WASHINGTON, DC June 27, 2007-Exposure to iron during the first weeks of life in combination with exposure later in life to a common herbicide may contribute to the subsequent degeneration of brain cells associated with the onset of Parkinson's disease (PD), according to a new study in mice. The findings also showed that a compound that protects cells in the body from damage from certain forms of oxygen, a kind of antioxidant, could suppress such neural degeneration.
Previous studies indicated that both early exposure to iron and later exposure to the herbicide paraquat independently increase oxidative stress — an environment in which damage from levels of reactive oxygen is more likely — in dopamine-producing regions of the brain, areas that are affected by PD. Julie Andersen, PhD, and her team at the Buck Institute for Age Research found that feeding iron to newborn mice made them more susceptible to paraquat, which increases levels of harmful forms of oxygen and damages dopamine-producing neurons as they grew older. The study appears in the June 27 issue of The Journal of Neuroscience.
"The importance of the study is that it points to a possible role of common mechanisms triggered by iron and paraquat as important in PD, and suggests that therapies that block their effects would be worth testing in patients," says Marie-Francoise Chesselet, MD, PhD, of UCLA, who did not participate in the study.
Ten-day-old mice were fed iron for a week. At ages from two months to two years, they were then exposed to paraquat for three weeks. By examining their brains, Andersen and her team found that by the time the mice were a year old, early iron consumption exacerbated damage to brain cells caused by paraquat exposure. The effect was even more pronounced at two years of age, the human equivalent of 60-70 years.
A subset of mice that received the antioxidant at the same time that they were exposed to paraquat exhibited reduced levels of dopamine-producing neuron death, suggesting they were protected from oxidative damage. Aging is the single major risk factor for PD, but the findings from Andersen and her colleagues show that exposure during the neonatal period may play a crucial role in the development of late-onset PD.
Future studies are likely to explore the role of antioxidants in helping to prevent and treat symptoms of PD, says Andersen. "The present findings suggest that antioxidants may be a viable therapeutic approach for neurodegenerative diseases associated with oxidative stress, such as PD."
The work was supported by a grant from the National Institutes of Health.
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 36,500 basic scientists and clinicians who study the brain and nervous system. Andersen can be reached at email@example.com.