Z-YVAD-FMK br Brain cell reactions Brain cells in common wit

Brain cell reactions Brain cells in common with all metabolic cells must contain chemically active primary compounds which spontaneously initiate and continue cell reactions under normal conditions of temperature and pressure (NTP). These compounds have been identified as monophosphoric and polyphosphoric acids plus hydroxylamine and hydrogen peroxide. The former are hydrating/dehydrating reagents involved in for example, protein formation and decomposition by amino Z-YVAD-FMK linkage and the reverse. These compounds originate from dietary phosphates. Hydrogen peroxide and hydroxylamine are known to exist in metabolic fluids are identified as the oxidation and reducing agents formed in all cells and are produced in cells by the Raschig reaction involving sulphite and nitrite ions [8]. The compounds function as either oxidation or reduction reagents according to the pH of the intracellular and intercellular fluids [8]. These four biochemically active inorganic compounds operate by being incorporated either singly or as complexes [H4P2O8, (NH3OH)3PO4] into the structures of different proteins giving rise to enzymes, for example, hydroxylamine oxidase [13]. The varying lattice structures and chemical composition of proteins involved control the compounds incorporated plus access to and reaction with these compounds. This means that the same reactions can involve a different enzyme associated with the same active reagent. The above pH dependencies is reflected in the enzyme sensitivity to pH value. Biochemical reactions, in common with all chemical reactions, proceed until a specific concentration of reaction products is present in the reaction zone. Under these conditions the reaction rate slows or stops and can proceed in reverse until a reaction product or products leave the reaction zone. The Fig. 1, Fig. 2, Fig. 3, Fig. 4 are show diagrammatically the molecular interactions leading to the formation of biochemicals associated with brain diseases involving the primary compounds described above. The formation of the benzene ring molecular structure in brain has been demonstrated as occurring cells through the primary brain cell reaction producing benzene ozonide from glyoxal [8]. The latter is derived from glucose and this mechanism means that benzene compounds are produced independently by the relevant brain cells as opposed to the present concept that these compounds arise mainly from the diet which contains such compounds formed by plants. In Fig. 1 the products are methanal (formaldehyde) and active/nascent oxygen. The decomposition of fructose by hydroxylamine shown in Fig. 2 produces glycoaldehyde and oxygen. Also shown in Fig. 1, Fig. 2 are brain reactions producing ethanolamine, methylglyoxal and aspartic acid. The Fig. 3 shows the formation of kynurenine and 3-hydroxykynurenine. The difference in formation between these compounds is the spatial orientation of the -OH group of aminophenol during reaction. This arises from the involvement of a structurally different polyphosphoric acid enzymes. Tryptophan is formed similarly except that glutamic acid replaces aspartic acid. The formation of neurotoxic quinolinic acid and charged phosphagen betaine derived from a percussion peroxide are shown in Fig. 4. The ethylene glycol required is formed from glycoaldehyde derived from fructose and urea from ammonium carbamate. The latter compound always exists in intracellular fluid containing both ammonium and carbonate ions. Ammonia is a product of the decomposition of fructose by hydroxylamine as shown and carbonate ion is present in metabolic fluids. Betaine formation through unstable peroxides is a general mechanism available for the formation of these biochemical compounds by brain cells.
Metabolic controls of brain compound formation Biochemical reactions must be subject to control mechanisms which ensure the type and rate of supply of the biochemicals for metabolic functions are available. In the first instance the concentration of polyphosphoric acid in brain cells is maintained by water leaving cells by osmosis, electro-osmosis plus the exit from cells of hydrated amino acids or proteins with a hydration halo [14]. The primary mechanism controlling the concentrations of hydrogen peroxide/hydroxylamine in brain fluids involves reactions with the ions of iron. In acid conditions (low pH) the Fe3+ ion is reduced to the Fe2+ state by hydroxylamine which is converted to water and nitrous oxide. In alkaline solution (high pH values) the Fe2+ state is oxidised to the Fe3+ producing ammonia. Hydrogen peroxide acts similarly producing nitrous oxide and water. These reactions produce a cyclic control mechanism for these reagents as the intracellular fluid pH alters with brain cell biochemical reactions involving the reversible change from monophosphoric to polyphosphoric acids as illustrated. A further control mechanism is available through the mutual interaction of hydrogen peroxide and hydroxylamine producing nitrous oxide and water. This mechanism operates when the former mechanism is compromised and the intracellular/intercellular concentration of these reagents becomes excessive. The oxidising characteristics of monatomic oxygen formed as shown are independent of pH and oxidise Fe2+ to Fe3+ either directly or through the formation of hydrogen peroxide by reaction with water. Any monatomic oxygen not removed by the latter functions transfers into the blood flow by diffusion becoming part of the haemoglobin cycle. The formation of oxygen by brain cell reactions can cause cessation of brain function through interruption of the blood circulation or supplying oxygen to the brain under high pressure. Both of these applications lead to oxygen accumulation in the brain cells causing brain reactions involving oxygen as detailed above to slow or stop.