Hemolytic activity of copper sulfate as influenced by epinephrine and chelating thiols
Abstract
AIM: To study the effects of epinephrine, homocysteine, and other complexing agents on the cytotoxicity of copper sulfate.
METHODS: In vitro suspensions of human red cells incubated with cupric sulfate were used, and hemolysis was determined by extracellular hemoglobin.
RESULTS: The hemolytic activity of CuSO4 (0.3 mmol.L-1) was enhanced by the presence of epinephrine and to a lesser extent by homocysteine, whereas D-penicillamine, succimer, and mercaptodextran reduced the copper-induced hemolysis. The latter 3 chelating thiols also reduced the copper-epinephrine-induced hemolysis. The plasma protein ceruloplasmin reduced markedly the copper-epinephrine-induced hemolysis, even upon concentrations < 20% of that of copper. Chromic chloride, as well, acted anti-hemolytically.
CONCLUSION: The latter protectors may interact with the production or activity of toxic oxygen, while classical copper chelators sequester cupric ions from interaction with epinephrine or homocysteine.
Keywords:
METHODS: In vitro suspensions of human red cells incubated with cupric sulfate were used, and hemolysis was determined by extracellular hemoglobin.
RESULTS: The hemolytic activity of CuSO4 (0.3 mmol.L-1) was enhanced by the presence of epinephrine and to a lesser extent by homocysteine, whereas D-penicillamine, succimer, and mercaptodextran reduced the copper-induced hemolysis. The latter 3 chelating thiols also reduced the copper-epinephrine-induced hemolysis. The plasma protein ceruloplasmin reduced markedly the copper-epinephrine-induced hemolysis, even upon concentrations < 20% of that of copper. Chromic chloride, as well, acted anti-hemolytically.
CONCLUSION: The latter protectors may interact with the production or activity of toxic oxygen, while classical copper chelators sequester cupric ions from interaction with epinephrine or homocysteine.