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Selenium and kidney deposits in experimental argyria. Electron microscopy and microanalysis
Pathologie-Biologie
|March 1, 1982
Summary
Selenium and silver salts accelerate renal argyria by forming deposits in basal membranes. Selenium replaces sulfur in silver deposits, enhancing toxicity and argyria symptoms.
Area of Science:
- Toxicology
- Biochemistry
- Materials Science
Background:
- Renal argyria is a condition characterized by silver deposition in kidney tissues.
- The interaction between selenium and silver in biological systems is not fully understood.
Purpose of the Study:
- To investigate the conjugate effects of selenium and silver salts on experimental renal argyria.
- To elucidate the mechanisms of silver and selenium deposition and interaction in renal tissues.
Main Methods:
- Experimental induction of renal argyria in animal models.
- Microanalysis and electron probe microanalysis for elemental localization and identification.
- Histological examination of kidney tissue sections.
Main Results:
- Silver and sulfur deposits were observed in basal membranes after silver salt treatment.
- Concomitant administration of selenium and silver salts significantly accelerated the formation of these deposits in glomerular basal membranes.
- Electron probe microanalysis revealed that selenium replaces sulfur within silver deposits.
- Selenium exhibited a complex action on silver, primarily increasing its toxicity and promoting argyria symptoms.
Conclusions:
- Selenium potentiates the deposition and toxicity of silver in renal tissues, accelerating the onset and severity of argyria.
- The mechanism involves selenium replacing sulfur in silver deposits, altering their properties and biological interactions.
- Understanding these interactions is crucial for managing heavy metal toxicity and related conditions.