Effect of pH on polarity of purines and pyrimidines

1968 ◽  
Vol 22 (2) ◽  
pp. 345-348 ◽  
Author(s):  
C.E. Hedrick ◽  
Gary McDougall
HortScience ◽  
1998 ◽  
Vol 33 (3) ◽  
pp. 550a-550 ◽  
Author(s):  
Royal G. Fader ◽  
Martin J. Bukovac

We have reported that NH4NO3 (AN, 8 mM, pH 4.2), applied as simulated spray droplets, enhanced penetration of 14C-NAA through isolated leaf and fruit cuticles. One explanation for this response is that AN depresses NAA (pKa= 4.2) dissociation, increasing the nondissociated moiety, which penetrates more readily than the anion (NAA'). Direct measurement of AN (concn. 0-800 mM) effect on NAA (215 μM) dissociation as indexed by change in solution pH revealed no significant effect, with a pH change from 4.19 to 4.05. This change is not sufficient to account for the observed enhancement. When 14C-NAA, buffered (20 mM sodium citrate) at pH 3.2, 4.2, 5.2, 6.2, was partitioned against chloroform, there was a marked increase in NAA partitioning into chloroform as pH was decreased. AN (8 mM) did not alter this partition behavior, also indicating no effect on NAA dissociation. However, in cuticle penetration studies, using a finite dose system with 14C-NAA buffered at pH 3.2, 4.2, 5.2, 6.2, and in the presence and absence of 8 mM AN, there was no marked or consistent pH or AN (-70 to + 232 % of no AN control) effect on penetration as indexed by initial slope (4-12 h) or penetration after 120 h. The possible effects of AN and buffer on penetration of 14C-NAA from the droplet deposit will be discussed.


Author(s):  
Debanjan Kundu ◽  
Vikash Kumar Dubey

Abstract:: Various neurodegenerative disorders have molecular origin but some common molecular mechanisms. In the current scenario, there are very few treatment regimens present for advanced neurodegenerative diseases. In this context, there is an urgent need for alternate options in the form of natural compounds with an ameliorating effect on patients. There have been individual scattered experiments trying to identify potential values of various intracellular metabolites. Purines and Pyrimidines, which are vital molecules governing various aspects of cellular biochemical reactions, have been long sought as crucial candidates for the same, but there are still many questions that go unanswered. Some critical functions of these molecules associated with neuromodulation activities have been identified. They are also known to play a role in foetal neurodevelopment, but there is a lacuna in understanding their mechanisms. In this review, we have tried to assemble and identify the importance of purines and pyrimidines, connecting them with the prevalence of neurodegenerative diseases. The leading cause of this class of diseases is protein misfolding and the formation of amyloids. A direct correlation between loss of balance in cellular homeostasis and amyloidosis is yet an unexplored area. This review aims at bringing the current literature available under one umbrella serving as a foundation for further extensive research in this field of drug development in neurodegenerative diseases.


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