In this work, a pharmacological approach is reported, aimed at deciphering the role of calcium as a second messenger in the transduction pathway leading to the inhibitory effect of 2,4-dichlorophenoxyacetic acid (2,4-D), selleckchem in regulating monoterpene indole alkaloid (MIA) biosynthesis in Catharanthus roseus cells. It is demonstrated here that auxin-dependent MIA biosynthesis is differentially

regulated by two distinct calcium release components from internal stores in C. roseus showing pharmacological profiles similar to those displayed by animal RyR and IP3 channels. MIA biosynthesis is stimulated by caffeine (Ca2+-release activator through RyR channels) and by heparin and TMB8 (Ca2+-release inhibitors of IP3 channels) whereas MIA biosynthesis is inhibited by mastoparan (Ca2+-release activator of IP3 channels) and by ruthenium red and DHBP (Ca2+-release inhibitors of RyR GDC973 channels). Furthermore, calcium,

as 2,4-D, acts on MIA biosynthesis by regulating the monoterpene moiety of the MIA biosynthesis pathway since calcium channel modulators preferentially modulate g10h expression, the gene encoding the enzyme of the secoiridoid monoterpene pathway, that is the major target of 2,4-D action. In addition, the simultaneous use of caffeine (an activator of RyR channel in animals) and TMB8 (an inhibitor of the IP3 channel) in 2,4-D treated cells triggers a synergistic effect on MIA accumulation. This finding suggests an opposite and co-ordinated action of multiple Ca2+-release pathways in 2,4-D signal transduction, adding a new level of complexity to calcium signalling in plants and questioning the existence of RyR and IP3 channels in plants.”
“Hulls from dry edible beans are rich in phenolic compounds recognized as possessing antioxidant

activity. The aim of this study was to characterize antioxidant properties of bean hull extract (BHE) and to determine whether BHE supplementation (at 400 or 800 mg/kg for 3 months) affects serum biochemical markers and bone structure in 12-month-old male C57BL/6 mice. Mice supplemented with 800 mg BHE/kg had lower serum tartrate-resistant acid phosphatase and parathyroid hormone concentrations than those on control diet or supplemented with 400 mg BHE/kg. BHE supplementation WH-4-023 clinical trial caused slight decrease in oxidized glutathione concentration in blood (P = 0.07). Compared to the control group, BHE supplementation at 800 mg/kg for 3 months improved bone structural indices, bone mineral density and trabecular thickness in the third lumbar vertebra. These results suggest that BHE supplementation may have beneficial effects on bone health in mice by decreasing bone resorption. Published by Elsevier Ltd.”
“Objective Non-disclosure of a cancer diagnosis is a common practice in many Asian cultures where family-based medical decision making is the norm.