Superiority of TiO<sub>2</sub> Supported on the Nickel Foam Over Ni Doped TiO<sub>2</sub> in the Photothermal Decomposition of Acetaldehyde
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Acetaldehyde decomposition was performed under heating at the temperature range of 25-125oC and UV irradiation on TiO2 doped by the metallic Ni powder and TiO2 supported on the nickel foam. Process was carried out in high temperature reaction chamber “The Praying MantisTM”, with simultaneous in situ FTIR measurements and UV irradiation. Ni powder was added to TiO2 in the quantity of 0.5 to 5.0 wt%. Photothermal measurements of acetaldehyde decomposition indicated, that the highest yield of acetaldehyde conversion on TiO2 und UV irradiation was obtained at 75oC. Doping of nickel to TiO2 did not increase its photocatalytic activity. Contrary to that, application of nickel foam as a support for TiO2 appeared to be highly advantageous, because increased decomposition of acetaldehyde from 31 to 52% at 25oC and then to 85% at 100oC by comparison with TiO2 itself. At the same time mineralisation of acetaldehyde to CO2 increased two times at the presence of nickel foam. However, oxidised nickel foam used as support for TiO2 was detrimental. Most likely, different mechanisms of electrons transfer between Ni-TiO2 and NiO-TiO2 occurred. Application of nickel foam greatly enhanced separation of free carriers in TiO2. As a consequence, high yields of the photocatalytic reactions were obtained.Keywords:
Non-blocking I/O
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Ethanol metabolism
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Acetaldehyde is an intermediate of alcohol metabolism,but its effect on alcohol dependence is not clear. It was performed with conditioned place preference(CPP)and conditioned taste preference(CTP) experiments to investigate the effects of acetaldehyde on the alcohol dependence in mice. The mice showed significant CPP to ethanol (n = 6,P 0.01)while training with ethanol for 8 times after pre-treatment with 0.8% ethanol for 7 days,but no significant CPP effect on acetaldehyde was observed (n = 6,P 0.05). While trained with 0.8% ethanol and with 0.4% acetaldehyde, the CPP effect to ethanol decreased (n=6, P 0.01). Mice also showed the CTP to ethanol after drinking water and 10% ethanol for 7 days (n = 6, P 0.01),but the CTP to ethanol decreased while 1% acetaldehyde was added in drinking water. Mice showed no CTP to ethanol after treated with 1% acetaldehyde for 7 days,but the drinking to the admixture of ethanol and acetaldehyde increased. The results showed that acetaldehyde had important roles in alcohol dependence behavior in mice.
Ethanol metabolism
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Acetaldehyde is one of the most important flavor ingredients in beer.Excess acetaldehyde produces a grassy or apple-like off-flavor.One target of beer production is to produce the beer with low acetaldehyde content.It was summarized about the properties of acetaldehyde,the metabolism of acetaldehyde in Saccharomyces cerevisiae during fermentation and aging,the factors impacting acetaldehyde content in beer,and some research progress on acetaldehyde content control.
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복어추출물이 acetaldehyde의 산화 효소에 어떤 영향을 주는가를 관찰할 목적으로 실험동물에 복어추출물을 투여한 다음 acetaldehyde의 대사에 미치는 영향을 관찰하였다. 복어추출물(100㎎/㎏)을 2주간 전처리하고 acetaldehyde(100㎎/㎏)를 투여하므로 혈액 및 간조직중 acetaldehyde의 농도가 acetaldehyde 단독 투여군보다 현저히 감소되었다. 한편, 25% alcohol 용액을 6주간 섭취케한 군에서도 복어추출물의 투여로 acetaldehyde의 농도가 감소됨을 관찰하였다. 복어추출물을 전처리하고 5g/㎏의 alcohol용액을 투여한 급성 중독실험에서 mitochodrial aldehyde dehydrogenase(Ald DH)의 활성이 alcohol 단독투여군 보다 약 30% 증가되었다. 25% alcohol용액을 6주간 섭취한 흰쥐에 복어추출물을 투여하므로 Ald DH의 활성이 alcohol의 단독투여로 억제되던 현상이 회복되었다. Disulfiram(300㎎/㎏)을 3일간 투여하므로 정상 동물군과 alcohol 투여군에서 Ald DH활성이 억제되던 것이 복어추출물의 투여로 정상 수준에 가깝게 증가되었다. 시험관내 실험에서 alcohol의 투여로 유도된 효소원에 복어추출물을 10㎎/ml까지 첨가하였으나 본 효소의 활성에는 별다른 영향이 없었다. 이상의 실험결과 복어추출물은 Ald DH의 활성을 조절하므로써 급성 및 아급성 alcohol 중독의 해독에 사용될 수 있는 가능성을 시사한 것으로 사료된다.
Disulfiram
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Human blood
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1. Removal of acetaldehyde and ethanol has been studied in perfused rat livers. 2. The maximum rate of ethanol oxidation was 2μmol/min per g of liver, which was less than the calculated capacity of the ethanol-oxidizing system. The lactate/pyruvate ratio of the medium increased with the rate of ethanol removal. At low ethanol concentrations most of the acetaldehyde formed was oxidized further, but at ethanol concentrations above 16mm about 60% of the acetaldehyde left the liver unmetabolized. 3. At lower concentrations the greater part of added acetaldehyde was oxidized, but above 5mm, 50–60% of that removed was recovered as ethanol. 4. When the reduction of acetaldehyde was blocked by pyrazole, removal was strongly diminished. There was no effect on the lactate/pyruvate ratio during oxidation of low concentrations of acetaldehyde, even in the presence of pyrazole, but at higher concentrations a gradual increase occurred. 5. The results indicate that during ethanol oxidation the ethanol/acetaldehyde pair is not in redox equilibrium with the lactate/pyruvate pair. Ethanol oxidation was abolished by addition of acetaldehyde. Under these conditions the lactate/pyruvate ratio was 1.5–1.8 times the ethanol/acetaldehyde ratio, indicating equilibration of the alcohol dehydrogenase and lactate dehydrogenase systems. 6. The results support the view that ultimately the rate of mitochondrial oxidation of NADH limits the removal of ethanol in the liver.
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Acetaldehyde, the first metabolite of ethanol oxidation, has been proposed as a major initiating factor in ethanol-induced liver injury. The aims of this study were to examine whether acetaldehyde is absorbable from the digestive tract and whether, when delivered chronically in drinking water, it is capable of inducing liver injury in rats. Acetaldehyde concentrations in the rat portal and peripheral blood were measured by head space gas chromatography after intragastric (5 ml) and intracolonic (3 ml) administration of 20 mM acetaldehyde solution. In the hepatotoxicity study, rats were exposed to acetaldehyde (20 and 120 mM) delivered in drinking water for 11 weeks and histopathological changes in the liver were morphometrically assessed. Peak blood acetaldehyde levels were found at 5 min after acetaldehyde infusion and were 235±11 μμ (mean±SE) after intragastric and 344±83 μμ after intracolonic infusion of 20 mM acetaldehyde solution. The exposure of rats to 120 mM acetaldehyde solution for 11 weeks resulted in the development of fatty liver and inflammatory changes. Morphometric analysis showed significantly more fat accumulation in rats receiving 120 mM acetaldehyde solution (85±2 per cent of hepatocytes occupied by fat) than in rats receiving 20 mM acetaldehyde solution (38±11 per cent) or in controls (36±10 per cent). The dose of extrahepatic acetaldehyde (500 mg/kg per day) producing liver injury corresponds to only around 3 per cent of that derived from hepatic ethanol oxidation in animals receiving an ethanol-containing totally liquid diet (15 g/kg per day). These results indicate that acetaldehyde delivered via the digestive tract can reach the liver by the portal circulation and that acetaldehyde of extrahepatic origin appears to be more hepatotoxic than acetaldehyde formed during ethanol oxidation within the liver.
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The aim of the present paper is to update the status regarding human acetaldehyde levels in blood, breath and saliva during normal ethanol oxidation, i.e. without deficiency in, or inhibition of, aldehyde dehydrogenase activity. The previous conclusion according to which no detectable (<0.5 microM), adequately determined 'free and/or loosely bound' acetaldehyde has not yet been found in venous blood, more or less, still holds. The only new findings within this context consist of low venous blood acetaldehyde levels (1-3 microM on average) observed in some women during the use of oral contraceptives or during the high oestradiol phases of normal menstrual cycle. Breath acetaldehyde levels are about 10-20 and 20-40nM at blood ethanol concentrations of about 10 and 20mM, respectively. Theoretically calculated corresponding blood acetaldehyde levels in pulmonary blood would be about 2-4 and 4-8 microM. The acetaldehyde in the breath most likely reflects pulmonary blood acetaldehyde, microbial and tissue acetaldehyde production in the aerodigestive tract. As well as with breath acetaldehyde, salivary acetaldehyde levels also correlate positively with the blood ethanol concentrations. At blood ethanol concentrations of about 10 and 20 mM the average acetaldehyde concentration in saliva is about 15-25 and 20-40 microM, respectively. Saliva acetaldehyde represents mostly microbial acetaldehyde formation in the oral cavity, but also, to some extent, ethanol oxidation in nearby tissues. More studies are still needed to clarify the proportion of the underlying sources for blood, breath and salivary acetaldehyde at different ethanol concentrations. The problem with rapid acetaldehyde oxidation, which may markedly affect the recovery of low acetaldehyde levels, also needs to be solved.
Venous blood
Ethanol metabolism
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Experiments on white rats were carried out to confirm an important role of acetaldehyde in pathogeny of alcoholism. It is evidenced by results of experiments when animals were given acetaldehyde and medichronal (a drug which combines acetaldehyde) and by data obtained in the course of studies of changes in the content of endogenic ethanol and acetaldehyde, activity of alcohol dehydrogenase and aldehyde dehydrogenase, concentration of biogenic amines (catecholamines and serotonin) in the blood and brain structures.
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