Purple sweet potato pigments protective against Cobalt-60 induced radiotoxicity. - GreenMedInfo Summary
Purple sweet potato pigments protect murine thymocytes from⁶⁰Co γ-ray-induced mitochondria-mediated apoptosis.
Int J Radiat Biol. 2010 Dec;86(12):1061-9. Epub 2010 Aug 10. PMID: 20698744
Department of Pharmacochemistry, Ocean University of China, Qingdao, PR China.
PURPOSE: Purple sweet potato (PSP) pigments have been widely accepted as antioxidants but their radioprotective effect still remains unclear. In this study we investigated the effect of PSP pigments on⁶⁰Co γ-ray-induced mitochondria-mediated apoptosis in murine thymocytes.
MATERIALS AND METHODS: The murine thymocytes were pretreated by PSP pigments before exposure to 4 Gy⁶⁰Co γ-rays. Flow cytometry analysis was used to measure apoptotic cells and mitochondrial membrane potential. Reactive oxygen species (ROS) were detected using 2',7',-dichlorofluorescein diacetate (DCFH-DA) probe and the activity of antioxidant enzymes was tested by biochemical assay after irradiation. Cytochrome c, caspase-3 and poly ADP-ribose polymerase (PARP) were measured by Western blotting.
RESULTS: After treatment with PSP pigments and exposure to 4 Gy radiation the apoptosis of thymocytes was reduced and the mitochondrial transmembrane potential was maintained compared to control cells. In the presence of PSP pigments, ROS were reduced and the activities of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) were protected and in some cases increased. All the pro-apoptotic proteins (cytochrome oxidase, caspase 3 and PARP) decreased in PSP pigments pretreated thymocytes compared to irradiated cells in the absence of PSP pigments.
CONCLUSIONS: Pre-treatment with PSP pigments significantly inhibited⁶⁰Co γ-ray-induced mitochondria-mediated apoptosis. This radioprotective effect might be related to ROS scavenging, the enhancement of the activity of antioxidant enzymes, the maintenance of mitochondrial transmembrane potential, and the sequential inhibition of cytochrome c release and downstream caspase and PARP cleavage.