Endocrine Disruptors

For the previous century, the humans have created an unintended and unwanted problem of endocrine disruptors as a potential threat to our public health. By the name of industrialization, endocrine disruptors are smuggling in the everyday life of people today. Although there are much debate on the reality of their emerging health threat, it is no doubt that there are certain classes of compounds that have the potential to affect hormonal status adversely, leading to abnormal development, reproductive dysfunction, and some cancers. The classes of endocrine disruptors are extensively diverse and even more increasing, such as, polychlorinated biphenyls (PCBs), dioxins, dieldrin, bisphenol A and toxaphene. Although these endocrine disruptors have been prohibited or tightly regulated, many of them are still unrecognized and still used without knowing their potential threat to the biological world. Once they are released into the environment, they usually persist without degradation and even undergo bioaccumulation and bioconcentration in food chain. Comparing with the great concern over the public health, we do not have enough information for these issues. It is now clear that we need further extensive studies for the risk assessment and the protection of human and ecological health from the potential hazards of endocrine disruptors. This article introduces a breif overview of the current status of our knowledge and research on endocrine disruptors.

The mechanism of phospholipase C-gamma1 regulation

Phospholipase C (PLC)1 hydrolyzes phosphatidylinositol 4,5-bisphosphate to generate the second messengers, inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 induces a transient increase in intracellular free Ca2+, while DAG directly activates protein kinase C. Upon stimulation of cells with growth factors, PLC-gamma1 is activated upon their association with and phosphorylation by receptor and non-receptor tyrosine kinases. In this review, we will focus on the activation mechanism and regulatory function of PLC-gamma1.