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JPMPH : Journal of Preventive Medicine and Public Health

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2 "immune response"
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Original Articles
Effect of Mercury Chloride on Humoral and Cell-mediated Immune Responses in Mice.
Jung Ho Youm
Korean J Prev Med. 1995;28(1):27-42.
  • 2,084 View
  • 23 Download
AbstractAbstract PDF
The in vivo and in vitro humoral and cell-mediated immune responses of lymphocytes of BALB/c mouse exposed to mercury chloride(HgC12) were investigated. In vitro exposure of the splenocytes to mercury chloride produced overt cytotoxicity in 3 hours period. The IC50(the concentration required to inhibit a splenocyte viability by 50%) for mercury chloride was >0.1mM for cytotoxicity. In vivo mercury chloride exposed mice were significantly depressed delayed type hypersensitivity(DTH) response to sheep red blood cells(SRBC) in a dose-dependent manner compared with control group. Mercury chloride inhibited the proliferative responses of splenocytes to lipopolysaccharide. pokeweed mitogen, concanavalin A and phytohemagglutinin in a dose-dependent manner. Hemagglutinin response to SRBC in mercury chloride exposed mice was significantly depressed in a dose-dependent manner compared with control group. After 7 weeks of mercury chloride exposure in vivo. mercury chloride induced an increase of nonspecific serum IgG1 and IgE levels in BALB/c mice.
Summary
HgCl2 Dysregulates the Immune Response of Balb/c Mice.
No Suk Kim, Dai Ha Koh, Chong Suh Kim, Jung Sang Lee, Nam Song Kim, Hwang Ho Lee
Korean J Prev Med. 1994;27(1):11-24.
  • 1,998 View
  • 21 Download
AbstractAbstract PDF
The studies reported here were undertaken to investigate the effects of mercury chloride on immune system of Balb/c mouse employing a flexible tier of in vitro and in vivo assays. Mercury chloride inhibited the proliferative responses of spleen cells to lipopolysaccharide, pokeweed mitogen, and phytohemagglutinin as a dose-dependent manner. This inhibitory effect was observed not only when HgCl2 was added 2nd or 3rd day of 3 days culture period but also when spleen cells was pretreated with HgC12 for 2 hours. Mercury chloride, however, potentiated the production of IgM and IgG from spleen cells. During the HgCl2 administration by drinking for 3 weeks, the weight gain of mice was significantly blunted than that of control group mice, while no overt signs related to mercury toxicity were noted in any mice of experimental group. There was no change in thymus and spleen weights, and in histological findings of kidney, bone marrow of femur, thymus, spleen, and politeful lymph node after 3 weeks of mercury exposure. However, HgC12 induced a significant increase of total serum IgM, IgG including IgG1, IgG2a and IgG2b, and IgE in Balb/c mice. Treatment in vivo with anti-IL-4 monoclonal antibody significantly abrogated the HgCl2-induced increase in total serum IgG1 and IgE. Whereas HgCl2 potentiated total serum IgM and IgG, there was, there was no difference in total serum hemagglutinin to SRBC(Sheep Red Blood cell) between experimental and control group mice when these mice were immunized with SRBC. All these findings observed in Balb/c mice suggest that mercury perturbates well-orchestrated regulation of immune responses before developing histopathological changes in lymphoid tissues.
Summary

JPMPH : Journal of Preventive Medicine and Public Health
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