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Quinone reductase (QR; EC 1.6.99.2) is recognized as a major antimutagenic/anticarcinogenic enzyme in the organism. Our recent studies demonstrated the presence of significant QR activity in the early human placenta; whether this enzyme is expressed by the mammalian embryo is not known at present. In the investigation reported here, we sought to determine whether or not QR activity is detected in porcine embryonal tissues and if so, how early this expression takes place. In addition, the enzyme activity in the embryo was compared to that present in adult porcine tissue. Enzyme activity was determined by a colorimetric method with menadione as substrate in the presence of tetrazolium salt (MTT). NADH was a preferable cofactor in the embryo, whereas in the adult tissues NADPH was a better cofactor. Results show that the enzyme is present in all the embryonal organs tested from a very early age (30 days of gestation). Among the organs tested, activity was highest in the porcine embryo liver, and the specific activity remained unchanged until Day 70. Activity in the embryonal kidney increased with advancing gestation. The enzyme activity in embryonal tissues was much lower than that measured in the adult liver (30-40-fold).These findings suggest that the embryo has the potential for inactivating carcinogens/mutagens that will subsequently be eliminated by the maternal organism, thus protecting against adverse environmental impacts during the most critical period of development.

Glial phagocytosis is critical for the development and maintenance of the CNS in vertebrates and flies and relies on the function of phagocytic receptors to remove apoptotic cells and debris. Glial phagocytic ability declines with age, which correlates with neuronal dysfunction, suggesting that increased glial phagocytosis may prevent neurodegeneration. Contradicting this hypothesis, we provide experimental evidence showing that an elevated expression of the phagocytic receptors Six-Microns-Under (SIMU) and Draper (Drpr) in adult Drosophilaglia leads to a loss of both dopaminergic and GABAergic neurons, accompanied by motor dysfunction and a shortened lifespan. Importantly, this reduction in neuronal number is not linked to neuronal apoptosis, but rather to phosphatidylserine-mediated phagoptosis of live neurons by hyper-phagocytic glia. Altogether, our study reveals that the level of glial phagocytic receptors must be tightly regulated for proper brain function and that neurodegeneration occurs not only by defective, but also excessive glial cell function.