Health Hypotheses; Antioxidants, Antibodies and Autoimmune Disease by Steven Wm. Fowkes
Posted Sep 11 2009 4:57pm
The involvement of free-radical reactions in the development of many degenerative diseases has been repeatedly documented by researchers across the world. What may not be so widely understood, especially in the popular press, is the involvement of the oxidation-reduction potential in these disease processes.
The activation of immune function by oxidizing conditions may be a generalized function. Immune cells secrete reactive oxygen species (oxidizing free radicals) when stimulated by their target antigens. This function creates localized oxidizing conditions just as exposure to atmospheric oxygen does.
Oxidation may even play a role in antibody sensitivity to antigen. This hypothesis, first advanced by physician Robert Cathcart, suggests that antibody conformation (shape) is influenced by redox potential. The Cathcart theory hypothesizes that under oxidizing conditions, the disulfide (sulfur-sulfur) bridges between the two halves of the antibody is in its oxidized, intact, and active conformation, and that under reducing conditions, one (or more) of the disulfide bridges may become broken by becoming temporarily reduced to the sulfhydryl form. Hypothetically, this could alter the antibody conformation and temporarily inactivate the antibody complex.
If the Cathcart hypothesis is correct, the oxidation (redox) gradient in body tissues is a significant factor in immune activation, and impaired ability to maintain reduced conditions may lead to chronic immune hyper-activation and autoimmune disease.
The redox-sensitivity hypothesis offers some interesting speculations regarding the influence of aging on immune competence. With aging, redox potential slowly becomes more oxidized. This may be responsible for systemic activation of antibodies and the increased likelihood of autoimmune disease associated with aging. It also would be predicted to diminishes the strength of the antibody attack on a localized antigen because of dilution and an increase in the oxidative diffusion from the local infection site.
The involvement of free-radical reactions in the development of many degenerative diseases has been repeatedly documented by researchers across the world. What may not be so widely understood, especially in the popular press, is the involvement of the oxidation-reduction potential in these disease processes.
The activation of immune function by oxidizing conditions may be a generalized function. Immune cells secrete reactive oxygen species (oxidizing free radicals) when stimulated by their target antigens. This function creates localized oxidizing conditions just as exposure to atmospheric oxygen does.
Oxidation may even play a role in antibody sensitivity to antigen. This hypothesis, first advanced by physician Robert Cathcart, suggests that antibody conformation (shape) is influenced by redox potential. The Cathcart theory hypothesizes that under oxidizing conditions, the disulfide (sulfur-sulfur) bridges between the two halves of the antibody is in its oxidized, intact, and active conformation, and that under reducing conditions, one (or more) of the disulfide bridges may become broken by becoming temporarily reduced to the sulfhydryl form. Hypothetically, this could alter the antibody conformation and temporarily inactivate the antibody complex.
If the Cathcart hypothesis is correct, the oxidation (redox) gradient in body tissues is a significant factor in immune activation, and impaired ability to maintain reduced conditions may lead to chronic immune hyper-activation and autoimmune disease.
The redox-sensitivity hypothesis offers some interesting speculations regarding the influence of aging on immune competence. With aging, redox potential slowly becomes more oxidized. This may be responsible for systemic activation of antibodies and the increased likelihood of autoimmune disease associated with aging. It also would be predicted to diminishes the strength of the antibody attack on a localized antigen because of dilution and an increase in the oxidative diffusion from the local infection site.
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