Quote: Originally posted by AJKOER  | |
.......related goal is to use the recycling ability of the aluminum ion with respect to transition metals to their lower valence states as a means to foster chemical decomposition reactions. The first alluded to article is ‘Oxidative Stress Gated by Fenton and Haber Weiss Reactions and Its Association with Alzheimer’s Disease’ by Tushar Kanti Das, et al, published in Archives of Neuroscience, July 2014 2(3): e20078, DOI: 10.5812/archneurosci.20078. The authors cite, in Figure 4, “ Formation of Aluminum Superoxide Semi reduced Radical Ion and Aluminum Superoxide Complex (43)”, with described reactions proceeding as follows (also adopting notation and water complexing from the second article): [Al(H2O)4](3+) + O2•− <-> [Al(O2•−)(H2O)4](2+) [Al(O2•−)(H2O)4](2+) + Fe(3+) --> O2 + [Al(H2O)4](3+) + Fe(2+) And, in the presence of H+ : [Al(H2O)4](3+) + O2•− + H+ <-> [Al(O2•−)(H+)H2O)4](3+) [Al(O2•−)(H+)H2O)4](3+) + [Al(O2•−)(H+)H2O)4](3+) --> 2 [Al(H2O)4](3+) + H2O2 + O2 Note per below, the action of hydrogen peroxide on ferric also leads to ferrous: H2O2 = H+ + HO2- Fe(3+) + HO2- --> Fe(2+) + •HO2 ( or, pH> 4.88, H+ + O2•− ) Hydroxyl radical can also be formed via the classic Fenton reaction: Fe(2+) + H2O2 --> Fe(3+) + •OH + OH- Another work: ‘Pro-oxidant Activity of Aluminum: Stabilization of the Aluminum Superoxide Radical Ion’ by J. I. Mujika, F. Ruiperez, I. Infante, J. M. Ugalde, C. Exley, and X. Lopez in J., published in Phys. Chem. A 2011, 115, 6717–6723, American Chemical Society, dx.doi.org/10.1021/jp203290b .Link: https://s3.amazonaws.com/academia.edu.documents/50520932/Pro... . In the Mujika article to quote “In addition, the presence of LMM ligands such as citrate could also have an indirect effect in the oxidation capacity of aluminum by augmenting the bioavailability of Al3+ species, shifting the formation of Al(OH)4- to higher pH’s. However, one should also take into account the effect of citrate chelation itself in the thermodynamic equilibrium of [AlO2•]2+ formation.” ADDITIONAL THEORY FOR AN EXPERIMENT With respect to the chemistry, some more reactions relating to formation of superoxide, solvated electrons electrons and ferric salts per a planned experiment: •OH + H2O2 = O2•− + H+ + H2O (or HO2• for pH < 4.88) Al --> Al3+ + 3 e- Fe2+ + 2 e- --> Fe ------------------------- Net Electrochemical Cell: Al + Fe2+ --> Al3+ + Fe + e- e- + n H2O = e-(aq) e-(aq) + O2 = O2•− From the added presence of Citric acid crystals, Fe2+ --> Fe3+ + e- e- + OH• --> OH- -------------------------- Fe2+ + OH• --> Fe3+ + OH- (the creation of a basic ferric citrate from a hydroxyl radical attack) Yet more chemistry from a prior thread (see http://www.sciencemadness.org/talk/viewthread.php?tid=77977 ):
An added quote from the Vidrio's work detailing the limited recycling ability of citrate (and ascorbate): “Similar reactions can occur with Cu, Cr and Ni. Furthermore, biological chelators and reductants can greatly enhance the production of ROS (Burkitt et al., 1991; Engelmann et al., 2003; Wenk et al., 2001). For example, in the presence of ascorbate (Asc), a biological reductant, the oxidized form of the transition metal produced by the Fenton reaction can be reactivated (R2 and R3), thus allowing additional ROS to be produced. Fe(III) + Ascn → Fe(II) + Ascn+1 (R2) Cu(II) + Ascn → Cu(I) + Ascn+1 (R3) “ ...... Note reference (43) is “Exley C. The coordination chemistry of aluminium in neurodegenerative disease. Coordina Chmst Rev. 2012;256(19-20):2142–6. Here is the Abstract and Highlights: “The coordination chemistry of aluminium in neurodegenerative disease, Link: https://doi.org/10.1016/j.ccr.2012.02.020 Abstract The coordination chemistry of a metal ion defines its optimal association with a biomolecule such that its binding by specific ligands on that molecule confers function and biological purpose. Aluminium is a non-essential metal with no known biological role which means that its coordination neurochemistry defines aluminium's putative role in a number of neurodegenerative diseases. In examining this chemistry it is found that very little is known about the complexes formed and ligands involved in aluminium's interactions with neurochemically-relevant ligands. Aluminium's action as a pro-oxidant as well as an excitotoxin are highlighted while the evidence for its interactions with amyloid beta, tau and DNA are discussed and it is concluded that it is too early to discount these ligands as targets for the neurotoxicity of aluminium. Highlights ► There are few quantitative data describing the coordination chemistry of aluminium in neurodegenerative disease. ► One compelling line of evidence relates to the putative aluminium superoxide semi-reduced radical ion (AlO22+) and its powerful action as a pro-oxidant. ► Another important candidate is aluminium's complex with ATP and its potential to disrupt neuronal signalling and induce excitotoxicity. ► Though there are no quantitative data to describe aluminium's interactions with amyloid beta this does not preclude their association in the brain. ► The biological reactivity of aluminium supports myriad as yet unidentified interactions with biomolecules associated with brain function in health and disease.” [Edited on 7-10-2018 by AJKOER] |