The evidence in Part 1 (Dickens, 1946) enables the following working hypothesis of the mode of action of oxygen on brain metabolism to be advanced with some confidence.(1) Exposure to unphysiologically high tensions ofoxygen causes irreversible damage to brain respiration and glycolysis.(2) This damage is sustained by the enzymes themselves rather than by their coenzymes, as shown by the lack of general protection in presence of excess of the more important coenzymes.(3) The following conditions tend to protect against oxygen poisoning: Presence of (a) glucose or (as shown in this paper) manganese ions, which protect succinoxidase in finely divided brain tissue; (b) ions of manganese, cobalt, or magnesium (and probably calcium), which protect the whole oxidative system in brain slices, with decreasing activity in the order of the above series.(4) The brain enzymes poisoned by oxygen are mainly those concerned in carbohydrate metabolism.Oxidation of glucose, fructose, lactate and pyruvate is inhibited, while the succinoxidase system, at least in intact tissue (slices) is much more resistant.There is support for the view that the inactivation of an -SH component of the pyruvate oxidase system may be a primary stage in oxygen poisoning, the resulting interference with resynthesis of adenosine triphosphate could then lead to general breakdown of aerobic and anaerobic carbohydrate metabolism.
No takes yet. Share an insight, caveat, or question.
F. Dickens (1946) studied this question.