Open AccessThiol compounds inhibit mercury‐induced immunological and immunopathological alterations in susceptible mice
Author(s) -
HU H.,
MO¨LLER G.,
ABEDIVALUGERDI M.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1997.d01-903.x
Subject(s) - in vivo , dithiothreitol , in vitro , antibody , immunoglobulin e , immune system , thiol , chemistry , spleen , microbiology and biotechnology , biology , immunology , biochemistry , enzyme
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.