Oxidative stress
 R.A.S HEMAT, MB;BCh, FRCSI, DUL.
Oxygen was discovered in 1775. In 1963, attention was attracted to the possible toxicity of pressured oxygen in divers. In 1968, vitamin E that was discovered in 1922, was recognized to be an essential vitamin because of its potential antioxidant properties.
Reactive oxygen species (ROS) are cytotoxic agents as a result of their ability: to inactivate proteins, to oxidize lipoproteins, to promote DNA strand scission, to degrade carbohydrates, to induce haemolysis and overall to initiate lipid peroxidation processes. Reactive nitrogen metabolities (free radical nitric oxide) and also sulphur-centered radical have been discovered. Oxidative stress occurs because there is profound disturbance in the proxidant-antioxidant balance in favour of the former leading to potential for damage.
Identifying oxidative stress in human disease, can be separated into nine categories
1- Detection of oxidized biological material.
2- Salicylate hydroxylation.
3- Measurement of endogenous antioxidants.
4- Determination of total antioxidant capacity of blood.
5- Evidence of free iron.
6- Neutrophils activation.
8- Electron spin resonance.
9- Antioxidant therapy.
The use of allopurinol, for xanthine oxidase inhibiting, significantly reduce the incidence of poor early renal function.
Ischemia inflicts damage to the mitochondria. Most mitochondria can resume activity after 60 min of ischemia. The ATP that is present or made available during ischemia is probably used mainly to pump ions against their thermodynamic gradients.
Mechanisms that cause membrane dysfunction and cell death are, calcium, osmolysis, free radicals, and acidosis.
The postischemic injury processes that lead to cell dysfunction and death are mutifactorial in nature and include oxidant generation, elaboration of inflammatory mediators, infiltration of leukocytes, Ca2+ overload, phospholipid peroxidation and depletion, impaired nitric oxide metabolism, and reduced ATP production.
Complement activation is potentiated by ischemia.
Intervention strategies to reduce postischemic injury
1-Limit OFR-mediated injury.
2-Limit leukocyte-mediated injury.
3-Block complement activation.
4-Limit Ca2+-mediated injury.
5-Modulate eicosanoid metabolism.
6-Limit intravascular coagulation.
7-Block phospholipase activation.
8-Modify adenine nucleotide metabolism.
9-Modulate nitric oxide metabolism.
10-Cytokines.
11-Stabilization of endothelial cytoskeletaton.
When oxygen is reintroduced after hypoxia-ischemia, arachidonic acid is metabolized, and OFRs are produced when prostaglandin G2 is converted to prostaglandin H2.
Respiring cells are capable of reducing molecular oxygen (dioxygen, O2) by four electrons to water (H2O) by way of cytochrome C oxidase....etc.
December, 2000
Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology, Principles of modern urology, Principles of Orthomolecularism, Andropathy, by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.
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