At 38 weeks of gestation, a woman with a previously unremarkable pregnancy was noted to have fetal tachycardia without obvious cause. Fetal echocardiography resulted in a presumptive diagnosis of fetal atrial flutter with a 2:1 block. The newborn resumed the same rhythm. The neonate underwent transesophageal incremental overdrive pacing. A normal sinus rhythm was restored. The infant had no recurrence to age 6 months.
Zn2+ is present at high concentrations in mammalian brain, and is released in chelatable form after excitation of certain glutamatergic neurons. Recent observations suggest that it may play an important role in excitotoxic-induced neural injury. Ascorbic acid has been widely studied as a stimulator or an inhibitor of lipid-peroxide formation, depending on concentration, and lipid peroxidation has been postulated to be involved in both acute and chronic neurogenerative diseases. We find that ascorbic acid and Zn2+, at concentrations that are achieved in the brain after prolonged synaptic depolarization, coordinately promote lipid-peroxide formation and cause dysfunction of membrane-bound proteins. This effect is unique to Zn2+, and other divalent cations do not share a similar synergism with ascorbate. We propose that the Zn2+-ascorbate interaction may be an overlooked mechanism of lipid-peroxide formation in brain injury.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.