The role of estrogen, testosterone, and parathyroid hormones in combination with conventional and sustained antioxidant treatment on lncap cells - biomed 2009.

As men age, they will begin to experience numerous changes in their bodies and sometimes these changes are life threatening. Unfortunately, these alteractions can result in protate cancer which tends to be a major public health issue and a leading cause of cancer-related deaths in males (Greenlee et a., 2001). Androgens are metabolites of testosterone (TST), which are essential for maintenance of the normal morphology and functionof the prostate gland. With advancing age, transpositions can result in reduced testosterone levels and alter the ratio between testosterone levels and alter the ratio between testosterone and the chief female hormone, estrogen (Harman 2005). Testosterone is the major circulating androgen and it plays a major role in the overall health and well-being of both sexes. Similarly, estrogen (EST) is equally important and has been shown to be a powerful antioxidant responsible for suppressing free radical-induced peroxidation chain reactions (Sugioka et al., 1987; Green et al., 1997). Parathyroid hormone (PTH) is also a significant hormone responsible for regulating the calcium and phosphate within ghe body. Research has been ongoing examining these hormones in specific conditions to determine their effects (Bhasin 2003; Tanaka et al 2004; Young et al 2004). In this study, three antioxidants, epigallocatehin -3-gallate (EGCG), thymoquinone (TQ), and tannic acide (TA) were analyzed in combination with the above hormones to compare the effects of conventional and sustained administration of TST, EST, and PTH. Data of the study demonstrated that regardless of the route of administration cell growth was suppressed. Overall results revealed that route of administration played a significant role in disrupting prostate cancer growth.

C5 is required for CD49d expression on neutrophils and VCAM expression on vascular endothelial cells following mesenteric ischemia/reperfusion.

Complement activation is critical in the development of local mucosal damage and inflammation as well as of remote organ injury after mesenteric ischemia/reperfusion. To further define the role of C5 activation in local and remote tissue injury, C5 deficient (C5(-/-)) and wild-type control (C5(+/+)) mice treated with an anti-C5 mAb were subjected to sham or ischemia followed by up to 4 h of reperfusion. The development of local (intestinal) and remote (lung) injury was associated with the expression of CD49d on the surface of circulating blood neutrophils and with VCAM on the endothelial cells of intestinal and lung vessels. Because CD49d heterodimerizes with integrin beta1 on the surface of neutrophils and can bind VCAM on the endothelium, we propose that complement activation causes organ damage by upregulating molecules that lead to inappropriate homing of neutrophils.