Reactive oxygen species (ROS) are constantly generated and eliminated in the
biological system and play important roles in a variety of physiological and
pathological processes. Previous studies indicate that modulation of cellular ROS affects cell proliferation.
Thymosin alpha 1 (Talpha1) is a naturally occurring thymic
peptide and has previously been shown to be a potential
therapy for some immunodeficiencies,
malignancies, and
infections. However, few reports have focused on manipulation of cellular ROS level effects of Talpha1. In this study, the Talpha1-treated leukomonocytes, which were isolated from mice spleens, exhibited a higher ROS level and a lower
reduced glutathione (GSH) level; however, HepG2 cells treated with Talpha1 exhibited lower ROS level and higher GSH level. In addition,
after treatment with Talpha1, the population of leukomonocytes in the G(2) phase increased, resulting in a slight increase in viability. However, in Talpha1-treated HepG2 cells, the cell cycle was delayed in the G(1) phase, thereby inhibiting
tumor cell proliferation; in addition, dephosphorylation of the
serine/threonine kinase Akt was detected. In conclusion, we show that Talpha1 has potent anti-proliferative activity against malignant human
hepatoma cells and proliferative activity against leukomonocytes associated with manipulation of oxidative stress levels which indicates the potential of Talpha1 as an
antitumor drug.