Department of Cell Physiology & Molecular Biophysics
Seminar Series
Antoinette Steinacker, Ph.D.
Research Associate Professor
Institute Neurobiology
UPR San Juan, PR
Room 5BC201, 10:00 – 11:00 a.m., October 30, 2008
"Sulfite, exocytosis and bronchoconstriction"
Sulfite is ubiquitous in the environment, in our foods and in many pharmaceuticals. It is found in all
eukaryotic cells as a toxic metabolic byproduct of sulfur containing amino acids. Sulfite is oxidized to the
harmless sulfate by the cellular enzyme, sulfite oxidase. An international registry of sulfite oxidase
deficient families exist. The individuals who carry two copies of the defective gene are not viable.
Heterozygotes are considered normal. Although there exists an in depth knowledge of the biochemistry
and genetics of sulfite oxidase and of the effects of sulfite on transmitter release and the critical role of
disulfide bonds in transmitter release, there has been very little application of this to the consideration of
sulfite toxicity in the human lung. The FDA requires the presence of sulfites in foods to be labeled, and
prohibits the use of sulfites on fresh produce intended to be sold or served raw to consumers (However,
exclusion is given for many foods, such as sliced potatoes for use in French fries and many sea foods,
drugs (such as lidocaine) and many intermediates in food and drug processing. The sudden deaths that
occur from sulfite exposure are from acute bronchoconstriction. Data from the speaker’s lab on sulfite
effects show long-term presynaptic increases of transmitter release and potentiation of the postsynaptic
muscle response. Recent data has detailed many of the molecular steps involved in vesicular secretion
(exocytosis). One of those steps is critically sensitive to NEM (N-ethylmaleimide) a reducing agent
chemically very similar to sulfite. Here lies the link between sulfite research and bronchoconstriction.
NEM was shown to produce the same effects on long-term outpouring of neurotransmitter as sulfite does
and the pathway for NEM activity is known. This infers that sulfite may produce bronchoconstrion by
causing release from mast cells and ACh terminals in the lung. Data will be shown that supports this
hypothesis.
Steinacker, A., Perez, R., Blanco, R.E. and Zuazaga, D.C. (2000) Morphological correlates of
electrophysiological properties of the sensory vestibular periphery. J. Physiol. 253:128-129p.
Steinacker, A. (2002) Ionic currents in vestibular hair cells. The Vestibular System of Fishes. Ed S.M
Highstein Springer-Verlag.
Persons with disabilities who may need auxiliary aids or services are requested to contact Crystal Perkins at least 24 hours prior
to this seminar so that appropriate arrangements can be made.
Department of Physiology: Crystal Perkins
STOP 6551 | 806-743-2520
Persons with disabilities who may need auxiliary aids or services are requested to contact Crystal Perkins at least 24 hours prior
to this seminar so that appropriate arrangements can be made.
Department of Physiology: Crystal Perkins
STOP 6551 | 806-743-2520