. Pathomorphological evaluations of the removed organs were performed using paraffin preparations, stained with hematoxylin and eosin. The aldolase activity in the pancreata was measured using colorimetric methods and the protein concentration by the Lowry method.In the case of group I, pathomorphological examinations of the lungs revealed the appearance of erythrorrhagia, hyperaemia, necrosis of epithelium cells, numerous macrophages in interalveolar septa, infiltrations in the area of blood vessels and emphysematous blebs. Focal vacuolar degeneration cells and inflammatory infiltrations appeared only in pancreata. The results confirmed that the administration of vitamins A and E and coenzyme Q has a counteracting influence upon the degenerative changes seen in the examined organs.     

氟砷联合染毒对大鼠子代大脑氧化性损伤的研究

目的 揭示氟砷共存时对子代健康的影响。方法 采用两代一窝繁殖实验的方法,测定Ｗｉｓｔａｒ大鼠暴露于氟砷后其子代大脑中氟砷蓄积情况、脂质过氧化水平。结果 随着暴露剂量的增加,大脑氟砷含量显著增加,ＳＯＤ和ＧＳＨ－Ｐｘ活性随之降低,而ＬＰＯ含量却逐渐增加,同代不同剂量组间比较,差异均有非常显著意义（Ｐ〈０．０１）,并出出明显的病理性变化;停止氟砷暴露８周后,大脑氟砷含量显著降低,酶的生有所恢复,而ＬＰ     

辣木籽对大鼠心肌缺血再灌注损伤的保护作用

目的 探讨辣木籽对大鼠心肌缺血再灌注损伤的保护作用.方法 选择SD大鼠75只,分为假手术组、模型组、高剂量组、中剂量组、低剂量组,假手术组和模型组分别给予同体积生理盐水灌胃,高中低剂量组分别给予辣木籽混悬液0.5 g/kg、1.0 mg/kg、2.0 g/kg灌胃.制作心肌缺血再灌注损伤模型,缺血30分钟,再灌注120分钟.观察心肌梗死范围,测定血清乳酸脱氢酶、磷酸肌酸激酶、丙二醛、超氧化物歧化酶水平.结果 模型组梗死区心肌梗死范围大于假手术组,高中低剂量组梗死区心肌梗死范围分别低于模型组,差异有统计学意义(P＜0.05).高中低剂量组乳酸脱氢酶、磷酸肌酸激酶、超氧化物歧化酶活性及丙二醛含量分别和模型组比较,差异有统计学意义(P＜0.05).结论 辣木籽对大鼠心肌缺血再灌注损伤有保护作用,可能与其抗氧化损伤作用有关.     

Influence of gender on oxidative stress, lipid peroxidation, protein damage and apoptosis in hearts and brains from spontaneously hypertensive rats

1. Hypertension leads to oxidative stress, lipid and protein damage, apoptosis and impaired cardiac contractile function. However, impact of gender on these hypertension-associated abnormalities has not been elucidated. 2. The present study evaluated the oxidative stress, lipid/protein damage, apoptosis in heart and brain tissues as well as cardiomyocyte contractile function in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) of both genders. Oxidative stress, lipid peroxidation, protein damage and apoptosis were assessed by glutathione (GSH) : reduced glutathione (GSSG) ratio, malondialdehyde (MDA) levels, protein carbonyl levels and caspase-3 activity, respectively. Cardiomyocyte contractile function was examined including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/-dL/dt). The SHR cardiomyocytes displayed reduced PS and +/-dL/dt compared with gender-matched WKY counterparts. Male but not female SHR cardiomyocytes possessed longer resting cell length, normal TPS and prolonged TR90. All mechanical parameters were comparable between male and female WKY rats with the exception of a higher TR90 in females. Hypertension did not significantly affect the GSH : GSSG ratio in the heart and brain tissues of either gender. Brain from female WKY rats displayed a reduced GSH : GSSG ratio. The MDA levels were unchanged and elevated, respectively, in SHR heart and SHR brain tissues from both genders. Protein carbonyl formation and caspase-3 activity were elevated in male but not female SHR hearts. Nonetheless, brain protein carbonyl level and caspase-3 activity were unaffected by hypertension or gender. 3. In summary, these results suggest that gender affects hypertension-associated oxidative stress, lipid and protein damage, apoptosis in heart and brain tissues and cardiomyocyte contractile function.     

Role of iron and oxidative stress in the exacerbation of allergic inflammation in murine lungs caused by urban particulate matter <2.5 μm and desert dust

Simultaneous exposure of lipopolysaccharide (LPS) and urban particulate matter <2.5 μm (PM2.5) or desert dust exacerbated murine asthma. In the present study, the role of iron (Fe) contained in particles and oxidative stress was investigated using Fe chelator deferoxamine (DFO) and oxidative stress scavenger N‐acetylcysteine (NAC) in a murine asthma model exacerbated by LPS + PM2.5 or LPS + Asian sand dust (ASD). When BALB/c mice were intratracheally challenged with ovalbumin (OVA) + LPS and either urban PM2.5 or ASD, LPS + PM2.5 and LPS + ASD caused exacerbation of OVA‐induced lung eosinophilia along with T‐helper 2 cytokine and eosinophil‐relevant chemokine production in bronchoalveolar lavage fluid as well as the production of OVA‐specific IgE in serum. LPS + PM2.5 with NAC tended to reduce the lung eosinophilia compared to the LPS + PM2.5 host, whereas LPS + PM2.5 with DFO did not reduce them. LPS + ASD with NAC moderately reduced the lung eosinophilia compared to the LPS + ASD host. LPS + ASD with DFO drastically reduced the lung eosinophilia compared to the LPS + ASD host. The concentration of Fe in urban PM2.5 and ASD were almost the same. However, the concentrations of trace metals Pb, Cu, As, Ni, Cr, Mo, Sb, Co, Se and Cd were greater in PM2.5 than in ASD. These results suggested that Fe and oxidative stress are at least partly involved in lung eosinophilia exacerbation caused by LPS + ASD. However, trace metals (except Fe) might also be involved in lung eosinophilia exacerbated by LPS + PM2.5.     

Oxidative modification of neurofilament-L and neuronal cell death induced by the catechol neurotoxin,tetrahydropapaveroline

Tetrahydropapaveroline (THP), which is an endogenous neurotoxin, has been suspected to be associated with dopaminergic neurotoxicity of l-DOPA. In this study, we examined oxidative modification of neurofilament-L (NF-L) and neuronal cell death induced by THP. When disassembled NF-L was incubated with THP, protein aggregation was increased in a time- and THP dose-dependent manner. The formation of carbonyl compounds and dityrosine were observed in the THP-mediated NF-L aggregates. Radical scavengers reduced THP-mediated NF-L modification. These results suggest that the modification of NF-L by THP may be due to oxidative damage resulting from the generation of reactive oxygen species (ROS). When THP exposed NF-L was subjected to amino acid analysis, glutamate, proline and lysine residues were found to be particularly sensitive. We also investigated the effects of copper ions on THP-mediated NF-L modification. At a low concentration of THP, copper ions enhanced the modification of NF-L. Treatment of C6 astrocyte cells with THP led to a concentration-dependent reduction in cell viability. When these cells were treated with 100 μM THP, the levels of ROS increased 3.5-fold compared with control cells. Furthermore, treatment of cells with THP increased NF-L aggregate formation, suggesting the involvement of NF-L modification in THP-induced cell damage.     

Effects of concentrated ambient particles on heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats during a dust storm event

Epidemiological studies have suggested that cardiovascular mortality and morbidity increased during Asian dust events. The findings were still inconclusive though. We have shown an increased pulmonary toxicity in diseased animals during a dust storm event. However, the toxicity nature of dust storm particles remains unclear. It is our objective in this study to further investigate the cardiovascular effects of concentrated PM(2.5) on spontaneously hypertensive rats during the same dust storm event. Four spontaneously hypertensive rats were implanted with radiotelemetry transmitters at the age of 10 wk. Baseline heart rate, mean blood pressure, and cardiac contractility (measured as QA interval, QAI) data were collected 4 wk before. Exposure group received concentrated ambient particles inhalation for 6 h during a dust storm event, while the control group received room air inhalation at the same time. Self-control data were collected 4 wk after the event during the same clock hours while there was no dust storm. Gravimetric analysis showed a particle mass concentration of 315.55 microg/m(3) during the 6 h of exposure. A linear mixed-effects model revealed sigmoid increases in heart rate (to a maximum of 93.8 +/- 18.8 bpm) and mean blood pressure (to a maximum of 14.8 +/- 5.4 mm Hg), and a sigmoid decrease of QAI (to a maximum of - 3.5 +/- 1.5 ms) during the exposure after an initial incubation period. We conclude that concentrated dust storm particles, which are different from products of automobile combustion process, may cause adverse cardiovascular effects on diseased animals.     

Oxidative stress,progressive damage in the substantia nigra and plasma dopamine oxidation,in rats chronically exposed to ozone

The purpose of our work was to determine the effects of oxidative stress on the neurodegeneration process in the substantia nigra, and to evaluate dopamine-oxidation metabolites in the plasma using a cyclic voltammetry (CV) technique. We have also studied the correlation between the increases in oxidized dopamine-species levels with the severity of lipid-peroxidation in the plasma. Sixty-four male Wistar rats were divided into four experimental groups and received air (Group I, control) or ozone (0.25 ppm) daily by inhalation for 4 h for 15 (Group II), 30 (Group III), and 60 (Group IV) days. The brains were processed for immunohistochemical location of dopamine and p53 in the substantia nigra. Plasma collected from these animals was assayed for oxidized dopamine products using CV and lipid-peroxidation levels were measured. Our results indicate that chronic exposure to low O₃ doses causes that the number of dopaminergic neurons decreased, and p53-immunoreactive cells increases until 30 days; which was a function of the time of exposure to ozone. Oxidative stress produces a significant increase in the levels of the dopamine quinones (DAQs) that correlated well (r = 0.962) with lipid peroxides in the plasma during the study period. These results suggest that DAQ could be a reliable, peripheral oxidative indicator of nigral dopaminergic damage in the brain.     

Protective Effect of Ginsenoside R0 on Anoxic and Oxidative Damage In vitro

To examine the neuroprotective effects of ginsenoside R0, we investigated the effects of ginsenoside R0 in PC12 cells under an anoxic or oxidative environment with Edaravone as a control. PC12 neuroendocrine cells were used as a model target. Anoxic damage or oxidative damage in PC12 cells were induced by adding sodium dithionite or hydrogen peroxide respectively in cultured medium. Survival ratios of different groups were detected by an AlamarBlue assay. At the same time, the apoptosis of PC12 cells were determined with flow cytometry. The putative neuroprotective effects of ginsenoside R0 is thought to be exerted through enhancing the activity of antioxidant enzymes Superoxide dismutases (SOD). The activity of SOD and the level of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), were measured to evaluate the protective and therapeutic effects of ginsenoside R0. Ginsenoside R0 treated cells had a higher SOD activity, lower MDA level and lower ROS, and their survival ratio was higher with a lower apoptosis rate. It is suggested that ginsenoside R0 has a protective effect in the cultured PC12 cells, and the protection efficiency is higher than Edaravone. The protective mechanisms of these two are different. The prevent ability of ginsenoside R0 is higher than its repair ability in neuroprotection in vitro.     

The toxic effects of indoor atmospheric fine particulate matter collected from allergic and non‐allergic families in Wuhan on mouse peritoneal macrophages

Recent studies have shown that fine particulate matter (PM_2.5) is associated with multiple adverse health outcomes and PM_2.5‐induced oxidative stress is now commonly known as a proposed mechanism of PM_2.5‐mediated toxicity. However, the association between allergic symptoms in children and exposure to PM_2.5 has not been fully elucidated, particularly the role of PM_2.5 on the indoor environment involved in allergy or non‐allergy is unknown. The aim of the present study was to explore whether indoor PM_2.5 from the homes of children with allergic symptoms had more increased risks of allergy than that of healthy ones and then compare the toxicity and inflammatory response of them. In this study, indoor PM_2.5 was collected from the homes of schoolchildren with allergic symptoms and those of healthy ones respectively, and components of PM_2.5 were analyzed. PM_2.5‐mediated oxidative damage and inflammatory response were further evaluated in mouse peritoneal macrophages based on its effects on the levels of reactive oxygen species accumulation, lipid peroxidation, DNA damage or cytokine production. It seems that oxidative stress may contribute to PM_2.5‐induced toxicity, and PM_2.5 from the allergic indoor environment produced more serious toxic effects and an inflammatory response on mouse peritoneal macrophages than that from a non‐allergic indoor environment. Copyright © 2015 John Wiley & Sons, Ltd.