Immune-Type Glomerulonephritis Induced in the Brown-Norway Rat with Mercury-Containing Pharmaceutical Products

Druet, Philippe; Teychenne, Paul F.; Mandet, Chantal; Bascou, C.; Druet, E

doi:10.1159/000182136

Cited by 25 publications

(10 citation statements)

References 2 publications

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“…The systemic nature of the HgCl, induced disease in experimental animals has been documented in a number of reports. The gastrointestinal tract was also among the tissues involved (2,4, 6,8,12,13). It seemed especially interesting to determine if the intestinal involvement in BN rats treated orally differed from that of i.m.-injected rats.…”

Section: Discussionmentioning

confidence: 99%

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Autoimmune Disease Induced by Oral Administration of Mercuric Chloride in Brown-Norway Rats

1986

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ABSTRACIOnly few reports are available on the consequences of chronic oral administration of low doses of mercuric chloride (HgClJ. Forty Brown-Nonvay rats received 150 p g HgCIJ100 g body weight 3 times a week by gavage or by i.m. injection with 100 pg twice pcr week. After 2 weeks of oral HgC12 administration, the rats lost weight and hair. Phases of proteinuria were observed in weeks 5-8 and then continuously from week 12 until the end ofthe experiment at week 39. Antibodies binding to renal, intestinal, and vascular basement membrane developed after 2 weeks; circulating immune complexes were detectable in increasing titers starting at week 3. There were linear deposits of IgG, IgM, and IgA in the glomemlar basement membrane and tubular basement membrane, and along the intestinal basement membrane. After week 1 1, the first granular immune deposits wcrc observed in renal and intestinal basement membranes. Light microscopy showed thickcning of glornerular bascment membrane, mesangial matrix, and tubular basement membrane. In addition, interstitial nephritis was observed in some animals. Interestingly, kidney involvement was as severe in the orally as the i.m.-treated animals.

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Section: Discussionmentioning

confidence: 99%

“…Druet et a1 produced renal lesions in BrownNorway (BN) rats by applying mercury-containing drugs to the skin, on wounds, into the vagina, and by mouth. Their findings provided strong evidence against the use of mercury-containing ointments and antiseptics (8).…”

Section: Introductionmentioning

confidence: 93%

Autoimmune Disease Induced by Oral Administration of Mercuric Chloride in Brown-Norway Rats

1986

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“…Previous studies have shown that treatment with mercury in its various chemical forms, using different routes of administration (subcutaneous injection, oral ingestion, inhalation), results in autoimmune responses to a variety of antigens (7)(8)(9)(10). Relatively low doses of mercury have been found to be effective in both rats and mice; for example, the immunotoxic effects of If -HgCI2 occur in BN rats at doses (3-25 ,g/100 g body weight) that are much lower than those causing the common nephrotoxic effects (11,12,Bigazzi et al, unpublished data).…”

Section: Methodsmentioning

confidence: 99%

Mercury-induced renal autoimmunity: changes in RT6+ T-lymphocytes of susceptible and resistant rats.

Kosuda

Greiner

Bigazzi

1993

Environ Health Perspect

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The repeated administration of mercury to rats of the Brown Norway (BN) inbred strain results in a self-limiting production of autoantibodies to renal antigens (e.g., laminin) and autoimmune glomerulonephritis. In contrast, rats of the Lewis (LEW) strain do not develop renal autoimmunity after mercury treatment. Suppressor T-cells and/or the idiotype-anti-idiotype network have been implicated in the control of autoimmunity in susceptible (BN) rats as well as the "resistant" state of nonsusceptible (LEW) animals. In our investigations of the immune regulation of mercury-induced autoimmune glomerulonephritis, we have performed a phenotypic analysis of lymphocyte subpopulation in the spleens and lymph nodes of mercury-treated and control LEW, BN, and (BN x LEW) F1 hybrid rats. Of particular interest were RT6+ T-cells, a subpopulation of lymphocytes that may have immunoregulatory properties and show a relative decrease in mercury-treated BN rats concomitantly with the development of autoimmune responses to renal autoantigens. LEW rats did not develop renal autoimmunity after mercury treatment and had no significant change in the ratio of RT6+ to RT6- T-lymphocytes. Interestingly, the administration of mercury to (BN x LEW) F1 hybrid rats caused effects similar to those observed in the BN strain. Auto-immune responses to antigens of the kidney coincided with a change in the balance within the RT6 cell population, which was altered in favor of T-lymphocytes that do not express the RT6 phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Various other inbred rat strains (Lewis, Wistar AG, August, PVG/c) do not produce such antibodies under the same experimental conditions [37]. The immune reaction in mercury-sensitive Brown Norway rats is accompanied by an autoimmune renal disorder, identified as a membranous glomerulonephropathy [14,38,39]. After inhalation of mercury vapor (0.3-1.0 mg Hg/m 3 air for up to 10 weeks), mercury-susceptible mouse strains produce antinuclear antibodies, followed by deposition of immunocomplexes in the glomerulus [40].…”

Section: Autoimmunity In Mercury-sensitive Rodent Strainsmentioning

confidence: 99%

Immunological effects of mercury (IUPAC Technical Report)

Schwenk

Klein

Templeton

2009

Pure and Applied Chemistry

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Republication or reproduction of this report or its storage and/or dissemination by electronic means is permitted without the Immunological effects of mercury (IUPAC Technical Report)Abstract: Various chemical species of mercury differ considerably with regard to their route of absorption and their distribution in the body, yet many of them and their metabolites exhibit high-affinity binding to sulfanyl groups of proteins. Among all metals, mercury appears to have the most diverse effects on the immune system. Depending on the animal species and experimental conditions, mercury compounds may cause immunosuppression or immunostimulation, autoimmune reactions, or hypersensitivity. Mercury-sensitive strains of rats and mice are often used as model organisms to study the time course and events in autoimmunity. Within about 14 days after onset of oral mercury(II) exposure, levels of immunoglobulins E and G (IgE and IgG) increase, including autoantibodies to biomolecules such as laminin and fibrillarin. Antigen-antibody complexes are formed and are the cause of subsequent autoimmune diseases of blood vessels and organs. Mercury may induce local mercury hypersensitivity in humans, but the evidence for a role of mercury in autoimmune disease of humans is at best weak. Models for the immune effects of mercury are presented on the basis of current knowledge.

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Immune-Type Glomerulonephritis Induced in the Brown-Norway Rat with Mercury-Containing Pharmaceutical Products

Cited by 25 publications

References 2 publications

Autoimmune Disease Induced by Oral Administration of Mercuric Chloride in Brown-Norway Rats

Autoimmune Disease Induced by Oral Administration of Mercuric Chloride in Brown-Norway Rats

Mercury-induced renal autoimmunity: changes in RT6+ T-lymphocytes of susceptible and resistant rats.

Immunological effects of mercury (IUPAC Technical Report)

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