Alcohol en zwangerschap*
Uit een laboratoriumstudie blijkt dat alcohol meer foetale hersencellen laat afsterven. Voor een normale groei van de hersenen van de foetus moet ongeveer de helft van pas gevormde zenuwcellen weer afsterven. Doch uit deze studie blijkt dat alcohol meer zenuwcellen doet afsterven dan normaal en dan alleen als de cellen een lage waarde van de belangrijke lichaamseigen antioxidant,
glutathion hebben. Alcohol zorgt voor oxidatieschade die bij voldoende glutathion herstelt
kan worden.
Low Antioxidant Level May Damage Fetal Neurons
— Fetal neurons that have low levels of a vital antioxidant, glutathione, are the first to die when exposed to alcohol in cell culture and possibly in the living brain, according to new research from the laboratory of George Henderson, Ph.D., professor of medicine and pharmacology at The University of Texas Health Science Center at San Antonio.
The researchers examined brain tissue from immature rats and neurons from rat fetuses.
Why do only some neurons die quickly?
“The scope of the study was to document, in a convincing manner, why only some neurons within a specific brain area are extremely sensitive to alcohol exposure and die very fast, while adjacent neurons are resistant and able to survive the same insult,” said Shivani Maffi, Ph.D., the lead author and assistant professor of medicine. “A deficiency in glutathione might explain it.”
Normal growth of the fetal brain in animals as well as humans requires that approximately half of the newly formed neurons die by a process called apoptosis. However, when fetal brains are exposed to alcohol, this neuron death is increased. There is evidence that this may be caused by oxidative stress similar to what may also occur in neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases.
When alcohol is involved, 3 percent to 5 percent more neurons die. “Typically when the fetal rat brain is exposed to alcohol, we have observed a 3 percent to 5 percent increase in neuron death that depends on the amount of alcohol and length of exposure,” Dr. Maffi said.
The answer could provide preventive therapies
Knowing how some of the neurons escape apoptotic death during alcohol exposure could tell researchers how to provide therapies to prevent at least some of the devastating consequences of fetal exposure to alcohol. These studies confirm previous findings that neurons can be protected from alcohol by supplementing their glutathione content.
The scientists noted a 37 percent increase in oxidative stress and a 23 percent drop in glutathione levels in exposed tissues.
One in 100 live births in Texas suffers from a fetal alcohol spectrum disorder. Of 370,000 live births in the state annually, 3,700 babies are affected, said Carolyn A. Smith, executive director of the Texas Office for Prevention of Developmental Disabilities. “Each child may need $1 million to $2 million worth of supportive services during his lifetime,” Smith said. “You can see that this is an expensive problem in human and economic terms.”
The studyis published in the Journal of Neuroscience Research. Dr. Henderson’s co-authors, all from the Health Science Center, are Drs. Rhoda Hamby-Mason, Mary Rathinam, Priscilla Cherian, William Pate, Steven Schenker and Dr. Maffi.
Support for the study was from the National Institute on Alcohol Abuse and Alcoholism to an established investigator (Dr. Henderson) and the Executive Research Committee at the Health Science Center to a new investigator (Dr. Maffi).
University of Texas Health Science Center at San Antonio (Januari
2008)
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