Thiol compounds inhibit mercury-induced immunological and immunopathological alterations in susceptible mice.

Abstract

In vitro mercury induces a high proliferative response in splenic lymphocytes and in vivo it induces a systemic autoimmune disease in susceptible mouse strains. This disease is characterized by increased serum levels of IgE and IgG1 antibodies, by the production of anti-nucleolar antibodies and by the formation of renal immune complex deposits. We have previously found that the presence of 2-mercaptoethanol (2-ME) inhibited mercury-induced cell proliferation in vitro. In this study, we tested the effects of four other thiol compounds, namely dithiothreitol (DTT), L-cysteine, meso-2,3-dimercaptosuccinic acid (meso-DMSA) and 2,3-dimercapto-1-propanesulfonic acid, Na salt (DMPS) on mercury-induced immunological changes both in vitro and in vivo. We found that in vitro, the addition of all thiol compounds abrogated mercury-induced cell aggregation and proliferation. In vivo, injection of meso-DMSA and/or DMPS (s.c. or i.p.) immediately following exposure to mercury markedly decreased IgG1 synthesis in spleen cells and serum IgE levels in mercury-susceptible SJL mice. Treatment with DMPS also prevented mercury-induced IgG1 anti-nucleolar antibody synthesis and the development of mesangial IgG1 immune complex deposits in SJL mice.