Toxic byproducts of bacteria or metabolism

Endotoxin depletes ascorbate...Protective effects of vitamins C and E against oxidative stress.

Submitted by Jim K on Sun, 2005-08-28 20:14

Endotoxin depletes ascorbate in the guinea pig heart. Protective effects of vitamins C and E against oxidative stress.

Rojas C, Cadenas S, Herrero A, Mendez J, Barja G.

Department of Animal Biology-II (Animal Physiology), Faculty of Biology Complutense University, Madrid, Spain.

The effect of acute endotoxin-induced septic shock on myocardium oxidative stress after low or high vitamin C and/or E dietary supplementation was studied in guinea pigs, laboratory animals which, like human, do not have capacity for ascorbate synthesis. Neither the antioxidant enzymes or GSH were modified by endotoxin and vitamin treatments. Vitamin E showed a strong capacity to protect the myocardium against both enzymatic and non-enzymatic lipid peroxidation even in the presence of endotoxin. Vitamin C supplementation increased heart ascorbate whereas endotoxic shock totally depleted the heart ascorbate of vitamin C supplemented animals without changing vitamin E. Endotoxin significantly increased myocardium uric acid, a marker of ischemia induced oxidative stress, in animals fed with low vitamin C levels. This increase was totally prevented in vitamin C supplemented, but not in vitamin E supplemented animals. Strongly depressed levels of plasma vitamin C have been recently described in sepsis in human patients. The results suggest that ascorbate is a primary antioxidant target in the heart of endotoxin treated mammals lacking the capacity to synthesize ascorbate and that ascorbate can have a protective value against endotoxin-induced free radical damage in the myocardium. Implications of these results for the possible preventive role of vitamin C in humans during sepsis are discussed.

David Wheldon Comments on endotoxins & reactions

Submitted by Jim K on Sun, 2005-08-28 13:38

Cpn endotoxin is about 100 times less powerful than Neisserial endotoxin, but there must be a lot of it released, particularly with the active killing by metronidazole. Hence the need for caution at this stage of treatment. The long-term damaging effect of far more potent endotoxins on the CNS is vividly illustrated by this story: http://www.endotoxin.gmxhome.de/ which resulted in a letter in the BMJ: http://oem.bmjjournals.com/cgi/content/full/60/5/378

One quite common side effect of Cpn treatment is vestibular disturbance. A number of other medics who treat CFS with antibiotics have noticed this. It can go on for months, tends to have a diurnal rhythm and can be quite incapacitating. Its severity seems to be linked to bacterial load. The diurnal pattern suggests that it may be of host origin, perhaps cytokine. Here's a link to a webpage which notes the association between vestibular disturbance and cognitive deficits. http://www.backgroundfacts.com/menieres/COGDIS.htm

Cholesterol levels, bacterial endotoxin, and inflammation

Submitted by Jim K on Wed, 2005-08-24 20:24

Acute inflammation and infection maintain circulating phospholipid levels and enhance lipopolysaccharide binding to plasma lipoproteins
Richard L. Kitchens1,*, Patricia A. Thompson*, Robert S. Munford*, and Grant E. O'Keefe,**
* Departments of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9113
Microbiology, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9113
Surgery, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9113
** Department of Surgery, University of Washington, Harborview Medical Center, Seattle, WA 98104-2499

To whom correspondence should be addressed. e-mail: richard.kitchens@utsouthwestern.edu

Reactions to Treatment: Endotoxins, cytokines, porphyria, etc.

Submitted by Jim K on Mon, 2005-08-22 21:09

Bacterial Endotoxin reactions, Cytokine (immune) reactions and inflammation

These are often casually referred to as “herx” reactions, or scientifically as “herxheimer-like” alluding to the Jarisch-Herxheimer reaction to bacterial toxins specifically from syphilis. All gram-negative bacteria, of which Cpn is one, have contain Lipopolysaccharide endotoxin which is released as a matter of course during infection and is partially responsible for the on-going symptoms of the infection. When these bacterial are killed en masse they release larger amounts of endotoxin causing significant symptoms during initial phases of treatment. If the amount of endotoxin exceeds the body's ability to get rid of it, these toxic effects can be life threatening. Even in less threatening amounts, the endotoxins and the resulting reactions can cause oxidative stress and damage to body organs.