On the interaction of carbon monoxide with ternary Cu/ZnO/Al2O3 catalysts: modeling of dynamic morphological changes and the influence on elementary step kinetics

M. Peter; J. Fendt; S. Pleintinger; O. Hinrichsen

doi:10.1039/c2cy20189e

Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

BMC Emergency Medicine ◽

10.1186/s12873-021-00405-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Hitoshi Koga ◽

Hideki Tashiro ◽

Kouta Mukasa ◽

Tomohiro Inoue ◽

Aya Okamoto ◽

...

Keyword(s):

Carbon Monoxide ◽

Qt Interval ◽

Troponin I ◽

Morphological Changes ◽

Carbon Monoxide Poisoning ◽

Myocardial Damage ◽

Qt Dispersion ◽

Ecg Changes ◽

Corrected Qt Interval ◽

Logistic Analysis

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

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Protection against cisplatin-induced nephrotoxicity by a carbon monoxide-releasing molecule

AJP Renal Physiology ◽

10.1152/ajprenal.00363.2005 ◽

2006 ◽

Vol 290 (4) ◽

pp. F789-F794 ◽

Cited By ~ 89

Author(s):

Yasin Tayem ◽

Tony R. Johnson ◽

Brian E. Mann ◽

Colin J. Green ◽

Roberto Motterlini

Keyword(s):

Carbon Monoxide ◽

Caspase 3 ◽

Morphological Changes ◽

Antineoplastic Agent ◽

Negative Control ◽

Water Soluble ◽

Plasma Urea ◽

Therapeutic Benefits ◽

Corticomedullary Junction

Nephrotoxicity is one of the main side effects caused by cisplatin (CP), a widely used antineoplastic agent. Here, we examined the effect of a novel water-soluble carbon monoxide-releasing molecule (CORM-3) on CP-mediated cytotoxicity in renal epithelial cells and explored the potential therapeutic benefits of carbon monoxide in CP-induced nephrotoxicity in vivo. Exposure of LLC-PK1 cells to CP (50 μM) caused significant apoptosis as evidenced by caspase-3 activation and an increased number of floating cells. Treatment with CORM-3 (1–50 μM) resulted in a remarkable and concentration-dependent decrease in CP-induced caspase-3 activity and cell detachment. This effect involved activation of the cGMP pathway as 1H-oxadiazole [4, 3-a] quinoxaline-1-ore (ODQ), a guanylate cyclase inhibitor, completely abolished the protection elicited by CORM-3. Using a rat model of CP-induced renal failure, we found that treatment with CP (7.5 mg/kg) caused a significant elevation in plasma urea (6.6-fold) and creatinine (3.1-fold) levels, which was accompanied by severe morphological changes and marked apoptosis in tubules at the corticomedullary junction. A daily administration of CORM-3 (10 mg/kg ip), starting 1 day before CP treatment and continuing for 3 days thereafter, resulted in amelioration of renal function as shown by reduction of urea and creatinine levels to basal values, a decreased number of apoptotic tubular cells, and an improved histological profile. A negative control (iCORM-3) that is incapable of liberating CO failed to prevent renal dysfunction mediated by CP, indicating that CO is directly involved in renoprotection. Our data demonstrate that CORM-3 can be used as an effective therapeutic adjuvant in the treatment of CP-induced nephrotoxicity.

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An atomic-level insight into the basic mechanism responsible for the enhancement of the catalytic oxidation of carbon monoxide on a Cu/CeO2 surface

Physical Chemistry Chemical Physics ◽

10.1039/c6cp05957k ◽

2017 ◽

Vol 19 (5) ◽

pp. 3498-3505 ◽

Cited By ~ 5

Author(s):

Kenichi Koizumi ◽

Katsuyuki Nobusada ◽

Mauro Boero

Keyword(s):

Carbon Monoxide ◽

Reaction Mechanism ◽

Catalytic Oxidation ◽

Morphological Changes ◽

Basic Mechanism ◽

Atomic Level ◽

Insight Into ◽

Oxidation Of Carbon Monoxide

Reaction mechanism of CO molecules onto a Cu/CeO2 surface and morphological changes.

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Effects of volatile organic compounds and carbon monoxide mixtures on learning and memory, oxidative stress, and monoamine neurotransmitters in the brains of mice

Toxicology and Industrial Health ◽

10.1177/0748233717747504 ◽

2018 ◽

Vol 34 (3) ◽

pp. 178-187 ◽

Cited By ~ 8

Author(s):

Fan Wang ◽

Zheng Fangfang ◽

Xiangmeng Guo ◽

Wanguang Chen ◽

Weiyun Yao ◽

...

Keyword(s):

Carbon Monoxide ◽

Volatile Organic Compounds ◽

Learning And Memory ◽

Organic Compounds ◽

Morphological Changes ◽

Quality Standard ◽

Monoamine Neurotransmitters ◽

Volatile Organic ◽

Total Antioxidant ◽

Exposure Experiment

In this study, we investigated the effect of inhaled mixtures of volatile organic compounds (VOCs) and carbon monoxide (CO) on neuroethology. Fifty 6-week-old male Kunming mice were exposed in five similar static chambers; zero (control) and four different doses of VOC and CO mixtures (G1–G4) for 10 consecutive days and 2 h/day. The compounds and concentrations were as follows: formaldehyde, benzene, toluene, xylene, and CO as 0.10 + 0.11 + 0.20 + 0.20 + 10.00 mg/m3, 0.20 + 0.22 + 0.40 + 0.40 + 20.00 mg/m3, 1.00 + 1.10 + 2.00 + 2.00 + 100.00 mg/m3, and 5.00 + 5.50 + 10.00 + 10.00 + 500.00 mg/m3, respectively, which corresponded to 1, 2, 10, and 50 times the indoor air quality standard in China. Morris water maze and grip strength tests were performed during the exposure experiment. One day following the final exposure, oxidative damage levels, monoamine neurotransmitters, monoamine oxidase (MAO), and morphology of mice brain were analyzed. Escape latency, dopamine, norepinephrine (NE), and serotonin decreased significantly, while total antioxidant capacity, glutathione peroxidase, and MAO increased significantly in G3 and G4. In addition, there were morphological changes and degeneration of neurons in the dentate gyrus regions of the hippocampus in G4. Results showed that the inhaled mixtures of VOCs and CO affected learning and memory of mice. The impairment of monoamine neurotransmitter associated with MAO may be one of the mechanisms of learning and memory impairment of the mice induced by the mixtures of VOCs and CO.

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Can Indices of Myocardial Damage Predict Carbon Monoxide Poisoning Outcomes?

10.21203/rs.3.rs-84717/v1 ◽

2020 ◽

Author(s):

Hitoshi Koga ◽

Hideki Tashiro ◽

Kouta Mukasa ◽

Tomohiro Inoue ◽

Aya Okamoto ◽

...

Keyword(s):

Carbon Monoxide ◽

Qt Interval ◽

Troponin I ◽

Morphological Changes ◽

Carbon Monoxide Poisoning ◽

Myocardial Damage ◽

Qt Dispersion ◽

Ecg Changes ◽

Corrected Qt Interval ◽

Logistic Analysis

Abstract Background: Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is not clear, however, whether the indices of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relation between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning.Results: Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P=0.0072, R2=0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P<0.001, R2=0.2358) and the corrected QT dispersion and carboxyhemoglobin (P<0.001, R2=0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were hyperbaric oxygen therapy (P=0.0182), corrected QT dispersion (P=0.0062), and troponin I level (P=0.0002).Conclusions: Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

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Can indices of myocardial damage predict carbon monoxide poisoning outcomes?

10.21203/rs.3.rs-43628/v1 ◽

2020 ◽

Author(s):

Hitoshi Koga ◽

Hideki Tashiro ◽

Kouta Mukasa ◽

Tomohiro Inoue ◽

Aya Okamoto ◽

...

Keyword(s):

Carbon Monoxide ◽

Qt Interval ◽

Troponin I ◽

Morphological Changes ◽

Carbon Monoxide Poisoning ◽

Myocardial Damage ◽

Qt Dispersion ◽

Ecg Changes ◽

Corrected Qt Interval ◽

Logistic Analysis

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is not clear, however, whether the indices of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relation between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Results Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were hyperbaric oxygen therapy (P = 0.0182), corrected QT dispersion (P = 0.0062), and troponin I level (P = 0.0002). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

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