A characteristic of iron present in brain fluids

A characteristic of iron present in brain fluids is considerable differences between measured values of ferritin and transferrin and the total iron content value (Table 1). Variation of the latter is compatible with differences in individual metabolisms. However differences between total iron content and the sum of the ferritin and transferrin values indicates the presence a presently unknown third iron complexing mechanism. Potassium and sodium polyphosphates also form soluble complexes with iron (sequestration) [24], [25]. Potassium is the dominant alkali metal element present in intracellular fluids and potassium polyphosphate is identified as the principle compound transporting polyphosphoric ion into cells. The amount of iron sequestered per 100g of polyphosphate increases with a reduced number of atoms in the phosphate and a more acidic (low pH) solution. Under these conditions a high CSF iron content indicates acidic intracellular and intercellular fluid conditions. As described above in (±)-J 113397 conditions (low pH) the Fe3+ ion is reduced to the Fe2+ state by hydroxylamine which is converted to water and nitrous oxide controlling the brain fluid content of this compound. Under conditions in which the fluid acidity remains high (low pH) the second part of this control cycle does not function and hydroxylamine content of brain fluids rises. Such conditions are associated with blood acidosis.
Alzheimer’s disease This disease exists in several variations with the general symptom of progressive failure of brain functions. associated with variations of hydroxykynurenine, an increase in glucose in the serum, high metabolic concentration of nitrates, an increase in the sulphur containing cysteine amino acid in the cerebrospinal fluid and reduced ethanolamine plasmologen formation [26], [27], [28], [29]. Also associated are an increase in alkaline phosphate enzyme in both serum and cerebrospinal fluids plus methylglyoxal formation in the brain [30], [31]. Long term use of diuretics is linked with a reduced risk of the development of the disease [32]. A reduced concentration of acetylcholine present in the relevant brain fluids. Alzheimer’s disease also results in the presence of solid bodies of protein in brain tissue, known as amyloid plaques. Failure of betaine formation by brain cells is proposed as leading to Alzheimer’s disease. Acetylcholine is a product of the hydrolysis of phosphagen betaine found in muscle cells and a reduced concentration of this compound indicates reduced formation of this betaine. As proposed above this leads to reduced general muscle activity observed. Indole-3-propionic acid is found in brain fluid and is formed by hydrolysis from tryptophan betaine (hypaphorine). By analogy with acetylcholine the latter and other betaines can be linked to the operation of the remaining four sensory functions [10]. Reduced formation of betaines indicates reduced concentration of hydroxylamine/hydrogen peroxide formation in brain cells. The increased nitrate observed to be of serum nitrate and the increase in serum cysteine both indicate reduction in the formation of nitrite and the diversion of sulphate available for use in the Raschig reaction. The observed ethanolamine plasmaolgen reduction in brain fluids produces an increase of unused glucose which supports an increase in aspartic acid. The latter is involved in the formation of kynurenine and kynurenine betaine. Aspartic acid is derived from malic acid generated from glucose in liver cells [33] The increase leads to the observed changes in hydroxykynurenine. Excess glucose also encourages the formation of quinolinic acid as shown. Methylglyoxal is produced by reaction of methanol and glyoxal formed from glucose and fructose respectively as shown. The formation of methylglyoxal diverts glyoxal from production of benzene ozonide. Failure to produce the latter ultimately results in cessation of all brain cell activity [9].