Biophysical and computational comparison on the binding affinity of three important nutrients to β-lactoglobulin: folic acid, ascorbic acid and vitamin K3

2017 ◽  
Vol 36 (14) ◽  
pp. 3651-3665 ◽  
Author(s):  
Somaye Shahraki ◽  
Ali Heydari ◽  
Maryam Saeidifar ◽  
Masoumeh Gomroki
1952 ◽  
Vol 194 (2) ◽  
pp. 711-714
Author(s):  
Morton A. Schwartz ◽  
J.N. Williams
Keyword(s):  

1952 ◽  
Vol 197 (1) ◽  
pp. 481-484
Author(s):  
Morton A. Schwartz ◽  
J.N. Williams
Keyword(s):  

1969 ◽  
Vol 36 (3) ◽  
pp. 447-454 ◽  
Author(s):  
J. E. Ford ◽  
J. W. G. Porter ◽  
S. Y. Thompson ◽  
Joyce Toothill ◽  
J. Edwards-Webb

SummaryThe vitamin content of ultra-high-temperature (UHT) processed milk was compared with that of the original raw milk. Three processes were used. In the first, which caused no change in oxygen content, the milk was heated and cooled in a plate-type heat exchanger. In the second, the milk was again heated indirectly and then evaporatively cooled, leaving in the milk about one-third of the initial oxygen content. In the third process the milk was heated by direct steam injection and cooled by evaporation and contained little or no residual oxygen.On processing and during subsequent storage for 90 days there was no loss of vitamin A, carotene, vitamin E, thiamine, riboflavine, pantothenic acid, biotin or nicotinic acid. There was little or no loss of vitamin B6or vitamin B12on processing, but up to 50% of each of these vitamins was lost during 90 days' storage. All the dehydroascorbic acid (DHA) and about 20% of the ascorbic acid (AA) was lost on processing. There was no further loss of AA during 90 days’ storage when no residual oxygen was present, but in milks containing more than about 1 ppm oxygen all the AA was lost within 14 days. About 20% of the folic acid was lost on processing; thereafter, as with ascorbic acid, the extent of the loss on storage depended on the residual oxygen content of the milk: in the absence of oxygen the folic acid was stable.


Author(s):  
Noer Abyor Handayani ◽  
Elsa Anisa Krisanti ◽  
Yunita Sadeli ◽  
Sutrasno Kartohardjono ◽  
Kamarza Mulia

2019 ◽  
Vol 3 (6) ◽  
pp. 993-1002
Author(s):  
Neelima Paladugula ◽  
Zia Fazili ◽  
Maya R Sternberg ◽  
Gwendolyn Gabey ◽  
Christine M Pfeiffer

Abstract Background Serum folate forms, and particularly tetrahydrofolate, are sensitive to oxidation. Methods Using a repeated measures design, we investigated the stability of folate forms in convenience samples with added ascorbic acid (AA; 5 g/L) analyzed initially and after variable (approximately 1–33 weeks) storage time at −70 °C. We examined the recovery of tetrahydrofolate added at different spiking levels to serum with and without AA (5 g/L). We also assessed the long-term frozen storage stability of folate forms. Results Repeat analysis produced consistent results with the initial analysis; the mean relative change (95% CI; Lin's concordance correlation between initial and repeat result; sample size) was 0.08% (−0.24% to 0.39%; rc = 0.999; n = 301) for 5-methyltetrahydrofolate, 4.23% (2.44%–6.05%; rc = 0.984; n = 211) for pyrazino-s-triazine derivative of 4α-hydroxy-5-methyltetrahydrofolate (MeFox), −0.22% (−1.90% to 1.49%; rc = 0.986; n = 214) for folic acid, and 1.49% (−2.71% to 5.88%; rc = 0.889; n = 81) for tetrahydrofolate. Linear regression testing for a time trend indicated an estimated average percent change of less than ±5% for samples retested after 4 months: 5-methyltetrahydrofolate Ptrend = 0.0007, folic acid Ptrend < 0.0001, MeFox Ptrend = 0.38, and tetrahydrofolate Ptrend = 0.0256. The mean ± SD tetrahydrofolate spiking recovery was 96.7% ± 9.4% for serum with added AA, but <50% for serum without added AA. We observed ≤10% loss for most serum folate forms during 4 years of storage at −70 °C. Conclusions Serum containing added AA showed acceptable stability of folate forms during repeat analysis from the same vial within 4 months, complete spiking recovery of tetrahydrofolate during sample processing, and long-term frozen storage stability of folate forms.


2008 ◽  
Vol 21 (1) ◽  
pp. 67-71 ◽  
Author(s):  
P. C. Leclerc ◽  
C. D. Proulx ◽  
G. Arguin ◽  
S. Belanger ◽  
F. Gobeil ◽  
...  

1990 ◽  
Vol 156 (6) ◽  
pp. 878-882 ◽  
Author(s):  
M. W. P. Carney

Recently, research into the connection between vitamins and psychiatric disorder, particularly affective changes, has been in the doldrums, with the exceptions perhaps of studies of folic acid and pyridoxine. The best way for research to proceed is first to establish that the association of a vitamin deficiency with a psychiatric disorder is beyond a chance finding. Then, questions should be asked about what mental symptoms it is linked with, and what the other associations (malnutrition, drugs, physical illness, etc) are. Lastly, queries should be raised about whether the association is causal or if the mental symptoms are merely secondary to the anorexia and poor diet so common in mental illness (or whether they are linked in a vicious circle as suggested by Reynoldset al(1971)). These questions became pertinent in the mid-1960s when reliable ways of assaying B vitamins such as folic acid became more generally available. In this review, I present evidence that deficiencies of folic acid, B12, thiamine, riboflavin, pyridoxine and ascorbic acid are not infrequently found in psychiatric practice. It should be remembered, however, that some ways of assaying vitamins are liable to give a larger proportion of spurious low results than other methods (false positives), although the adoption of more reliable ways of assaying vitamins should reduce this.


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