Aluminum-induced entropy in biological systems: implications for neurological disease

Abstract

Over the last 200 years, mining, smelting, and refining of aluminum (Al) in various forms have increasingly exposed living species to this naturally abundant metal. Because of its prevalence in the earth's crust, prior to its recent uses it was regarded as inert and therefore harmless. However, Al is invariably toxic to living systems and has no known beneficial role in any biological systems. Humans are increasingly exposed to Al from food, water, medicinals, vaccines, and cosmetics, as well as from industrial occupational exposure. Al disrupts biological self-ordering, energy transduction, and signaling systems, thus increasing biosemiotic entropy. Beginning with the biophysics of water, disruption progresses through the macromolecules that are crucial to living processes (DNAs, RNAs, proteoglycans, and proteins). It injures cells, circuits, and subsystems and can cause catastrophic failures ending in death. Al forms toxic complexes with other elements, such as fluorine, and interacts negatively with mercury, lead, and glyphosate. Al negatively impacts the central nervous system in all species that have been studied, including humans. Because of the global impacts of Al on water dynamics and biosemiotic systems, CNS disorders in humans are sensitive indicators of the Al toxicants to which we are being exposed.

Figure 1

Semirigid hydration and cooperativity ((a) and (b)) a water molecule in the solvation shell of a cation (a) and an anion (b). Dielectric relaxation measurements probe the reorientation of the permanent dipole vector p. Femtosecond infrared spectroscopy is sensitive to the reorientation of the OD-stretch transition dipole moment μ. The dotted arrows indicate reorientation in a cone, in the case of semirigid hydration. (c) Proposed geometry, in which the water dynamics are locked in two directions because of the cooperative interaction with the cation and the anion. Figure 1 is reproduced here from (Tielrooij et al. 2010) [153] with permission of the American Association for the Advancement of Science.

Figure 2

Depiction of how Gadolinium (Gd³⁺) vibronic side band luminescence spectroscopy (GVSBLS) acts as a probe of the coordination of biologically-relevant sites of cation sequestration. The figure is reproduced here from (Guo and Friedman 2009) [139] with permission of the American Chemical Society. Copyright 2009 American Chemical Society.

Figure 3

Illustration of the devastating effects of Aluminum on a typical cell related to sulfate inactivation, G-protein signaling, and calmodulin signaling. (a) A healthy cell without Al contamination. eNOS, attached to the membrane at a caveola, produces sulfate, which maintains a healthy glycocalyx with sufficient negative charge. (b) Al binds to the sulfates, eliminating the negative charge, which allows cytokines to penetrate through the glycocalyx, activating G-protein coupled receptor signaling cascades. AlF₄ ⁻ disrupts the signal, acting as a phosphate mimic, and Al binds to CaM, inducing eNOS detachment from the membrane. Phosphorylation cascades activate eNOS to produce abundant NO released into the cytoplasm, instead of producing sulfate to enrich the glycocalyx.

Figure 4

Schematic of the biosemiotic levels at which Al can impact the body and CNS.