Methylmercury: Decreased Antibody Formation in Mice

Koller, Loren D.; Exon, Jerry H.; Brauner, Julie A.

doi:10.3181/00379727-155-39859

Cited by 33 publications

(11 citation statements)

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“…A known volume of this mixture was spread in Cunningham chambers, and incubated for 1 h. The IgM antibody secreted by sensitised mononuclear cells, lysed the SRBC around them and formed a plaque. Each plaque, represented an IgM secreting cell, was counted under microscope (Cunningham and Szenberg, 1968;Koller et al, 1977;Dogra et al, 1993). The anti-SRBC IgM antibody titer of serum, collected from above animals, was assayed by haemagglutination assay method, in a 96 well microtiter plate.…”

Section: Immune Function Studiesmentioning

confidence: 99%

Immunotoxicological effects of piperine in mice

2004

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Section: Immune Function Studiesmentioning

confidence: 99%

Immunotoxicological effects of piperine in mice

2004

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“…This indicates that autoregulation of mercury‐induced antibody/autoantibody synthesis was not owing to a general immune suppression. This statement contradicts the general idea that exposure to mercury induces a suppression in the humoral immune responses [32–34]. We think that the reason for this contradiction lies in the form of mercurial compounds which have been used in each study.…”

Section: Discussionmentioning

confidence: 77%

Spontaneous Downregulation of Antibody/Autoantibody Synthesis in Susceptible Mice upon Chronic Exposure to Mercuric Chloride is not Owing to a General Immunosuppression

et al. 2002

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Administration of mercuric chloride into susceptible rats and mice induces a systemic autoimmune disease, which is characterized by a T-cell-dependent polyclonal B-cell activation, an increase in serum levels of immunoglobulin (Ig)G1 and IgE, production of antibodies of different specificities and development of renal IgG deposits. A peculiar feature of mercury-induced autoimmunity is that the polyclonal B-cell activation spontaneously disappears in spite of continuous injection of mercury. The exact mechanism(s) for autoregulation of mercury-induced autoimmunity is not well understood. In the present study, we analysed the regulation of mercury-induced immune/autoimmune responses in mice and tested whether spontaneous downregulation of these responses is owing to a general immunosuppression. Mercury-susceptible [SJL (H-2 s )] and -resistant [DBA/2 (H-2 d )] mice were injected with mercury for 4, 10, 15 and 17 weeks. Immune/autoimmune responses were monitored in these mice. Thereafter, mercury-injected mice for 17 weeks were further immunized with horse red blood cells (HRBC) to study whether the subsequent humoral immune response to a foreign antigen is suppressed. We found that except for IgG1 anti-nucleolar antibody production and renal IgG1 deposition, other characteristics of mercury-induced autoimmunity were downregulated in SJL (H-2 s ) mice after chronic treatment with mercury. However, these mice did not show any reduction in the number of splenic antibody-secreting cells and/or in serum titres of specific IgM, IgG1 and IgG2a anti-HRBC antibodies in response to HRBC as compared with naõÈ ve mice. Similarly, in mercury-resistant DBA/2 (H-2 d ) mice, chronic treatment with mercury did not either suppress specific antibody responses against HRBC. Our findings show that the autoregulation of mercury-induced immune/ autoimmune responses observed after chronic treatment with mercury is not owing to a general immunosuppression.

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“…Likewise, HgCl2 at doses of 250 and 500 ppm administered to chickens orally for 35 days or at 300 pg/ml for 11 weeks diminished their ability to produce specific IgM and IgG antibodies to SRBC (61,62). A NOAEL of 125 (63,64). A LOAEL value of 1 ppm was identified for MeHg.…”

Section: Experimenal Studies In Vivomentioning

confidence: 97%

Immunotoxicity of heavy metals in relation to Great Lakes.

Bernier

Brousseau

Krzystyniak

et al. 1995

Environ Health Perspect

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Heavy metals including mercury, lead, and cadmium are present throughout the ecosystem and are detectable in small amounts in the Great Lakes water and fish. The main route of exposure of humans to these metals is via the ingestion of contaminated food, especially fish. Extensive experimental investigations indicated that heavy metals alter a number of parameters of the host's immune system and lead to increased susceptibility to infections, autoimmune diseases, and allergic manifestations. The existing limited epidemiologic data and data derived from in vitro systems in which human peripheral blood leukocytes were used suggested that the human immune system may also be at increased risk following exposure to these metals. The magnitude of the risk that the presence of such metals in the Great Lakes may pose to the human immune system, and consequently to their health, is not known. In this review, the available data with respect to potential adverse effects of heavy metals on the immune system of humans and experimental animals are discussed, and additional data requirements are suggested. Environ Health Perspect 103(Suppl 9): 23-34 (1995)

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Methylmercury: Decreased Antibody Formation in Mice

Cited by 33 publications

References 0 publications

Immunotoxicological effects of piperine in mice

Immunotoxicological effects of piperine in mice

Spontaneous Downregulation of Antibody/Autoantibody Synthesis in Susceptible Mice upon Chronic Exposure to Mercuric Chloride is not Owing to a General Immunosuppression

Immunotoxicity of heavy metals in relation to Great Lakes.

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