In this study, we attempted to investigate the potency of allicin against C. albicans, the predominant fungal species isolated from human infections. Allicin alone could exhibit antifungal activity, and when used in synergy with antimicrobial agents, it increased the efficacy of the therapeutic agents (Aala et al., 2010; Khodavandi et al., 2010). For example, combination of allicin

with amphotericin B and fluconazole has been demonstrated to have a significant synergistic effect in a mouse model of systemic candidiasis (An et al., 2009; Guo et al., 2010). Garlic and some of its derivatives destroy the Candida cell membrane integrity (Low Pembrolizumab cost et al., 2008), inhibit growth (Lemar et al., 2002) and produce oxidative stress (Lemar et al., 2005) in C. albicans. Most of these abilities are related to an SH-modifying potential, because the activated disulfide bond of allicin has an effect on thiol-containing Selleckchem ERK inhibitor compounds such as some proteins; however, the main targets of allicin on Candida are not well understood. It has been demonstrated that the antifungal activity

of allicin in vivo may be related to some secondary metabolites such as ajoene, diallyl trisulfide and diallyl disulfide, because the chemical structure of allicin is too unstable and converts to these secondary products immediately (Miron et al., 2004). Nonetheless, little is known about the potential in vivo activity of allicin against Candida. In this study, we used fluconazole as the standard anticandidal drug for comparison against allicin. The MICs of allicin Anacetrapib and fluconazole against C. albicans fell within the ranges 0.05–12 and 0.25–16 μg mL−1, respectively (Table 1), which is similar to findings from previous reports (Ankri & Mirelman, 1999; Khodavandi et al., 2010). All of the samples were sensitive to fluconazole and drug resistance was not seen. The time–kill study demonstrated a significant inhibition of Candida growth comparing untreated controls against those treated with allicin

and fluconazole, using inoculum sizes of 1 × 106 Candida cells mL−1 (P<0.05) and 1 × 104 Candida cells mL−1 (P<0.001) after 2- and 4-h incubation, respectively. This demonstrates that allicin decreased the growth of C. albicans almost as efficiently as fluconazole (P>0.05) for both inoculum sizes of Candida, demonstrating a comparable ability to inhibit the growth of the yeast cells (Fig. 1). The presence of pits on the cell surface and cellular collapse with high concentrations of allicin indicates that the cell membrane could be one of the targets of allicin in Candida (Lemar et al., 2002), whereas fluconazole in high concentrations can destroy the Candida cell entirely (Fig. 2).