## Heavy Metal Chelation: Mechanism and Treatment ### Mercury and Sulfhydryl Binding **Key Point:** Mercury has an extremely high affinity for sulfhydryl (-SH) groups on cysteine residues in proteins and enzymes. This is the basis for its toxicity and the rationale for dimercaprol (BAL) therapy. ### Mechanism of Mercury Toxicity 1. Mercury binds to sulfhydryl groups in: - Mitochondrial enzymes - Glutathione (GSH) - Protein thiols 2. This inactivates critical enzymes and disrupts cellular respiration 3. Results in neurological damage (tremor, ataxia, personality changes) ### Chelation Therapy: Heavy Metals and Their Agents | Heavy Metal | Chelating Agent | Mechanism | Indication | |---|---|---|---| | **Mercury** | Dimercaprol (BAL) | Binds -SH groups; forms stable complex | Acute & chronic mercury poisoning | | **Lead** | EDTA, DMSA, DMPS | Binds divalent cations | Lead poisoning with high levels | | **Arsenic** | DMSA, DMPS | Binds trivalent As; forms water-soluble complex | Acute arsenic poisoning | | **Cadmium** | DTPA, EDTA | Less effective; mainly supportive care | Limited chelation efficacy | | **Chromium** | No specific chelator | Mainly supportive care | Occupational exposure management | ### Why BAL (Dimercaprol) for Mercury? **High-Yield:** Dimercaprol contains two sulfhydryl groups that compete with mercury for binding to tissue thiols. The mercury–BAL complex is: - Water-soluble - Readily excreted in urine - More stable than mercury–tissue complexes **Clinical Pearl:** BAL must be given early (within 24 hours of acute exposure) for maximum efficacy. It is less effective in chronic mercury poisoning because mercury has already crossed the blood–brain barrier and bound irreversibly to CNS proteins. **Mnemonic:** **BAL = Bivalent And Lipophilic** — it crosses the blood–brain barrier and reaches CNS deposits of mercury, unlike EDTA. [cite:Forensic Medicine & Toxicology by Reddy & Murthy Ch 12]
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