Immunological Alterations Inducible by Mercury Compounds

Pietsch, P; Vohr, Hans-Werner; Degitz, Klaus; Gleichmann, Ernst

doi:10.1159/000234999

Cited by 63 publications

(1 citation statement)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have demonstrated that in susceptible mouse strains, mercury treatment results in the formation of high levels of autoantibodies against nucleolar antigens [5][6][7]131. Many of these ANolA were found to be directed against fibrillarin, a 34-kDa protein, which is a component of the U3 and U8 small nuclear ribonucleoproteins [19][20][21].…”

Section: Mercury Induces Anola In Sjl Mice But Not In (Nzb X Nzw)fl mentioning

confidence: 99%

Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZB × NZW)F1 hybrids

Al‐Balaghi

Möller

et al. 1996

Eur J Immunol

View full text Add to dashboard Cite

It is well established that in susceptible mouse strains, chronic treatment with subtoxic doses of mercuric chloride (HgCl2) induces a systemic autoimmune disease, which is characterized by increased serum levels of IgG1 and IgE antibodies, by the production of anti-nucleolar antibodies and by the development of immune complex-mediated glomerulonephritis. Susceptibility to mercury is partly under the control of major histocompatibility complex genes. To study the susceptibility to mercury further, we investigated the in vivo effects of mercury in young autoimmune disease prone (NZB x NZW)F1 (H-2d/z) mice prior to establishment of spontaneous autoimmune disease. Mercury-susceptible SJL (H-2s) mice and mercury low-responder BALB/c (H-2d) mice were used as positive and negative controls, respectively. In (NZB x NZW)F1 mice, treatment with mercury stimulated an intense antibody formation characterized by increased numbers of splenic IgG1 and IgG3 antibody-producing cells as well as by elevated serum IgE levels. Injection with mercury also induced an increased production of IgG1, IgG2b and IgE antibodies in SJL, but not in BALB/c mice. The mercury-induced IgG1 response in (NZB x NZW)F1 and SJL mice was found to be polyclonal and autoantibodies against double-stranded (ds)DNA, IgG, collagen, cardiolipin, phosphatidylethanolamine as well as antibodies against the hapten trinitrophenol were produced. In addition, SJL, but not (NZB x NZW)F1 or BALB/c mice, produced IgG1 anti-nucleolar antibodies after treatment with mercury. Further studies demonstrated that (NZB x NZW)F1 and SJL mice developed high titers of renal mesangial immune complex deposits containing IgG1 antibodies 3 weeks after injection with mercury. Thus, a mouse strain genetically prone to develop spontaneous autoimmune diseases is highly susceptible to mercury-induced immunopathological alterations.

show abstract

Section: Mercury Induces Anola In Sjl Mice But Not In (Nzb X Nzw)fl mentioning

confidence: 99%

Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZB × NZW)F1 hybrids

Al‐Balaghi

Möller

et al. 1996

Eur J Immunol

View full text Add to dashboard Cite

show abstract

Silver and Gold

Juberg¹,

Hearne²

2001

Patty's Toxicology

View full text Add to dashboard Cite

Silver, an element of the II(B) Group, is in the second transition series of the periodic table. It is a white, lustrous, relatively soft and very malleable metal. Silver has high thermal and electrical conductivity and resists oxidation in air that is devoid of hydrogen sulfide. Silver is insoluble in water although it can exist in an aqueous environment in three cationic forms, Ag(I), Ag(II), and Ag(III), in addition to its metallic state (AgO). Most silver compounds are made from silver nitrate, which is prepared from silver metal. The toxicological properties of many substances depend on the particular chemical species of that substance, and silver is no exception. Although silver exists in its elemental state and many references within the scientific literature are simply to “silver,” it is important to stress that speciation is critical to understanding the potential for toxicity and subsequent health effects. As with many substances, a discussion of each silver species' toxicological properties would appear rather incomplete due to the lack of information available. Given these factors, it is more logical to discuss silver based on specific target organs or endpoints of concern (i.e., irritation, carcinogenicity) and to provide information on relevant silver species within this context. An explanation for the apparent lack of toxicity information on numerous species of silver is that many of the commonly used forms are insoluble in aqueous media and therefore are not readily tested in laboratory animal species. This property of many silver species may, in part, also explain its apparent lack of acute or chronic toxicity in humans based on years of occupational and workplace experience. Gold is a dense, yet malleable, lustrous, yellow metal widely found in nature as elemental gold or in combination with sulfides in igneous rocks and ores. Gold is very stable and nonreactive and does not burn or oxidize in air. Other than in its atomic state, the metal does not react with oxygen, sulfur, or selenium at any temperature. Gold does react with various oxidizing agents at ambient temperatures provided a good ligand is present to lower the redox potential below that of water. Therefore, gold is not attacked by most acids under ordinary conditions and is stable in basic media. Early uses of gold were in medicinal, antibacterial, and dental applications dating back to the ancient Chinese and Egyptians. Gold salts have been used therapeutically, without notable success in treating several diseases, including asthma, leprosy, syphilis, and tuberculosis. Presently, gold salts have therapeutic usefulness (chrysotherapy) limited to treating rheumatoid arthritis of the peripheral joints and in certain rare skin diseases. Gold salts are most efficacious in the early stages of arthritic disease and reduce the inflammatory process but without inducting any repair process in the joints. Two generally recognized disadvantages to chrysotherapy include relapse following discontinuation of treatment and potential toxicity associated with gold salts. Because of its distribution in the body and short half‐life, colloidal radioactive gold, has been used as a radiation source in treating cancer. As noted for silver, a discussion of the toxicological properties for each gold compound is not practical from the standpoint of available information. Therefore, this discussion on gold and its toxicity potential centers on particular aspects of gold toxicology, and within this framework, where a particular gold compound has been evaluated, it are discussed.

show abstract

The toxic effects of organometals on the lands cycle in HL‐60 cells

Krug

1992

Applied Organom Chemis

View full text Add to dashboard Cite

The concentration of free fatty acids within cells is mainly dependent upon the following enzyme activities: liberation by phospholipase A, (PLA,), activation of free acids by acyl-CoA-synthetase and re-esterification by lysophospholipid acyltransferase (LAT). In many cell types, especially those of the haematopeotic system, this deacylation-reacylation cycle ('Lands cycle') plays an important role in the regulation of free fatty acid concentration, above all that of arachidonic acid.We have shown here that heavy-metal compounds affect this cycle mainly at two points and thereby lead to an increase of free fatty acids. On the one hand, organometals cause an inhibition of the reacylation of lysophospholipids; and on the other, the induction of PLA2 activity produces the same result. All compounds investigated such as methylmercury chloride (MeHgCI), diethyl-, triethyl-, and trimethyl-lead chloride (EGPbCI, , Et3PbC1, Me,PbCI) as well as trimethyltin chloride (EtgnCl) and di-t-butyltin dichloride (t-Bu,SnCI,) show at least one of these effects. In the case of Et3PbC1, the use of PLA,-inhibitors or pertussis toxin causes a drastic decrease in the amount of arachidonic acid liberated. These experiments demonstrate that the organometallic compounds inhibit the reacylation andlor stimulate the deacylation of fatty acids that are involved in many important biological or pathological mechanisms.The results suggest that in differentiated HL-60 cells the organometal compounds stimulate the Lands cycle by increasing the activity of the PLA, , possibly via a signal-transduction mechanism, and this effect is intensified via an inhibition of reesterification.

show abstract

Immunological Alterations Inducible by Mercury Compounds

Cited by 63 publications

References 22 publications

Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZB × NZW)F1 hybrids

Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZB × NZW)F1 hybrids

Silver and Gold

The toxic effects of organometals on the lands cycle in HL‐60 cells

Contact Info

Product

Resources

About