On October 23-26 I visited Albuquerque with a great view of the city and the hot air balloons dotting the horizon early in the morning. I presented information about mold toxins and how they decrease the function of the enzymes that make glutathione resulting in a decrease in glutathione. These toxins are fat soluble, so they find their way into cells to cause problems. The basis of the information I presented comes from an article published in 2014 titled “Deficient Glutathione in the Pathophysiology of Mycotoxin-Related Illness” and is available online, just click the link. The history of finding out how the loss of these enzymes was found is reviewed in the paper and is interesting as presence of the mold toxins should increase glutathione, but a deficit was found.
This is a very important topic because the loss of expression of the glutamate-cysteine ligase (GCL) has been found in other conditions including chronic astham and HIV disease. The loss of the enzymes controlling GCL (called the modifier unit or GCLM) is discussed in the paper “Glutathione supplementation improves macrophage functions in HIV“. The abstract for this article is on line. Contact me for information about the whole article. The article discusses the pathways depicted in the presentation slides. You can find out more about the role of glutathione in the innate immune cells ( antigen presenting cells and neutrophils) in the following articles, which are available online: “Characterization of Dendritic Cell and Regulatory T Cell Functions against Mycobacterium tuberculosis Infection” and “An Elucidation of Neutrophil Functions against Mycobacterium tuberculosis Infection“.
The slide presentation: Glutathione depletion by mold toxins and other causes AAEM Fall 2014 Mycotoxin