Identification of apoptosis-associated protein factors distinctly expressed in cigarette smoke condensate-exposed airway bronchial epithelial cells.

Smoking is associated with an increased risk of respiratory diseases, including lung cancer and asthma. However, the mechanisms or diagnostic markers for smoking-related diseases remain largely unknown. Here we investigated the role of cigarette smoke condensate (CSC) in the regulation of human bronchial epithelial cell (BEAS-2B) behavior. We found that exposure to CSC significantly inhibited BEAS-2B cell viability, impaired cell morphology, induced cell apoptosis, triggered oxidative damage, and promoted inflammatory response, which suggests a deleterious effect of CSC on bronchial epithelial cells. In addition, CSC markedly altered the expression of apoptosis-associated protein factors, including p21, soluble tumor necrosis factor receptor 1, and Fas ligand. In sum, our study identified a panel of novel protein factors that may mediate the actions of CSC on bronchial epithelial cells and have a predictive value for the development and progression of smoking-related diseases, thus providing insights into the development of potential diagnostic and therapeutic strategies against these diseases.

Endocrine Disruption Activity of 30-day Dietary Exposure to Decabromodiphenyl Ethane in Balb/C Mouse.

OBJECTIVE: This study aimed to evaluate the hepatotoxicity, metabolic disturbance activity and endocrine disrupting activity of mice treated by Decabromodiphenyl ethane (DBDPE). METHODS: In this study, Balb/C mice were treated orally by gavage with various doses of DBDPE. After 30 days of treatment, mice were sacrificed; blood, livers and thyroid glands were obtained, and hepatic microsomes were isolated. Biochemical parameters including 8 clinical chemistry parameters, blood glucose and hormone levels including insulin and thyroid hormone were assayed. The effects of DBDPE on hepatic cytochrome P450 (CYP) levels and activities and uridinediphosphate-glucuronosyltransferase (UDPGT) activities were investigated. Liver and thyroid glands were observed. RESULTS: There were no obvious signs of toxicity and no significant treatment effect on body weight, or liver-to-body weight ratios between treatment groups. The levels of ALT and AST of higher dose treatment groups were markedly increased. Blood glucose levels of treatment groups were higher than those of control group. There was also an induction in TSH, T3, and fT3. UDPGT, PROD, and EROD activities were found to have been increased significantly in the high dose group. Histopathologic liver changes were characterized by hepatocyte hypertrophy and cytoplasmic vacuolization. Our findings suggest that DBDPE can cause a certain degree of mouse liver damage and insufficiency. CONCLUSION: DBDPE has the activity of endocrine disruptors in Bal/C mice, which may induce drug-metabolizing enzymes including CYPs and UDPGT, and interfere with thyroid hormone levels mediated by AhR and CAR signaling pathways. Endocrine disrupting activity of DBDPE could also affect the glucose metabolism homeostasis.

Subacute effect of decabromodiphenyl ethane on hepatotoxicity and hepatic enzyme activity in rats.

Information regarding decabromodiphenyl ethane (DBDPE) effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.

Single wall carbon nanotube induced inflammation in cruor-fibrinolysis system.

OBJECTIVE: To study single wall carbon nanotubes (SWCNT) and its role in inducing inflammatory cytokines in the cruor-fibrinolysis system of rat. METHODS: Twenty one Wistar rats were divided into four groups: 1) control; 2) low-dose SWCNT (0.15 mg/kg BW); 3) medium-dose SWCNT (0.75 mg/kg BW); 4) high-dose SWCNT (1.5 mg/kg BW). Intratracheal instillation of SWCNT suspensions was administered to rats once per day for 21 days. In order to assess the exposure effect of SWCNT to the rats, activity of Inflammatory cytokine was measured and markers of cruor-fibrinolysis system were studied via ELSIA. Also, change in clotting time was recorded and histopathology was studied. RESULTS: IL-6 and IL-8 concentrations of rats exposed to SWCNT were significantly higher than those in controls (P<0.05). The activity of inflammatory cytokines and histopathological change indicated that oxidative damage occurred. Change in clotting time in rats exposed to SWCNT decreased compared with controls. Meanwhile, t-PA (tissue-tupe plassminogen activator) and AT-III (antithrombin-III) levels in rats exposed to particulates increased or decreased significantly compared with controls (P<0.05). A similar trend was observed for D-dimer (D2D) levels, indicating that SWCNT can impact the cruor-fibrinolysis system of rat. CONCLUSION: The results from our study suggest that an increased procoagulant activity and reduced fibrinolytic activity in rats exposed to SWCNT can cause pulmonary oxidative stress and inflammation, due to the release of pro-thrombotic and inflammatory cytokines into the blood circulation of rat.

Cytotoxicity and apoptosis induction in human HepG2 hepatoma cells by decabromodiphenyl ethane.

OBJECTIVE: To investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro. METHODS: HepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125-100.0 mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied. RESULTS: As evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays and nuclear morphological changes, DBDPE inhibited HepG2 viability in a time- and dose-dependent manner within a range of 12.5 mg/L to 100 mg/L and for 48 h and 72 h. Induction of apoptosis was detected at 12.5-100 mg/L at 48 h and 72 h by propidium iodide staining, accompanied with overproduction of reactive oxygen species (ROS). Furthermore, N-acetyl-L-cysteine, a widely used ROS scavenger, significantly reduced DBDPE-induced ROS levels and increased HepG2 cells viability. CONCLUSION: DBDPE has cytotoxic and anti-proliferation effect and can induce apoptosis in which ROS plays an important role.

Impact of traffic emissions on local air quality and the potential toxicity of traffic-related particulates in Beijing, China.

OBJECTIVE: Air-borne particulates from different sources could have different physicochemical properties and inflammatory potentials. This study aims to characterize the chemical compositions and the toxicity of ambient particulate matter (PM) associated with traffic emissions. METHODS: The concentrations of trace elements, organic carbon (OC), elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 and PM10 were measured in samples collected at sites in Beijing, China. Their toxic effects on the pulmonary system of rats were investigated. Biochemical parameters (LDH, T-AOC, TP) and inflammatory cytokine(IL-6, IL-1, TNF-a) levels were measured in the lungs of rats exposed to traffic-related PM. Oxidative damage was observed. PM samples were taken from a near road site and an off road site in summer time in 2006. RESULTS: The concentrations of the USEPA priority pollutant PAHs in both PM10 and PM2.5 were higher (299.658 and 348.412) at the near road site than those (237.728 and 268.472) at the off road site. The similar trend was observed for the concentrations of trace elements in PM. Compared to coarse particles (PM10), fine particles (PM2.5) have a greater adsorption capacity to enrich toxic elements than inhalable particles. Decrease in antioxidant capacity and an increase in the amount of lipid peroxidation products in rat lung tissues was observed. CONCLUSION: The findings of the present study suggest that the differing inflammatory responses of PM collected from the two road sites might have been mediated by the differing physicochemical characteristics.

Single-wall carbon nanotubes induce oxidative stress in rat aortic endothelial cells.

Oxidative stress is a major factor contributing to endothelial cell damage. Single-wall carbon nanotubes (SWCNTs) have oxidative properties; however, the oxidative effects of SWCNTs on endothelial cells are not fully understood. In the present study, we investigated the effects of oxidative stress induced by SWCNTs on rat aortic endothelial cells (RAECs). Various markers of cellular damage were assessed, such as biochemical and ES immunity indexes, and DNA and protein damage. Our findings suggest that RAEC endured oxidative damage following SWCNT exposure. Specifically, after SWCNTs exposure, non-enzymatic antioxidant glutathione was activated prior to superoxide dismutase activation in order to defend against oxidative stress. Additionally, it was found that as SWCNT concentration increased, so did the stress protein, heme oxygenase-1 (HO-1), expression levels. These changes may induce RAEC damage, and result in many serious diseases.

[Effects of nanopolystyrene nanoplastic exposure on the development and neurotoxicity of fetal rats during gestation].

Objective: To investigate the effects of polystyrene nanoplastics (PS-NPs) exposure during gestation on the growth and neurotoxicity of fetal rats. Methods: Twenty-seven SD pregnant rats were randomly divided into 9 groups with three rats in each group. The experimental group of PS-NPs was given 0.5, 2.5, 10 and 50 mg/kg of PS-NPs suspension with different particle sizes (25 and 50 nm) by gavage, wihe the control group was given ultrapure water by gavage. The time of gavage is from the 1st to the 18th day of pregnancy. The morphological changes of the placenta were observed; compare the number of male and female fetuses, live/dead/absorbed fetuses, body weight, body length, placental weight, and organ coefficients of kidney, liver, brain and intestine of fetal rats; the prefrontal cortex, hippocampus and striatum of the fetal rats were taken to measure related biochemical indicators. Results: Compared with the control group, the placenta of the PS-NPs exposed group was found to have structural damage, which increased in a dose-dependent manner. The area ratio of trophoblast was significantly increased (P＜0.05), and the area ratio of labyrinth was significantly decreased (P＜0.05); In the prefrontal cortex, hippocampus and striatum of fetal rats, the levels of IL-1ß, IL -6 and TNF-α were significantly increased in the 10 and 50 mg/kg PS-NPs exposed group (P＜0.05), and more significantly elevated in the 25 nm group than those in the 50 nm group at 10 mg/kg exposure (P＜0.05) the CAT activity was significantly decreased in 2.5, 10 and 50 mg/kg PS-NPs exposure groups (P＜0.05), while the SOD and GSH-Px activities were significantly decreased in 25 nm exposure groups and 2.5, 10 and 50 mg/kg 50 nm PS-NPs exposure groups (P＜0.05), the MDA content was significantly increased in 10, 50 mg/kg 25 nm PS-NPs exposure groups and 50 mg/kg 50 nm PS-NPs exposure groups (P＜0.05). Conclusion: Maternal PS-NPs exposure during gestation may affect the growth and development of fetal rats by damaging the placental barrier and produce neurotoxicity in fetal rats, causing oxidative stress and inflammatory responses in various brain regions, and smaller particle sizes and higher doses of polystyrene nanoplastic exposure have more significant neurotoxic effects on the offspring.

[Effects of early life PM2.5 exposure on prefrontal cortex of offspring male rats].

Objective: To investigate the effects of PM2.5 exposure at different stages of early life on the prefrontal cortex of offspring rats. Methods: Twelve pregnant SD rats were randomly divided into four groups: Control group (CG), Maternal pregnancy exposure group (MG), Early postnatal exposure group (EP) and Perinatal period exposure group (PP), 3 rats in each group. The pregnant and offspring rats were exposed to clean air or 8-fold concentrated PM2.5. MG was exposed from gestational day (GD) 1 to GD21. EP was exposed from postnatal day (PND) 1 to PND21, and PP was exposed from GD1 to PND21. After exposure, the prefrontal cortex of 6 offspring rats in each group was analyzed. HE staining was used to observe the pathological damage in the prefrontal cortex. ELISA was employed to detect neuroinflammatory factors, and HPLC/MSC was applied to determine neurotransmitter content. Western blot and colorimetry were applied for detecting astrocyte markers and oxidative stress markers, respectively. Results: Compared with MG and CG, the pathological changes of prefrontal cortex in PP and EP were more obvious. Compared with MG and CG, the neuroinflammatory factors (IL-1, IL-6, TNF-α) in PP and EP were increased significantly (P＜0.01), the level of MT were decreased significantly (P＜0.05), and the level of oxytocin (OT) showed a downward trend; the level of neurotransmitter ACh was also increased significantly (P＜0.01). Compared with MG and CG, the GFAP level of PP and EP showed an upward trend, the level of oxidative stress index SOD in PP and EP was decreased significantly (P＜0.01), and the level of ROS was increased significantly (P＜0.01). Compared with the offspring rats of CG and MG, the CAT level of PP was decreased significantly (P＜0.01, P＜0.05). Compared with the offspring rats of CG, the CAT level of EP was decreased significantly (P＜0.05). There was no significant difference in IL-1, IL-6, TNF-α, MT, OT, ACh, GFAP, SOD, ROS and CAT levels between PP and EP, or MG and CG. Conclusion: PM2.5 exposure in early life has adverse effects on the prefrontal cortex of offspring male rats, and early birth exposure may be more sensitive.

[Effect of epithelial-mesenchymal transition on cardiac fibrosis induced by oil mist particulate matter].

Objective: To investigate the effects of oil-mist particulate matter (OMPM) on cardiac tissue structure fibrosis in rats and the role of epithelial-mesenchymal transition (EMT). Methods: Six-week-old Wistar rats (half male and half female) were randomly divided into 3 groups: control group (without OMPM exposure), low-dose exposure group (50 mg/m3) and high-dose exposure group (100 mg/m3), 18 rats in each group, with 6.5 hours per day of dynamic inhalation exposure. After 42 days of continuous exposure, cardiac tissues were collected for morphological observation; Western blot was used to detect fibrosis markers collagen I and collagen III levels, epithelial marker E-cadherin levels, interstitial markers N-cadherin, fibronectin, vimentin, alpha-smooth muscle actin (α-SMA) levels, and EMT transcription factor Twist protein levels; Real-time polymerase chain reaction (RT-qPCR) was used to detect collagen I and collagen III mRNA levels. Results: After OMPM exposure, myocardial cell edema and collagen fiber deposition were increased gradually with increasing exposure dose. Western blot results showed that compared with the control group, the expression levels of collagen I, collagen III, N-Cadherin, fibronectin, vimentin, α-SMA, and Twist protein were increased significantly in the low-dose exposure group and the high-dose exposure group (P＜0.01), and protein expression levels were higher in the high-dose exposure group than those in the low-dose exposure group (P＜0.01). In contrast, E-Cadherin protein expression levels were decreased significantly, and lower in the high-dose exposure group (P＜0.01). RT-qPCR results showed that compared with the control group, collagen I and collagen III mRNA levels were increased significantly in the low-dose exposure group and the high-dose exposure group (P＜0.01), and were increased with increasing exposure dose. (P＜0.01). Conclusion: OMPM may induce cardiac fibrosis in rats by promoting EMT process.

[Effects of ozone sub-chronic exposure on lncRNA expression profiles in rat heart].

Objective: This article aims to observe the changes in long noncoding RNA (lncRNA) expression profiles in rat hearts after ozone sub-chronic exposure. To provide scientific data to explore the role and mechanism of differentially expressed lncRNA in damaged hearts caused by ozone sub-chronic exposure. Methods: Eighteen Wistar rats were randomly divided into filtered air and ozone exposure groups, with nine rats in each group. The rats in filtered air group were exposed to filtered air, while the rats in ozone exposure group were exposed to ozone at 0.5 ppm(0.980 mg/m3)for 90 days at a frequency of 6 hours per day. After ozone exposure, cardiac tissues were collected and the total RNA was extracted. The expression level of lncRNA in the hearts of two groups was detected by microarray and qRT-PCR method and the potential functions of the differentially expressed lncRNA were analyzed by bioinformatics. Results: Compared with the filtered air group, lncRNA's expression profile was significantly altered in the rat hearts of ozone exposure group. A total of 167 lncRNA were up-regulated significantly and 64 lncRNA were down-regulated significantly. GO analysis indicated that the up-regulated lncRNA might involve in the process of regulating growth and development, and the down-regulated lncRNA might participate in nutrient catabolic. KEGG results showed that the up-regulated lncRNA might be involved in regulating the PI3K-Akt signaling pathway. The down-regulated lncRNA might regulate the metabolic processes of various vitamins and main energy-supplying substances. Conclusion: Ozone sub-chronic exposure can cause changes in the expression profile of lncRNA in rat hearts, which may regulate the effects of ozone sub-chronic exposure on the heart through the metabolism of energy and nutrients.

[Effects of repeated immobilization stress on hypothalamic-pituitary- ovarian axis in female rats].

Objective: To explore the effects of repeated immobilization stress on hypothalamic-pituitary-ovarian axis in female rats. Methods: Forty female SD rats were randomly divided into two groups: control group (n=20) and experimental group (n=20). One group was fed normally, the other group was subjected to incremental load restraint stress. Brake stress once a day in the retainer (starting at 9: 00 a.m.), braking for 2 hours on the first day, increasing load by 0.5 hours a day for two weeks. Body weight, estrous cycle, sex hormone, organ coefficient, pathology and expression of related genes were detected to explore the harm of hypothalamic-pituitary-ovarian axis. Results: Repeated immobilization stress caused weight loss, prolonged estrous cycle, and changed the organ coefficient and morphology of ovaries and uterus. QPCR technique was used to detect the related genes. It was found that the expressions of gonadotropin releasing hormone, pituitary gonadotropin releasing hormone receptor, follicle stimulating hormone and luteinizing hormone mRNA were decreased significantly, while the expressions of ovarian follicle stimulating hormone and luteinizing hormone receptor mRNA were increased significantly. The expression of estrogen receptor mRNA in ovary and uterus was decreased significantly. Conclusion: Repeated immobilization stress may disrupt the estrous cycle by interfering with the endocrine regulation of the hypothalamic-pituitary-ovarian axis, thus damaging the gonadal and reproductive endocrine function of female animals.

[Inflammatory mechanism of hippocampal tissue injury induced by PM2.5 in nasal drip in mice].

Objective: To investigate the inflammatory mechanism of nasal instillation of fine particulate matter (PM2.5)on hippocampal tissue injury in mice.Methods: Thirty C57BL/6J mice were randomly divided into 3 groups(n=10):control group, low-dose group, high-dose group. The nasal instillation doses of PM2.5 in the low-dose group and the high-dose group were 1.5 mg/kg BW and 7.5 mg/kg BW, respectively, and the control group was given saline with an equal volume. Saline was sprayed once every other time for 12 times. The serum levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) were determined by ELISA method. HE staining and electron microscopy were used to observe the pathological changes and ultrastructure of lung tissue and hippocampus. The inflammatory cytokine levels in hippocampus were detected by antibody chip technique. Results: There was no significant effect of PM2.5 nasal instillation on serum TNF-α, IL-1ß and IL-6 levels (P＞0.05), and there was no obvious pathological changes in lung tissue structure. In hippocampus, low-dose and high-dose PM2.5 exposure could lead to disordered neuronal arrangement in the hippocampal CA3 region, and there were neurological changes around the neuron cells and ultrastructural changes such as edema around small blood vessels. Compared with the control group, the levels of inflammatory cytokines such as CX3CL1, CSF2 and TECK in the low-dose group were increased significantly (P ＜0.05), while sTNFR1 was decreased significantly (P＜0.05); the inflammatory factors CX3CL1, CSF2, and TCA-3 were significantly increased in the high-dose group (P＜0.05), while leptin, MIG, and FASLG were significantly decreased (P＜0.05). Conclusion: Nasal instillation of PM2.5 can induce tissue damage in the hippocampus of mice, and its mechanism of action may be the olfactory brain pathway. The increasing of TNF-α and IL-6 and the decreasing of sTNFR1 and FASLG may be involved in inflammatory mechanisms.

Oxidative damage to lung tissue and peripheral blood in endotracheal PM2.5-treated rats.

OBJECTIVE: To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats. METHODS: PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase (GSH-Px) and concentration of malondialdehyde (MDA) were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length (microm) and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. RESULTS: The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length (microm) and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. CONCLUSION: PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length (microm) and rate of tail are simple and valuable biomarkers of PM2.5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.

[Effects of oral exposure to zinc oxide nanoparticles on the peripheral organs of C57BL/6J mice].

OBJECTIVE: To investigate the effects of oral exposure of zinc oxide nanoparticles on multiple peripheral organs of C57BL/6J mice. ;Methods: Twenty male C57BL/6J mice were randomly divided into control group and experimental group, with 10 mice in each group. The experimental group was treated with continuous gavage administration of zinc oxide nanoparticle solution at a dose of 20 mg/kg body weight for 60 days, and the control group was given the corresponding amount of normal saline; the mice were weighed once a week. After the end of the exposure, blood samples was collected from the eyeballs, and the levels of blood sugar and lipids, liver and kidney function, and inflammatory factors such as platelet activating factor (PAF), interleukin-6 (IL-6) and tumor septicemia (TNF-α) were detected. Then, tissues sections of the heart, liver, spleen, lung, kidney and small intestine were prepared and their morphological changes were observed after hematoxylin-eosin staining. ;Results: There was no significant difference in body weight between control group and the experimental group. Compared with control group, the serum levels of albumin (ALB), albumin/globulin ratio(A/G), alkaline phosphatase (ALP) activity, aspartate aminotransferase/alanine aminotransferase ratio(AST/ALT), uric acid (UA) and blood urea in the experimental group were increased significantly (P＜0.05 or P＜0.01). There was no significant change in serum inflammatory factors. Pathological examination showed myocardial turbidity, mild inflammatory lesions (focal or small necrosis) in liver, decreased pigmentation in spleen, mild or moderate interstitial inflammation in lungs, and no obvious pathological changes in the kidneys or small intestine. ;Conclusion: Sixty days of oral exposure to nanometer zinc oxide did not cause inflammation in the blood system of C57BL / 6J mice, but it could induce mild pathological changes in the heart, liver, spleen and lungs, and lead to abnormal liver and kidney function.

[Injury of rat blood vessels caused by acute ozone exposure and its mechanism].

OBJECTIVE: To investigate the vascular damage effects and possible mechanism of acute exposure to ozone (O3) in male Wistar rats. METHODS: One hundred and twenty male Wistar rats were randomly divided into six groups, 20 in each group. The experimental animals were placed in a gas poisoning cabinet, the control group was exposed to filtered air, and the treatment group was exposed to ozone at concentrations of 0.12 ppm, 0.5 ppm, 1.0 ppm, 2.0 ppm, and 4.0 ppm, respectively, for 4 hours. Arterial blood pressure data were obtained by PC-lab medical physiological signal acquisition system. Blood rheology indicators and blood biochemical indicators were detected by Tianjin Dean Diagnostic Laboratory. Serum endothelin-1 (ET-1), homocysteine (HCY), von Willebrand factor (vWF), 8-hydroxydeoxyguanosine (8-OhdG), interleukin (IL-6) and tumor necrosis factor alpha (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA) microplate assay. Oxidative stress indicators superoxide dismutase (SOD) activity and malondialdehyde (MDA) were determined by xanthine oxidase method, thiobarbituric acid (TBA) method, reduced glutathione (GSH) and nitric oxide (NO) were tested by using microplate colorimetry. Paraffin sections were prepared from thoracic aorta tissue, and vascular structure was observed by HE staining. RESULTS: Acute exposure to 0.12 ppm ozone could cause a significant increase in arterial systolic blood pressure (SBP). Exposure to different concentrations of ozone could cause a significant increase in plasma viscosity, and the K value of the ESR equation was significantly increased in the 1.0 ppm ozone exposure group. Both the relative and reduced viscosities were significantly reduced at ozone concentrations of 0.5 ppm and 4.0 ppm, while the red blood cell deformation index was increased significantly at ozone concentrations of 0.12 ppm, 0.5 ppm, 1.0 ppm, and 2.0 ppm. Acute ozone exposure resulted in the decrease of total cholesterol content. The content of high-density lipoprotein cholesterol (HDL-C) was significantly reduced in the 0.12 ppm ozone exposure group. When the ozone concentration was higher than 1.0 ppm, the body may also had an inflammatory reaction (increased TNF-α) and oxidative stress (increased MDA, decreased GSH). Acute exposure to ozone could lead to elevated levels of ET-1 in the blood, with significant differences in the 4.0 ppm concentration group, while HCY levels were decreased firstly and then increased, reaching the highest in the 1.0 ppm concentration group. No obvious pathological changes were observed in the thoracic aorta. CONCLUSION: Acute ozone exposure can affect arterial blood pressure, blood rheology and cholesterol metabolism in rats. The possible mechanism is that ozone exposure leads to inflammatory reaction and oxidative stress reaction, causing vascular endothelial function damage, and vascular endothelial cells increase with ozone exposure concentration.

[Effects of acute ozone exposure on genotoxicity of lung cells in rats].

OBJECTIVE: To clarify the genotoxicity induced by acute exposure of ozone with different concentrations on pulmonary cells in rats. METHODS: Thirty-six Wistar rats were randomly divided into control group (filtered air exposure) and ozone exposure group (0.12 ppm, 0.5 ppm, 1.0 ppm, 2.0 ppm, 4.0 ppm) with 6 in each group. After rats were exposed to different concentrations of ozone for 4 h, lung tissues were taken and single cells were isolated. Then, 8-hydroxydeoxyguanosine (8-OHdG) was quantitatively detected by enzyme-linked immunosorbent assay. Comet assay, micronucleus test and DNA- protein cross-linking assay were used to analyze DNA and chromosome damages. RESULTS: Compared with the control group, the content of 8-OHdG in lung tissue was increased significantly from the ozone exposure concentration of 0.12 ppm, reaching the highest value at 0.5 ppm. With the increase of ozone exposure concentration, the tail rate of comets was increased gradually, and there was a significant dose-effect relationship. The cross-linking rate of DNA- protein was increased first and then was decreased with a maximum value at 2.0 ppm group. Although the micronucleus rate of lung cells showed an upward trend, there was no significant difference compared with the control group. CONCLUSION: Acute exposure of ozone at low concentrations (0.12 ppm) could lead to DNA damage in the pulmonary cells of rats, while no significant chromosome damage was found even in the group with ozone concentration reached to 4 ppm.

Impacts of passive smoking on learning and memory ability of mouse offsprings and intervention by antioxidants.

OBJECTIVE: To determine the impact of passive smoking and the protective effect of antioxidants such as vitamin E and quercetin on learning and memory ability of mouse offsprings. METHODS: A passive smoking model of pregnant mice was established. Learning and memory ability was evaluated by the water maze test and long term potentiation (LTP). Nitric oxide (NO), content, nitric oxide synthase (NOS), acetylcholinesteras (Ache) activity in brain, vitamin E concentration, and reactive oxygen species (ROS) in serum were determined. The latency period (the time during which the mice swim from the starting position to the ending position) and errors (the number of mice entering the blind end) in control and antioxidant intervention groups were compared with those in the smoke exposure group after 6 days. RESULTS: The latency period as well as errors in the air, control diet, tobacco smoke (TS), and vitamin E diet groups were decreased significantly as compared with the TS and control diet groups (P<0.05). LTP was restrained in the TS and control diet groups. LTP in all the antioxidant diet groups was significantly increased compared with the TS and control diet groups. In addition, NOS and acetylcholinesteras (Ache) activitiy was significantly higher in the TS and control diet groups than in the air and control diet group. NO content was not significantly different among the different groups, and significantly lower in the TS and vitamin E diet groups than in the TS group, control diet group, quercetin diet group, and mixture diet group (P<0.05). Vitamin E concentration and ROS activity in serum were correlated with the outcome of water maze and LTP. CONCLUSION: Passive smoking reduces LTP formation by disturbing the hippocampus function of mice, by decreasing NOS and Ache activity and increasing NO content. Antioxidants (especially vitamin E) partially improve the learning and memory ability of offsprings whose mothers are exposed to tobacco smoke during pregnancy.