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2074678 
Technical Report 
Antagonists For Toxic Heavy Metals 
Jones, MM 
1984 
NIOSH/00146611 
27 
163-167 
Antagonists for toxic heavy metals are reviewed. Antagonism of the toxic action of heavy metals is generally based on manipulating bonding preferences of the toxic metal through transfer to an appropriate metal/chelate complex. Donor preferences of the metal ions must be studied to estimate effectiveness of proposed chelating agents and their rate of replacement. The acceptor preferences of the chelating agents represent the other side of the coin. Chelating agents of therapeutic usefulness are not specific for a given metal ion but can be matched to a number of ions with related patterns of behavior. If measured values of the stability constants are available they can give a clue as to the best chelate antagonists for a given toxic metal. The chelating agent must reach the toxic ion, form a complex with it, and be disposed of, preferably by excretion. The mode of excretion can have an effect on the net detoxification achieved. For many toxic metals delay in the beginning of chelation therapy results in increased permanent damage. Non chelate antagonists also cover a variety of situations. Absorption in the gastrointestinal tract, for example, is useful if orally ingested thallium is not yet absorbed by the intestines. Ascorbic-acid is an antidote for vanadate. The use of non chelate antagonists sometimes allows a completely different therapeutic approach but there seems to be no reliable technique for predicting efficiency of non chelates prior to experimentation. There are many unsolved problems in antagonizing toxic heavy metals. Thallium and some of the rare earths require development of more effective agents. An oral agent is needed to induce excretion of iron from persons receiving multiple blood transfusions. Aluminum, cis-platinum, gallium-nitrate, selenium, and the organometallic compounds all require further study. The author concludes that, in general, methods are needed to shift excretion of toxic metals from the sensitive renal route to the less sensitive fecal route.