Gold cyanide is the electrolyte used in commercial electroplating of gold onto base metals and electroforming. Gold chloride (chloroauric acid) solutions are used to make colloidal gold by reduction with citrate or ascorbate ions. Gold chloride and gold oxide are used to make cranberry or red-colored glass, which, like colloidal gold suspensions, contains evenly sized spherical gold nanoparticles. Gold, when dispersed in nanoparticles, can act as a heterogeneous catalyst of chemical reactions. Toxicity
Pure metallic (elemental) gold is non-toxic and non-irritating when ingested and is sometimes used as a food decoration in the form of gold leaf. Metallic gold is also a component of the alcoholic drinks Goldschläger, Gold Strike, and Goldwasser. Metallic gold is approved as a food additive in the EU (E175 in the Codex Alimentarius). Although the gold ion is toxic, the acceptance of metallic gold as a food additive is due to its relative chemical inertness, and resistance to being corroded or transformed into soluble salts (gold compounds) by any known chemical process which would be encountered in the human body. Soluble compounds (gold salts) such as gold chloride are toxic to the liver and kidneys. Common cyanide salts of gold such as potassium gold cyanide, used in gold electroplating, are toxic by virtue of both their cyanide and gold content. There are rare cases of lethal gold poisoning from potassium gold cyanide. Gold toxicity can be ameliorated with chelation therapy with an agent such as dimercaprol.
Buspirone also has lower affinities for the serotonin 5-HT2A, 5-HT2B, 5-HT2C, 5-HT6, and 5-HT7 receptors.In addition to binding to serotonin receptors, buspirone is an antagonist of the dopamine D2 receptor with weak affinity. It preferentially blocks inhibitory presynaptic D2 autoreceptors, and antagonizes postsynaptic D2 receptors only at higher doses. In accordance, buspirone has been found to increase dopaminergic neurotransmission in the nigrostriatal pathway at low doses, whereas at higher doses, postsynaptic D2 receptors are blocked and antidopaminergic effects such as hypoactivity and reduced stereotypy, though notably not catalepsy, are observed in animals. Buspirone has also been found to bind with much higher affinity to the dopamine D3 and D4 receptors, where it is similarly an antagonist.A major metabolite of buspirone, 1-(2-pyrimidinyl)piperazine (1-PP), occurs at higher circulating levels than buspirone itself and is known to act as a potent α2-adrenergic receptor antagonist. This metabolite may be responsible for the increased noradrenergic and dopaminergic activity observed with buspirone in animals. In addition, 1-PP may play an important role in the antidepressant effects of buspirone. Buspirone also has very weak and probably clinically unimportant affinity for the α1-adrenergic receptor. However, buspirone has been reported to have shown "significant and selective intrinsic efficacy" at the α1-adrenergic receptor expressed in a "tissue- and species-dependent manner".Unlike benzodiazepines, buspirone does not interact with the GABAA receptor complex. Pharmacokinetics
Buspirone has a low oral bioavailability of 3.9% relative to intravenous injection due to extensive first-pass metabolism. The time to peak plasma levels following ingestion is 0.9 to 1.5 hours.