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Bacterial Endotoxin (lipopolysaccharide) Stimulates The Rate Of Iron Oxidation

Discussion in 'Scientific Studies' started by md_a, Mar 9, 2020.

  1. md_a

    md_a Member

    Aug 31, 2015
    Bacterial endotoxin (lipopolysaccharide) has affinity for a number of cations, including iron.
    Previous investigations have demonstrated that lipopolysaccharide can affect the oxidation rate of iron; heme-bound ferrous iron in hemoglobin is oxidized to ferric iron when hemoglobin binds lipopolysaccharide.

    A series of sugars, starches and a preparation of purified O-chain polysaccharide (the carbohydrate portion of the lipopolysaccharide macromolecule) had no effect on the rate of iron oxidation, whereas phospholipid-enriched brain tissue extracts (similar to the lipid A component of lipopolysaccharide) stimulated oxidation.

    We conclude that the lipid moiety of bacterial lipopolysaccharide is responsible for the stimulation of iron oxidation. This process may contribute to the ability of lipopolysaccharide to cause oxidation of heme-bound iron in hemoglobin.


    Iron appears to play a number of diverse roles in the promulgation of bacterial infection and sepsis. Iron is an essential nutrient for bacterial proliferation, and bacteria have high affinity siderophores in order to utilize host sources of iron. It has long been hypothesized that hypoferremia, a characteristic of infections and sepsis, represents a host response to limit bacterial proliferation.

    Iron-containing hemoglobin is also a pathogenic factor in infection. Enhanced morbidity and mortality from infection has been documented in the settings of hemorrhagic peritonitis, hemoglobinemia secondary to hemolysis during sepsis, or when cell-free hemoglobin (a red blood cell substitute) is infused in the presence of sepsis. In these conditions, it is possible that heme-derived iron may become available for bacterial growth. Alternatively, a variety of mechanisms other than providing nutrient iron may be involved in the deleterious combination of hemoglobin and infection, including inhibition by iron of leukocyte anti-bacterial activity, depression of reticulo-endothelial cell system function, and enhancement of lipopolysaccharide-mediated toxicity.


    We believe that the processes of iron binding to LPS, with subsequent oxidation, may have relevance to bacterial infections. Bacterial virulence is enhanced by administration of iron, and bacteria, as well as other organisms, require iron for growth. Since the solubility of iron at physiological pH is very limited, it is logical that microorganisms have evolved sophisticated mechanisms for iron sequestration. Many micro-organisms synthesize and secrete chelators that can bind iron and maintain its solubility at physiological pH. However, these chelators have not been reported to associate with, or bind to, endotoxin. In addition, bacterial cell membranes have been demonstrated to have metal binding sites that serve as transmembrane redox systems, and LPS could be part of such a system.


    In conclusion, bacterial LPS-dependent oxidation of Fe2+ is likely to occur through a variety of mechanisms, including simple iron ‘auto-oxidation’ as well as free radical formation. In previous studies, we have demonstrated that the binding of iron to endotoxin decreased the biological activity of LPS and, if endotoxin undergoes free radical attack during iron binding and oxidation, perhaps its chemical structure, composition, or aggregation state is altered. Finally, an interaction between iron and the LPS in the membrane of Gram-negative bacteria may directly contribute to bacterial virulence.

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  2. methylenewhite

    methylenewhite Member

    Aug 21, 2018
    Iron is involved in bacterial quorum sensing and biofilm formation.