Shedding light on age-promoting agents

Multiple tools have been established to readily evaluate the carcinogenic potential of environmental agents; however, few options are available to examine the ability of an environmental agent to accelerate molecular aging. Expression of p16^INK4a is associated with cellular senescence and increases with age and in age-related diseases. Jessica Sorrentino and colleagues took advantage of a recently developed mouse strain (p16^LUC mice), in which luciferase production correlates with transcription of p16^INK4a, to evaluate potential age accelerating compounds (gerontogens). Several candidate gerontogens were tested in p16^LUC mice, including arsenic, a high-fat diet, UV light, and cigarette smoke. The authors found that a high fat diet did not enhance or accelerate p16^INK4a expression, arsenic produced a moderate increase of p16^INK4atranscription, while exposure to either UV light or cigarette smoke dramatically increased p16^INK4a expression. This study demonstrates the usefulness of p16^LUC mice for evaluating the age-promoting potential of environmental agents and suggests that DNA damaging agents are strong gerontogens. The above image is a representative luciferase-detecting scan of 24 week old p16^LUC mice exposed to ambient air (left 2 animals),  24 week old control mice (center), and 24 week old p16^LUC mice exposed to cigarette smoke (right 2 animals).

Published December 16, 2013, by Corinne Williams

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