Sophorolipid exhibits antifungal activity by ROS mediated endoplasmic reticulum stress and mitochondrial dysfunction pathways in Candida albicans.

In the present study, we investigated the mechanism of cell death in C. albicans due to treatment with sophorolipid (SL). SL is an extracellular glycolipid biosurfactant produced by various species of non-pathogenic yeasts and is known to inhibit the growth and biofilm formation of C. albicans. This study revealed that treatment of C. albicans cells with SL increases the ROS production and expression of oxidative stress-related genes significantly (SOD1, CAT1). Increased ROS level within the cells causes ER stress and release of Ca(2+) in the cytoplasm and alteration of the mitochondrial membrane potential (MMP). Quantitative real time-polymerase chain reaction (qRT-PCR) data showed that SL also upregulates the Endoplasmic Reticulum (ER) stress marker HAC1. Flow cytometric analysis (AnnexinV/PI) indicated that the cell death may have occurred due to necrosis which was further confirmed by LDH release assay and transmission electron microscopy (TEM). Further experiments with the null mutant Δ hog1 strain of C. albicans SC5314 indicated the activation of the osmotic stress response pathway (HOG-MAPK) and SAP9. This study gave an insight into the mechanism of cell death initiation by glycolipids and indicated that further modification of these molecules can lead to the development of new therapeutic agent against C. albicans.