Meeting Abstract
P2.82 Saturday, Jan. 5 Programmed cell death by reactive oxygen species in tail of tadpoles, Xenopus laevis MANZO, W.J.*; GARDNER, E.; MENON, J.; William Paterson University; William Paterson University; William Paterson University menonj@wpunj.edu
During metamorphosis, anuran tadpoles undergo morphological, biochemical and physiological changes in order to adapt to a different habitat. The process involves reorganization of the body plan and regression of the tail which are controlled by several pathways of apoptosis including autophagy. Autophagy induces cell death in regressing tail in response to reactive oxygen species (ROS). Several antioxidant systems regulate the presence of oxidant species such as superoxide dismutase (SOD), glutathione, ascorbic acid, catalase etc. Nitric oxide synthase(s) (NOS) leads to production of nitric oxide (NO), a free radical, important in cellular signaling. We performed a cellular, biochemical and molecular analysis of SOD, catalase, NOS, in situ staining for NO and mitochondria in the tail of tadpoles Xenopus laevis. NO also has profound effect on the mitochondrial function as mitochondria possess their own NOS enzyme. Spatiotemporal distribution of SOD and catalase showed significant co-localization (overlap coefficient of 95%) during earlier stages of metamorphosis. However, during climax (just before the tail regression begins), there was a significant decrease in activity of these enzymes as well as reduction in overlap coefficient (49%) which suggests an elevated ROS accumulation. Expression for nNOS and iNOS was found to be stage specific and both enzymes co-localized in epidermis and muscle tissue of tail, their expression being controlled by thyroxin as evidenced by RT-PCR studies. Additionally, NO and mitochondrial staining also shows co-localization suggesting that NO is derived from mitochondria. These findings are discussed in terms of putative functional importance of ROS and mitochondria derived NO in programmed cell death in tail tissue.
