To explore the underlying mechanism of cancer cell growth inhibition by brassinosteroids (BS), reactive oxygen species (ROS) generation under treatment with 28-homocastasterone and its synthetic derivatives (22S,23S)-28-homocastasterone was measured in A549 human lung adenocarcinoma cells. BS induced ROS generation in A549 cells and their growth in a time and dose-dependent manner. The maximal effect was observed for (22S,23S)-28-homocastasterone which at 30μM concentration showed a 6-fold increase of ROS generation in comparison with the control.
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