I received my doctorate in pharmacology at the University of Georgia College of Pharmacy studying the effects of dietary fats on carcinogen metabolic activation. After a postdoctoral fellowship at the Mayo Clinic, where I studied the metabolism of anesthetics and halogenated compounds by the cytochrome P450 enzyme system, I came to The University of Iowa in 1984. At the time, there was interest in the metabolism and toxicity of small fluorinated compounds as they were employed not only as anesthetics but as the new non-chlorinated refrigerant substitutes. In addition to defining metabolic pathways, I uncovered a unique P450 mechanism by which exposure to certain fluorinated compounds, including anesthetics, greatly increased the metabolism and potential toxicity of unsaturated fluoro- and chloro-ethylenic type compounds.

Having more of a clinical influence at Iowa, I eventually involved myself in application of fluorine chemistry to anesthesia. Fluorine is a most unique halogen, being the most electronegative element. When added to small molecules, it results in a number of desired properties, particularly good compound stability and volatility. The downside of fluorine additions is that it involves unique and sometimes dangerous chemical reactions to perform. My “dangerous” chemical endeavors involved use of the very reactive and toxic chemical bromine trifluoride to formulate a new way to make sevoflurane and to make a deuterated form of sevoflurane which is less metabolized to fluoride than sevoflurane. I have also investigated the breakdown of sevoflurane on CO absorbents, as well as authored articles on the chemical mechanisms of sevoflurane decay that remains a problem in both absorbents and vaporizers.

A hiatus from fluorine chemistry involved my work with propofol under industry sponsorship. Propofol is certainly a desirable anesthetic, but emulsion formulations containing different antimicrobial agents were thought to cause untoward chemical reactions in the emulsions. I was able to show that this was indeed the case. Sulfite, an additive in one formulation, could cause free radical formation, which in turn caused propofol and emulsion oxidation quickly after exposure to air. I also was able to show that there was a unique three-way reaction between sulfite, emulsion lipids, and propofol.

I enjoy the process of innovation and have more recently turned my attention toward the synthesis and use of fluorine in phenolic compounds related to propofol. I have been issued a number of patents for these compounds. In addition to some of these compounds having anesthetic properties, screens by the National Institutes of Health have shown a few to have low sedative, but significant anticonvulsant properties. Anticonvulsant properties are usually associated with anesthetics, but not useful for “everyday” epilepsy treatment due to their high sedative effects. I hope to also apply newly created fluorocompounds to such problems as bronchoconstriction and central nervous system imaging with fluorine tags.

In addition to research, I enjoy teaching and interacting with students. In my spare time, I can most likely be found working on my home improvement and gardening projects, amassing too many tools for such projects, or riding my bike.

Max T. Baker, Ph.D.
Associate Professor