the inhibitory properties of and mode of action of plant essential oils ...

Lemon balm, also known as balmint, has been tested in vitro against T. brucei and L.
major both of which have conventional treatments available but are currently
expensive or have strong side effects. The essential oil was found to inhibit the
growth of T. brucei (ED50 3.9 µg ml -1 ; Suramin ED50 0.5 µg ml -1 ) and L. major (ED50
7 µg ml -1 ; amphotericin B ED50 0.3 µg ml -1 ) (Mikus et al. 2000). When tea tree oil
(TTO) was used in these experiments the results for T. brucei inhibition indicated
that this oil might be an alternative to Suramin ® for the treatment of trypanosomiasis
(ED50 0.5 µg ml -1 for both compounds). One of the major constituents of TTO is
terpinen-4-ol which has a greater inhibitory action on the blood stream forms of T.
brucei (ED50 0.02 µg ml -1 ) and was over a 1000 fold more toxic to the parasite than
the human cell line HL-60 (Mikus et al. 2000). It was proposed that a deeper
investigation of these compounds trypanocidal activity should be undertaken to
determine their effectiveness as a new drug therapy.
Antitrypanosomal activity of PEOs
Again garlic appears to be the most active compound, with the constituent allicin
being of particular importance (Table 1.1). The chemically stable transformation
product of allicin is diallyl trisulphide (DAT) and is effective in inhibiting the growth
of the many species of the bloodstream form of trypanosomes, especially those
responsible for African trypanosomiasis (Lun et al. 1994). These include T. brucei
brucei, T. b. rhodesiense, T. b. gambiense, T. evansi, T. congolense and T.
equiperdum with DAT inhibiting growth at concentrations comparable to the
commercial drug Suramin ® (trypanosome IC50 = 0.8 - 5.5 µg ml -1 (4.5 – 31 µM);
Suramin ® IC50 = 10 µM; Lun et al. 1994). This compound has been reported to have
been used in China for the treatment of many diseases, such as bacterial and fungal
infections, with only mild side effects (Lun et al. 1994). A condensation product of
allicin is effective against both the epimastigote amastigote forms of T. cruzi to an
even greater degree. Ajoene immediately inhibits the proliferation of epimastigotes at
a concentration of 80 µM, reducing their proliferation by 50% with 40 µM and
causing cell lysis within 24 h with 100 µM (Urbina et al. 1993). Concentrations as
low as 40 µM were enough to completely eliminate T. cruzi amastigotes from Vero
cells in vitro within 96 h. The inhibition of epimastigote growth was accompanied by
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