It is also important to note that allicin could be toxic for mammalian cells in high concentrations (>60 μg mL−1), but the lethal dosage for fungus is lower (Rabinkov et al., 1998). In this study, two dosages of antifungal agents,

1 and Buparlisib order 5 mg kg−1 day−1, were selected. The results showed that allicin could reduce the morbidity and the fungal load in tissues of mice infected with C. albicans. However, these effects cannot be directly attributed to allicin, as it is not stable and converts immediately to other products such as ajoene, which may also have antifungal potential. The fungal load in liver of treated mice showed a significant reduction with increasing time intervals. Although after 1-week postinfection, the fungal load in mice treated with 5 mg kg−1 day−1 of allicin was lower (log10 mean CFU g−1=3.16 Smad3 signaling ± 0.42) compared with the other treated groups, mice treated with 5 mg kg−1 day−1 of fluconazole showed a more significant decrease

in fungal load (log10 mean CFU g−1=2.16 ± 0.20) thereafter. The results seen in other organs were similar to those seen in the liver (Table 2). Our findings also showed that the fungal load for all concentrations of antifungals during the first week were approximately similar, but after this time the differences between treated groups were significant. This may be due to the intrinsic murine immune responses of BALB/c mice (Ashman & Papadimitriou, 1988) infected at sites surrounding the infection for as long as 5 days postinfection, whereas treated mice were able to suppress Candida infection after at least 1 week. On the other hand, our data suggest that the conditions were approximately constant C1GALT1 after 2 weeks postinfection until the last day of the experiments. Data analysis showed a significant reduction in mortality for the two groups treated with fluconazole when compared with untreated control (P<0.05), whereas no significant difference was observed between the allicin groups treated

with 1 and 5 mg kg−1 day−1 dosages and the untreated control group at levels P=0.163 and P=0.067, respectively. However, the survival study suggests that allicin could increase the MST until 16 days, whereas the untreated control group showed an MST of 8.5 days. The percentage of mortality was reduced to 50% by treatment with allicin (Table 3, Fig. 3). The results from the MIC determination seem to suggest a more significant anticandidal potential in vitro of allicin than of fluconazole. However, the time–kill curve showed that allicin is comparable to fluconazole in terms of fungal load reduction. The combined results from both the survival studies and fungal load reduction studies in the present work demonstrate that allicin is slightly less efficacious than fluconazole in the treatment of candidiasis. Therefore, it is necessary to discover better treatment modalities or to increase the dosage of allicin, which will require further experiments.