Myristicin (5-allyl-1-methoxy-2,3-methylenodioxybenzene) is the main component of nutmeg essential oil [
1], which exists in the nutmeg nut (
Myristica fragrans Houtt.) and in mace, the waxy red covering of the nutmeg seed. Readily accessible on local markets, these spices have, at times, been drugs of abuse. On the other hand, nutmeg and mace are used in Asia as traditional medicines treating stomach cramps, diarrhea, and rheumatism. Information currently available on myristicin explains why its effects range from harmful to beneficial. As reported in the literature [
2], this alkenylbenzene acts as a serotonin receptor antagonist and as a hallucinogenic compound. Moreover, it induces: neurotoxicity in human neuroblastoma SK-N-SH cells [
3]; P450 liver enzyme in several families of rat, including the P450 1A enzyme [
4], which is also induced by polyaromatic hydrocarbons, dioxins, and polychlorinated biphenyls; glutathione S-transferase [
5] and forms DNA adducts in rodent livers. The ability to form DNA adducts is a common property of most chemical carcinogens and their metabolites [
6]. Several tests have shown myristicin to be a weak monamine oxidase (MAO) inhibitor [
7]. Acutely toxic doses of myristicin can cause organ damage [
8]. Myristicin poisoning can lead to many health problems such as convulsions, delirium, blurred vision, palpitations, nausea, dehydration, general body pain, and others [
9]. Those symptoms usually occur 3–6 h after the ingestion of myristicin or foodstuffs containing it, and persist up to 72 h [
10]. In recent years, many cases of nutmeg poisoning have been reported, including several fatal myristicin cases [
11‐
13]. Such poisonings can result not only from the toxic effect of myristicin itself but also from the combined toxic effects of its use with other substances [
12]. Because of potential widespread human exposure through foods and beverages and the possibility of adverse effects in diverse populations, myristicin was presented to the Chemical Selection Working Group (CSWG) for review.
Two publications describing myristicin determination in biofluid can be found in the literature [
14,
15]. The first concerns the myristicin metabolism in rats, but the results presented in the article were not obtained in a quantitative fashion. As a result, it is difficult to judge the method used for myristicin estimation in the reported study [
14]. Moreover, the described method involves a derivatization process, which is frequently inconvenient in GC analysis (the formation of deposits in the liner of GC injector or in chromatographic column). In the second study [
15], a method for HPLC determination of myristicin in rat serum is described. The procedure involves deproteinization, separation, and fractionation concentration of myristicin by appropriate switching of columns in the HPLC system. However, it should be stressed that the removal of serum proteins in the HPLC process can lead to the loss of analytes forming analyte–protein complexes. The present report describes the GC procedure for myristicin analysis in human plasma. The procedure involves a protein precipitation process, which generally degrades drug–protein complexes, and solid-phase extraction (SPE) isolation of myristicin from the examined materials. The proposed analytical approach can be considered as a method of choice for the estimation of myristicin in human fluids.