Toxicity complexes

It behaves like quinine in many ways but does not inhibit haem polymerase. It probably acts by forming toxic complexes with free haem that damages membranes and interacts with other plasmodial components. 

In theory, K (i.e., kjki) should be the same whether determined by kinetic or equilibrium approaches. In practice, however, moderate differences arise that are often attributed to technical problems associated with separating bound from free rapidly without losing a significant proportion of receptor-toxicant complex. This problem is troublesome, particularly when estimating the amount bound at early time points in association or dissociation experiments, when the amount of bound ligand is changing rapidly. Large differences between the KD as determined in saturation and kinetic experiments, however, may indicate that the reaction is more complex than a simple bimolecular reversible reaction. 

The Type III insect represented by A. kuehniella was baffling to the early investigators. Neither spores nor crystals by themselves, nor any other ratio of both agents (other than the natural combination of one spore to one crystal), killed all the insects. When equal weights were fed, spores alone caused 4 to 8% mortality crystals caused 12 to 13% mortality. Original culture spore-crystal ratio 1 to 1 caused 80 to 92% mortality. A previously undetected soluble toxic material, known as the McConnel-Richards toxic complex, is produced in... 

The treatment of poisoning with metals includes the use of drug chelating agents. The latter form stable and non-toxic complexes with metals and are quickly eliminated from the body. 

Schmitz, F. J., Hollenbeak, K. H., and Campbell, D C. (1978) Marine natural products halitoxin, toxic complex of several marine sponges of the genus Haliclona J. Org. Chem. 43, 3916-3922. 

A. Because a toxic complex with iron may be formed, avoid concurrent iron replacement therapy. 

Table V shows that some activity is observed for metal salts in lethality studies. These metal ions are not as active as the inert complexes in the lethality assay, and none of these ions has been found to be active in reversion studies. Perhaps the difference is that the metal ions rapidly come to equilibrium in the cell and form kinetically labile and non-toxic complexes with DNA. As strand separation occurs, the labile ions that are on the DNA can be rapidly displaced and thus are not able to interfere with replication. On the other hand, the inert ions undergo substitution at rates which are slow compared to cell division. When they undergo ligand substitutions and become attached to DNA, they remain fixed to the DNA long enough to cause errors during replication.

Smith H, Stoner HB. Anthrax toxic complex. Fed Proc 1967 26(5) 1554-1557. 

ABSTRACT. Non-toxic complexation agents/solubilizers have numerous applications in the biomedical field. Results obtained in the author s laboratory are reviewed here. This work resulted in (a) the development of a system enabling more efficient therapeutic use of retinoids, (b) the development of an agent eliminating mycoplasma infections in cell cultures, (c) the development of a detoxification process for hypervitaminosis A, and (d) the development of a system for effective sublingual administration of sex hormones. 

Life as we know it depends heavily on intermolecular forces— the attractions that keep molecules together. Without them, water—perhaps the most essential ingredient in life— would not be a hquid. On this occasion, though, intermolecular forces caused two contaminants in infant formula, each relatively innocuous by itself, to form a highly toxic complex that caused many thousands of babies in China to develop acute kidney failure. 

The synergistic behavior of crotoxin subunits was further demonstrated by studying the differential stability of crotoxin isoforms differing in their toxicity and their enzymatic activity (Faure et al. 1993). More toxic isoforms are less enzymatically active, block neuromuscular transmission of chick biventer cervicis more efficiently, are more stable and dissociate more slowly than less toxic complexes. Therefore, less toxic crotoxin isoforms, because of their lower stability, are more likely to dissociate en route before reaching their target, CA being no more able to prevent CB non specific binding. 

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