Solvent effect of aqueous ethanol on complex formation and protolytic equilibria in nicotinic acid solutions

2008 ◽  
Vol 53 (12) ◽  
pp. 1943-1947 ◽  
Author(s):  
N. N. Kuranova ◽  
S. V. Dushina ◽  
V. A. Sharnin
2020 ◽  
Vol 94 (10) ◽  
pp. 2030-2033
Author(s):  
N. N. Kuranova ◽  
N. A. Chesnokova ◽  
A. S. Gushchina ◽  
K. V. Grazhdan ◽  
V. A. Sharnin

2012 ◽  
Vol 116 (39) ◽  
pp. 12057-12064 ◽  
Author(s):  
Yunqi Li ◽  
Ji Li ◽  
Qiuyang Xia ◽  
Boce Zhang ◽  
Qin Wang ◽  
...  

1965 ◽  
Vol 43 (6) ◽  
pp. 1770-1777 ◽  
Author(s):  
R. Anantaraman ◽  
K. Saramma

The rates of mercuric chloride catalyzed solvolysis of some alkyl chlorides in aqueous acetone and ethanol solvents have been compared. It is found that the increase in rate on changing from the acetone to the ethanol solvent is less in the catalyzed than in the normal reaction. On the basis that the electrophilic activity of the catalyst is less in aqueous ethanol than in aqueous acetone an explanation for the anomaly has been suggested. The effect, on the rates of solvolysis, of added chloride ions is in accord with the suggested explanation.


1970 ◽  
Vol 23 (4) ◽  
pp. 757 ◽  
Author(s):  
VK Grover ◽  
YK Gupta

Oxidations of DL-atrolactic and 2-hydroxyisobutyric acids by cerium(IV) in sulphuric acid solution occur in accordance with the empirical rate law: (see equation in article) where k1 is a complex rate constant and A is an unspecified constant. Spectrophotometric results suggest complex formation between cerium(1v) and the organic acid, but no kinetic evidence was obtained. Manganese(11) catalyses the reactions. DL-Atrolactic acid is more reactive than 2-hydroxyisobutyric acid. The products of oxidations were acetophenone and acetone respectively.


1967 ◽  
Vol 21 (3) ◽  
pp. 547-556 ◽  
Author(s):  
K.-H. Kiessling ◽  
L. Pilström

1. Feeding rats with a 15% ethanol solution for several weeks caused structural and functional changes in their liver mitochondria, although their intake of solid food was about the same as that of the controls.2. Attempts were made to counteract these effects of ethanol by increasing the intake of amino acids, vitamins, lipotropic compounds and electrolytes beyond that which is adequate when water is the drinking fluid.3. An increased intake of nicotinic acid, together with aqueous ethanol, caused a further enlargement of the mitochondria above that obtained with ethanol solution alone. the diluted matrix observed with the ethanol and nicotinic acid treatment suggested that water imbibition by the mitochondria caused this further enlargement.4. In rats receiving ethanol fortified with magnesium sulphate and lipotropic compounds (choline, methionine) there was a further increase in mitochondrial size, as compared with those receiving ethanol alone. The matrix was, however, of the same density as in the mitochondria from the rats receiving ethanol alone. the oxidation rate of pyruvate and succinate was unchanged, but α-glycerophosphate and β-hydroxybutyrate were oxidized at a higher rate than in mitochondria from rats drinking ethanol or water.5. When the ethanol solution was supplemented with amino acids (casein hydrolysate), vitamins and electrolytes, the mitochondrial enlargement after 120 days of treatment was less than with ethanol alone and was completely absent after 300 days. the oxidation rate of pyruvate and succinate was, however, not fully restored to normal.


1974 ◽  
Vol 28a ◽  
pp. 1089-1100 ◽  
Author(s):  
Sten Ahrland ◽  
Jan-Olov Bovin ◽  
Aase Hvidt ◽  
Arne Kjekshus ◽  
Bernt Klewe ◽  
...  

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