Inhibition of adenosine triphosphatases by gold

Nechay, Bohdan R.

doi:10.1002/art.1780230409

Cited by 26 publications

(13 citation statements)

References 16 publications

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“…If ATPase is inhibited by a metallic ion such as cadmium, ciliary activity would be adversely affected. This would be reasonable in light of the data of Sugawara (28) and Nechay (29). Both investigators demonstrated that cadmium levels as low as 10' M significantly inhibited (Na+ + K+) ATPase and (Mge ') and (Mg2 + + Ca2 +) ATPase in animal tissues.…”

Section: Resultssupporting

confidence: 59%

Cytotoxicity and Ciliostasis in Tracheal Explants Exposed to Cadmium Salts

Gabridge¹,

Meccoli²

1982

Environmental Health Perspectives

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Cadmium salts were examined for their biological effects on ciliated respiratory epithelium in hamster tracheal explants. Cadmium chloride and cadmium acetate both caused significant decreases in ciliary motion when tested at 100 ,uM and above. Reductions in relative ciliary activity were dose-dependent and were first demonstrable at 8-32 hr. The decreased ciliary motion was accompanied by decreases in two key metabolic compounds (ATP and dehydrogenase) which are normally associated with cell viability. Histopathological examination of cadmium-treated tissues showed an epithelium thinner than normal, with extensive vacuolization and few, if any, intact ciliated cells. The various biological effects exerted by cadmium are presented, along with potential mechanisms of pathogenesis for the observed ciliostasis and cytonecrosis. Decreases in adenosine triphosphate appear to play a critical role in the development of cadmium-related effects on cellular function and metabolism.

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Section: Resultssupporting

confidence: 59%

Cytotoxicity and Ciliostasis in Tracheal Explants Exposed to Cadmium Salts

Gabridge¹,

Meccoli²

1982

Environmental Health Perspectives

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“…For half-maximal inhibition of the mic rosomal enzyme, similar concentrations ranging between 1.2 and 1.6 x 10 4M were noted for human [48], rat, rabbit, mouse, and sheep kidney and of 2.1 and 3.2 x 10 AM for cortex and outer medulla, respectively, of the dog and guinea pig kidney [49]. Mg-ATPase was approximately 10 times less sensitive to this metal (table IV).…”

Section: Discussionmentioning

confidence: 99%

In vitro Inhibition of Na-K-ATPase by Trace Metals: Relation to Renal and Cardiovascular Damage

Kramer¹,

Gonick

1986

Nephron

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The potential role of trace metals in the pathogenesis of various disease states, especially of renal and cardiovascular disease, has been recognized increasingly. Moreover, altered membrane transport was recently incriminated to play a role in renal tubular syndromes, such as the Fanconi syndrome, as well as in the pathogenesis of volume dependent hypertension. We therefore investigated the possible in vitro effects of various trace metals on Na-K-ATPase, the biochemical correlate of active cellular transmembrane sodium and sodium-dependent transport. To more closely mimic the in vivo situation, we deliberately chose as enzyme source renal tissue homogenate, which may contain protective agents. Under these experimental conditions, the metals studied inhibited the enzyme quantitatively in the following order: Hg > Pb > Cd > Ur > Cu > Zn > Mn > Ba > Ni > Sr. Enzyme kinetic studies showed that Hg, Pb, and Cd competitively, and Cu noncompetitively, inhibited the enzyme. In general, Mg-ATPase was significantly less sensitive to the trace metals. Accumulation of these metals may present serious health hazards by producing a general defect in cell membrane transport. From the other metals studied, i.e., Mn, Ba, Ni and Sr, some may have toxic effects via other mechanisms, whereas some may exert a protective role against toxicity of other agents including metal ions.

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“…Suggested mechanisms underlying the therapeutic efficacy ofthese drugs include the inhibition oflysosomal or other cellular enzymes (26)(27)(28), interference with complement activation (29,30), inhibition ofprostaglandin biosynthesis (31,32), alterations in protein interactions (33)(34)(35)(36) and sulfhydryl reactivity (37), and nonspecific antiinflammatory activity (38). It has also been suggested that they block the accessory cell functions of macrophages, leading to regression of cell-mediated immunological reactions (39).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of human endothelial cell proliferation by gold compounds.

Matsubara¹,

Ziff²

1987

J. Clin. Invest.

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Neovascularization has a role in the propagation of rheumatoid synovitis because the spread of mononuclear cell infiltration and the growth of pannus are dependent on the growth of new blood vessels. Growth of such vessels requires local endothelial cell (EC) proliferation. Inhibition of synovial EC proliferation, therefore, would have the potential to diminish rheumatoid inflammation. We have, therefore, studied the effects of gold sodium thiomalate (GST), auranofin, and gold chloride on the proliferation of human umbilical vein EC. GST suppressed both basal and EC growth factor-induced tritiated thymidine incorporation into EC in a dose-dependent fashion. Inhibition was observed with concentrations as low as 1 lsg/ml GST, 5 jg/ml gold chloride, and 0.1 ;g/ml auranofin, levels attainable in blood and synovium of patients. These results suggest that gold compounds have an antiangiogenic effect. The low concentrations inhibiting EC proliferation suggest that gold compounds may suppress rheumatoid synovitis by reducing the number of small blood vessels available for mononuclear cell infiltration and synovial tissue proliferation.

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Inhibition of adenosine triphosphatases by gold

Cited by 26 publications

References 16 publications

Cytotoxicity and Ciliostasis in Tracheal Explants Exposed to Cadmium Salts

Cytotoxicity and Ciliostasis in Tracheal Explants Exposed to Cadmium Salts

In vitro Inhibition of Na-K-ATPase by Trace Metals: Relation to Renal and Cardiovascular Damage

Inhibition of human endothelial cell proliferation by gold compounds.

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