Animals ; Carbon Monoxide ; physiology ; Humans ; Hydrogen Sulfide ; toxicity ; Hypertension, Pulmonary ; etiology ; Hypoxia ; complications ; Nitric Oxide ; physiology

OBJECTIVETo study the genotoxicity of components of diesel engine exhausts with ethanol-diesel blending fuel. To provide scientific arguments to find more economical and less polluted fuels.

METHODSAmes test, comet assay and GC-MS technique were used to test the genotoxicity and 16 kinds of PAHs on diesel engine exhausts with different proportions of ethanol (E0, E5, E10, E20).

RESULTSBoth Ames test and comet assay were positive. It shows that diesel engine exhausts can lead to mutation and DNA damage, especially in pure diesel oil. But the content of 16 kinds of PAHs and DNA damage level decreased in exhausts of E5. With the increase of ethanol proportion in diesel oil, the content of 16 kinds of PAHs and DNA damage level increased.

CONCLUSIONCompared with pure diesel oil and high proportion of ethanol fuel, E5 can reduce the genotoxicity and the brake specific exhausts of PAHs.

Air Pollutants ; toxicity ; Air Pollution ; Carbon Monoxide ; Comet Assay ; DNA Damage ; Ethanol ; toxicity ; Gasoline ; toxicity ; Mutagenicity Tests ; Particulate Matter ; Vehicle Emissions ; toxicity

The use of exogenous carbon monoxide releasing molecules (CORMs) provides promise for clinical application; however, the hazard potential of CORMs in vivo remains poorly understood. The developmental toxicity of CORM-3 was investigated by exposure to concentrations ranging from 6.25 to 400 μmol/L during 4-144 h post fertilization. Toxicity endpoints of mortality, spontaneous movement, heart rate, hatching rate, malformation, body length, and larval behavior were measured. CORM-3 disrupted the progression of zebrafish larval development at concentrations exceeding 50 μmol/L, resulting in embryonic developmental toxicity.
Animals ; Carbon Monoxide ; pharmacology ; Cardiotonic Agents ; toxicity ; Dose-Response Relationship, Drug ; Embryo, Nonmammalian ; drug effects ; Embryonic Development ; drug effects ; Organometallic Compounds ; toxicity ; Zebrafish ; embryology ; metabolism

BackgroundAsthma is a common chronic respiratory disease and is related to air pollution exposure. However, only a few studies have concentrated on the association between air pollution and adult asthma. Moreover, the results of these studies are controversial. Therefore, the present study aimed to analyze the influence of various pollutants on hospitalization due to asthma in adults.

MethodsA total of 1019 unrelated hospitalized adult asthma patients from Northeast China were recruited from 2014 to 2016. Daily average concentrations of air pollutants (particulate matter <2.5 μm [PM], particulate matter <10 μm [PM], sulfur dioxide [SO], nitrogen dioxide [NO], and carbon monoxide [CO]) were obtained from the China National Environmental Monitoring Centre website from 2014 to 2016. Cox logistic regression analysis was used to analyze the relationship between air pollutants and hospital admissions in adult asthma.

ResultsThe maximum odds ratio (OR) value for most air pollutants occurred on lag day 1. Lag day 1 was chosen as the exposure period, and 8 days before onset was chosen as the control period. Three pollutants (PM, CO, and SO) were entered into the regression equation, and the corresponding OR (95% confidence interval) was 0.995 (0.991-0.999), 3.107 (1.607-6.010), and 0.979 (0.968-0.990), respectively.

ConclusionsA positive association between hospital admissions and the daily average concentration of CO was observed. CO is likely to be a risk factor for hospital admissions in adults with asthma.

Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Asthma ; epidemiology ; Carbon Monoxide ; toxicity ; China ; Environmental Monitoring ; statistics & numerical data ; Female ; Hospitalization ; statistics & numerical data ; Humans ; Male ; Odds Ratio ; Particulate Matter ; toxicity ; Risk Factors ; Sulfur Dioxide ; toxicity

OBJECTIVETo observe the protection of carbon monoxide (CO) inhalation on lipopolysaccharide (LPS)-induced rat multiple organ injury.

METHODSSprague-Dawley rats with multiple organ injury induced by 5 mg/kg LPS intravenous injection were exposed to room air or 2. 5 x 10(-4) (V/V) CO for 3 hours. The lung and intestine tissues of rats were harvested to measure the expression of heme oxygenase-1 (HO-1) with reverse transcription-polymerase chain reaction, the levels of pulmonary tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intestinal platelet activator factor (PAF), intercellular adhesion molecule-1 (ICAM-1) with enzyme-linked immunosorbent assay, the content of maleic dialdehyde (MDA) and the activity of myeloperoxidase (MPO) with chemical method, the cell apoptosis rate with flow cytometry, and the pathological changes with light microscope.

RESULTSCO inhalation obviously up-regulated the expression of HO-1 in lung (5.43 +/- 0.92) and intestine (6.29 +/- 1.56) in LPS + CO group compared with (3.08 +/- 0.82) and (3.97 +/- 1.16) in LPS group (both P < 0.05). The levels of TNF-alpha, IL-6 in lung and PAF, ICAM-1 in intestine of LPS + CO group were 0.91 +/- 0.25, 0.64 +/- 0.05, 1.19 +/- 0.52, and 1.83 +/- 0.35 pg/mg, respectively, significantly lower than the corresponding values in LPS group (1.48 +/- 0.23, 1.16 +/- 0.26, 1.84 +/- 0.73, and 3.48 +/- 0.36 pg/mg, all P < 0.05). The levels of MDA, MPO, and cell apoptosis rate in lung and intestine of LPS + CO group were 1.02 +/- 0.23 nmol/mg, 1.74 +/- 0.17 nmol/mg, 7.18 +/- 1.62 U/mg, 6.30 +/- 0.97 U/mg, 1.60% +/- 0.34%, and 30. 56% +/- 6.33%, respectively, significantly lower than the corresponding values in LPS group (1.27 +/- 0.33 nmol/mg, 2.75 +/- 0.39 nmol/mg, 8.16 +/- 1.49 U/mg, 7.72 +/- 1.07 U/mg, 3.18% +/- 0.51%, and 41.52% +/- 3.36%, all P < 0.05). In addition, injury of lung and intestine induced by LPS was attenuated at presence of CO inhalation.

CONCLUSIONCO inhalation protects rat lung and intestine from LPS-induced injury via anti-oxidantion, anti-inflammation, anti-apoptosis, and up-regulation of HO-1 expression.

Animals ; Base Sequence ; Carbon Monoxide ; administration & dosage ; DNA Primers ; Inhalation Exposure ; Lipopolysaccharides ; toxicity ; Male ; Multiple Organ Failure ; chemically induced ; Rats ; Rats, Sprague-Dawley

Carbon monoxide gas is found in the atmosphere whenever society has become industrialized. In addition to the fact that Korea has become industrialized, bituminous coal is used to heat homes here, in heating systems that, if not very carefully maintained, leak this gas, resulting in a number of deaths and near deaths each winter. It has only rarely been reported by investigators that genetic damage may be done transplacentally to a human fetus by a pregnant woman's being poisoned by CO. We explored this by evaluating the damage done to the mouse fetus through an in vivo experiment, using micronucleus and sister chromatid exchange (SCE) tests. Mice were mated and pregnant ones divided into a group that received acute exposures on 3 different days, a group that received chronic exposure, and a control group. In the meantime in the control group the incidence of both micronuclei and SCE was less on the maternal side, in both the acute and chronic exposure groups, whereas the incidences of both micronuclei and SCE were more on the maternal side. However, the incidence on the fetal side was not far behind. Increasing, the dosage of carbon monoxide with gestational age increased the incidence of both micronuclei and SCE in the mother and fetus alike.
Animal ; Carbon Monoxide/toxicity* ; Cell Nucleus/drug effects* ; Female ; Fetus/drug effects* ; Maternal-Fetal Exchange ; Mice ; Mice, Inbred ICR ; Mutagens* ; Pregnancy ; Sister Chromatid Exchange/drug effects*

To explore the underlying mechanism(s) of pulmonary arterial hypertension in endotoxic shock, the roles of N-acetylcysteine (NAC), nitric oxide (NO) and carbon monoxide (CO) were investigated. Pulmonary arterial rings (3-mm width) were prepared from 24 rabbits. Lipopolysaccharide (LPS), after 7-hour incubation, decreased the endothelium-dependent relaxation response of the arterial ring (pre-contracted with phenylephrine) to acetylcholine (1 mumol/L), but did not affect the endothelium-independent relaxation response to sodium nitroprusside. The LPS effects were reduced by a concomitant incubation with the free radical scavenger (NAC), NO donor (L-arginine), and CO donor (hemin), respectively. On the other hand, the LPS effects were enhanced by applying heme oxygenase-1 (HO-1) inhibitor (zinc protoporphyrin) to block CO production. The response to acetylcholine changed from relaxation to contraction, however, the contractile response to phenylephrine increased significantly after pre-incubation with nitric oxide synthase (NOS) inhibitor (L-NAME) to block NO production, confirming the importance of CO and NO. These results show that LPS impairs endothelium-dependent relaxation of the pulmonary artery, which can be greatly reduced by the antioxidant, or by supplying with NO and CO. Thus, multiple factors are involved in this model of endotoxin-induced pulmonary hypertension.
Acetylcysteine ; metabolism ; Animals ; Carbon Monoxide ; metabolism ; Hypertension, Pulmonary ; etiology ; physiopathology ; Lipopolysaccharides ; toxicity ; Male ; Nitric Oxide ; metabolism ; Pulmonary Artery ; drug effects ; physiopathology ; Rabbits ; Shock, Septic ; complications

OBJECTIVETo observe the effects of nicotine on endogenous carbon monoxide (CO) concentration and nitric oxide synthase (NOS) activity in the corpus cavernosum of adult male rats, and explore the possible mechanism of cigarette smoking affecting erectile dysfunction.

METHODSForty adult male rats were equally divided into three treatment groups to receive subcutaneous injection of nicotine at 0.5 mg/kg pre d for 1, 2 and 3 months, and a control group to receive saline only. After treatment, the corpus cavernosum was harvested for detection of CO concentration by modified two-wavelength spectrophotometry and NOS activity by improved Griess measurement.

RESULTSCO concentration and NOS activity were decreased by 9.05 and 13.37%, respectively, after 1 month of nicotine injection (P < 0.01), 16.47 and 22.5% after 2 months (P < 0.01), and 22.99 and 31.74% after 3 months (P < 0.01), as compared with (13.664 +/- 0.404) umol/mg prot and (9.721 +/- 0.470) U/mg prot in the control group.

CONCLUSIONNicotine can reduce endogenous CO concentration and NOS activity in the corpus cavernosum of adult male rats, which suggests the involvement of endogenous CO and NOS in the pathophysiological process of smoking-induced erectile dysfunction .

Animals ; Carbon Monoxide ; metabolism ; Erectile Dysfunction ; chemically induced ; Male ; Nicotine ; toxicity ; Nitric Oxide Synthase ; metabolism ; Penis ; metabolism ; Rats ; Smoking ; adverse effects

Carbon monoxide has been proved to be an important signal molecule in body. Transition metal carbonyl compounds are solidified form of carbon monoxide. Numerous studies have shown that Ruthenium carbonyl carbon monoxide releasing molecules have a strong pharmacological activity. In this paper, five Ruthenium (II) carbonyl CORMs 1-5 were synthesized and their toxicology, tissue distribution and interaction with blood endogenous substances were investigated. The results showed CORMs' IC50 to fibroblasts are ranged from 212.9 to 2089.2 micromol x L(-1). Their oral LD50 to mouse is between 800 to 1600 mg x kg(-1). After repeated administration, CORMs 1 and CORMs 5 haven't shown an obvious influence to rats' liver and kidney function, but caused the injury to liver and kidney cells. The in vivo distribution result revealed the majority of CORMs were distributed in blood, liver and kidney, only a small part of CORMs distributed in lung, heart and spleen. They could scarcely cross the blood-brain barrier and distribute to brain. The non-CO ligands in structure have an obvious relevance to their in vivo absorption and distribution. Interestingly, CORMs could enhance the fluorescence of bovine serum albumin, and this enhancement was in direct proportion with the concentration of CORMs. Under different conditions, interaction of CORMs with glutathione got different type of products, one is Ruthenium (II) tricarbonyl complexes, and Ruthenium (II) dicarbonyl complexes.
Animals ; Carbon Monoxide ; chemistry ; pharmacokinetics ; toxicity ; Fibroblasts ; drug effects ; Kidney ; drug effects ; Liver ; drug effects ; Mice ; Molecular Structure ; Organometallic Compounds ; chemical synthesis ; chemistry ; pharmacokinetics ; toxicity ; Rats ; Rats, Wistar ; Ruthenium ; chemistry ; pharmacokinetics ; toxicity ; Tissue Distribution

OBJECTIVES: The association between concentrations of sulfur dioxide (SO), nitrogen dioxide (NO), carbon monoxide (CO), ozone (O), and emergency ambulance dispatches (EADs) for asthma was explored in the central Sichuan Basin of southwestern China for the first time. METHODS: EADs for asthma were collected from the Chengdu First-Aid Command Center. Pollutant concentrations were collected from 24 municipal environmental monitoring centers and including SO, NO, CO, daily 8-h mean concentrations of O (O-8 h), and particulate matter less than 2.5 μm in aerodynamic diameter (PM). The climatic data were collected from the Chengdu Municipal Meteorological Bureau. All data were collected from years spanning 2013-2017. A time-stratified case-crossover design was used to analyze the data. RESULTS: After controlling for temperature, relative humidity, and atmospheric pressure, IQR increases in SO (13 μg/m), NO (17 μg/m), and CO (498 μg/m) were associated with 18.8%, 11.5%, and 3.1% increases in EADs for asthma, respectively. The associations were strongest for EADs and SO, NO, and CO levels with 3-, 5-, and 1-day lags, respectively. CONCLUSIONS This study provides additional data to the limited body of literature for potential health risks arising from ambient gaseous pollutants. The results of the study suggest that increased concentrations of SO, NO, and CO were positively associated with emergency ambulance dispatches for asthma in Chengdu, China. Further studies are needed to investigate the effects of individual air pollutants on asthma.
Air Pollutants ; analysis ; toxicity ; Asthma ; chemically induced ; epidemiology ; Carbon Monoxide ; analysis ; toxicity ; China ; epidemiology ; Cities ; Cross-Over Studies ; Emergency Medical Dispatch ; statistics & numerical data ; Environmental Monitoring ; statistics & numerical data ; Humans ; Nitrogen Dioxide ; analysis ; toxicity ; Ozone ; analysis ; toxicity ; Particle Size ; Particulate Matter ; analysis ; toxicity ; Risk ; Sulfur Dioxide ; analysis ; toxicity