1. An Overview
Mercury compounds have been administered for medical purposes since the earliest times, applied directly to the skin, or given by mouth, and more recently by intramuscular or intravenous injection. Hypersensitivity (i.e., contact sensitivity) to mercury as a consequence of medicinal administration was first described in 1895 (93). Like other transition group elements and highly electropositive heavy metals, such as lead and cadmium, mercury can act as a coordination center for electronegative groups (SH groups and disulfide bridges, cysteinyl and histidyl residues) present in proteins, purines, and pteridines. Such complexation can cause conformational changes and hence immunogenicity (94). Hypersensitivity reactions to host proteins haptenized by mercury following skin contact or systemic exposure can be (a) of type I or anaphylactic, mediated by immunoglobulin E (IgE) (presenting clinically as urticaria); (b) of type III or Arthus reactions involving antigen-antibody complexes with the kidneys as main target organ; and (c) type IV or delayed hypersensitivity mediated by macrophages and sensitized T lymphocytes, resulting in contact dermatitis.
2. Autoimmunity ja
Exposure to mercury or mercurials induces autoimmune disease described as s type III or Arthus reaction in several species including humans. Such reactions, J
characterized by lymphoproliferation, are mediated mainly by IgG and involve o generation of antigen-antibody complexes. A genetic predisposition appears to be an important etiological factor for such metal-induced autoimmunity. For mer- | cury, immune complexes are preferentially deposited in the vascular endothelium of the kidneys, leading to destructive inflammatory reactions and glomerulone- |
phritis (70-72,95). Workers chronically exposed to mercury vapor in the indus- <->
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