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Discover Supplement-Drug Interactions

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Last Updated: a month ago

Possible Interaction: Manganese and Aminosalicylic Acid

Research Papers that Mention the Interaction

Here we compared the effects of manganese on gill innervation in the presence of PAS, EDTA or Acetylsalicylic acid (ASA), and examined whether co-treating animals with PAS could block the deleterious effects of manganese on the oyster's dopaminergic innervation of the gill.
In other experiments, animals exposed to three day treatments with manganese produced a dose dependent impairment of the dopaminergic, cilio-inhibitory system, which was decreased by co-treatment with PAS.
Pre-treating gill preparations with PAS or EDTA blocked the neurotoxic effects of manganese , while ASA did not.
The study shows that PAS protects the animal against neurotoxic effects of manganese and the mechanism of action of PAS in alleviating Manganism is more likely related to its chelating abilities than its anti-inflammatory actions.
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP  •  2010  |  View Paper
Abstinence and treatment with EDTA, levodopa, and para-aminosalicylic acid was associated with decreasing blood manganese concentrations and subjective improvement, but no change in objective findings.
Clinical toxicology  •  2009  |  View Paper
Co-… with Mn plus Ebs … Mn plus PAS caused a significant decrease in blood and brain Mn concentrations (compared to rats treated with Mn alone), concomitant with reduced brain E₂ prostaglandin (PGE₂) and enhanced brain glutathione (GSH) levels, decreased serum prolactin (PRL) levels, and increased ambulation and rearing activities.
Toxicology and applied pharmacology  •  2012  |  View Paper
Furthermore, PAS and AcPAS seem to be effective in reducing manganese levels in brain.
Drug Metabolism and Disposition  •  2011  |  View Paper
These data suggest that PAS likely acts as a chelating agent to mobilize and remove tissue Mn.
Neurotoxicology  •  2009  |  View Paper
The study found that high levels of Mn had a toxic effect on gill mitochondrial O(2) consumption and that this effect could be blocked by the drugs caEDTA, PAS and ASA.
In vivo  •  2011  |  View Paper