Aloin induces apoptosis in Jurkat cells

Abstract

Aloe is widely used as a dietary supplement. However, there are continuing concerns over the toxicity and the purity of aloe-based products. The primary class of compounds responsible for aloe-induced toxicity are anthraquinones. One of these, aloe-emodin, has been extensively investigated for apoptosis inducing effects. Conversely, the precursor to aloe-emodin, aloin, has been subjected to only minimal investigation of any cytotoxic effects. Jurkat T cells, an established model for the study of compound toxicity, were used to evaluate the effect of aloin on cell viability. Cells were analyzed using flow cytometry and microscopy for cell size and granularity, cell membrane integrity, mitochondrial membrane potential, and cell cycle profile. Treatment with aloin resulted in a reduction in cell size, compromised membrane integrity, and loss of mitochondrial membrane potential in a dose-dependent manner. Additionally, treatment with aloin resulted in alteration of the cell cycle, specifically a block at G2/M phase. Importantly, the loss of cell membrane integrity was preceded by a loss of mitochondrial membrane potential, suggesting a mitochondrial-dependent pathway for aloin-induced apoptosis. These observations provide insight into the potential mechanisms of aloin-induced toxicity and thus, perhaps, aloe preparation-induced toxicity. Furthermore, because of the concern over the safety of aloe-based supplements, this work suggests that aloe supplements not containing aloin may be safer than aloe supplements containing aloin, and that aloin should be considered in addition to concentrations of aloe-emodin.