Abstract:Summary: The effects of administration of ambilhar to rats poisoned with mercury for two weeks were investigated. The results showed that administration of ambilhar to rats dosed with mercuric Chloride, resulted in a significant increase in the faecal excretion of mercury. At the same time a significant decrease in the urinary Output of the metal was found. Chelation of ambilhar with mercury to form a polar complex with a higher molecular weight could explain its biliary rather than its urinary excretion. The … Show more
“…Later, Abdel Aziz et al (5) reported that niridazole stimulated the biliary excretion of mercury in rats. This finding was explained by the formation of a polar complex with mercury of a higher molecular weight, which undergoes biliary rather than urinary excretion.…”
Summary:Administration of niridazole to rats poisoned with copper caused a significant increase in both the urinary and biliary excretion of the metal. Although the urinary excretion of iron was increased by the drug, iron excretion was significantly decreased during the drug-induced excretion of copper after copper poisoning. Formation of a copper-niridazole chelate or chelates before excretionjn the bile or urine may explain these findings. Polarity and molecular weights of the metal-drug chelates formed in vivo may be the directing forces not only in the selection of the metal for chelation, but also for its urinary or biliary excretion. The laboratory preparation of two copper-niridazole complexes lends support to these conclusions.
“…Later, Abdel Aziz et al (5) reported that niridazole stimulated the biliary excretion of mercury in rats. This finding was explained by the formation of a polar complex with mercury of a higher molecular weight, which undergoes biliary rather than urinary excretion.…”
Summary:Administration of niridazole to rats poisoned with copper caused a significant increase in both the urinary and biliary excretion of the metal. Although the urinary excretion of iron was increased by the drug, iron excretion was significantly decreased during the drug-induced excretion of copper after copper poisoning. Formation of a copper-niridazole chelate or chelates before excretionjn the bile or urine may explain these findings. Polarity and molecular weights of the metal-drug chelates formed in vivo may be the directing forces not only in the selection of the metal for chelation, but also for its urinary or biliary excretion. The laboratory preparation of two copper-niridazole complexes lends support to these conclusions.
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