No abstract

Curcumin exhibits antioxidant properties in normal cells where the uptake is low, unlike in tumor cells where uptake is high and curcumin increases reactive oxygen species (ROS) production and cell death. Mitochondria are the main source and primary target of cellular ROS. We hypothesized that curcumin would regulate cellular redox status and mitochondrial function, depending on cell sensitivity and/or curcumin concentration in normal cells. We examined the differences between low and high concentrations of curcumin, with specific attention focused on ROS levels, mitochondrial function, and cell viability in mouse C2C12 myoblast under normal and simulated conditions of diabetes.Cells incubated with high concentrations of curcumin (10-50 μM) resulted in decreased cell viability and sustained robust increases in ROS levels. Mechanistic studies showed that increased ROS levels in cells incubated with 20 μM curcumin induced opening of mitochondrial permeability transition pores and subsequent release of cytochrome c, activation of caspases 9 and 3/7, and apoptotic cell death. Low concentrations of curcumin (1-5 μM) did not affect cell viability, but induced a mild increase in ROS levels, which peaked at 2 hr after the treatment. Incubation with 5 μM curcumin also induced ROSdependent increases in mitochondrial mass and membrane potential. Finally, pretreatment with 5 μM curcumin prevented high glucose-induced oxidative cell injury. Our study suggests that mitochondria respond differentially depending on curcumin concentrationdependent induction of ROS. The end result is either cell protection or death. Curcumin may be an effective therapeutic target for diabetes and other mitochondrial diseases when used in low concentrations.

In the United States, people who use artificial reproductive technologies have the option of choosing the sex, for nonmedical purposes, of the child they would like to conceive. This is in sharp contrast to many areas of the world in which this practice has been banned. In this paper, the process of prenatal sex selection is explained and compared to other forms of sex selection. Policy regarding nonmedical sex selection in the U.S. is then contrasted to that of other countries, followed by a discussion of the ethical considerations of this practice with a particular focus on the potential dangers it could pose to women. The paper then ends with policy and regulation recommendations as well as an examination of how sex selection relates to larger conversations regarding abortion, genetic engineering, and cloning.