Speakers Bureau
Kenneth E. McMartin, PhD
LSU Health Sciences Center – Shreveport 1980 - present
Coe College, Cedar Rapids, Iowa, BA, Chemistry, 1973
University of Iowa, Ph.D., Pharmacology. 1977, Advisor: Thomas Tephly
Postdoctoral Fellow, Karolinska Institute, Huddinge, Sweden, 1977 – 1979, Advisor: Rolf Blomstrand
Visiting Faculty, Medical University of South Carolina, Charleston (1989 - 1990) with Donald Sens
Visiting Faculty, University of Minnesota – Duluth School of Medicine (2002 – 2003) with Kendall Wallace
SOT positions
Clinician-Scientist Engagement Task Force 2015–2020, Co-Chair 2016–2017, Chair 2017–2018
Collaborative Conferences Committee 2020–2021
Committee on K–12 Education Chair 2005–2006
Disease Prevention Task Force 2012–2013
Education Subcommittee for K–12 Education 2003–2006
IUTOX Councilor 2013–2016
Specialty Section Collaboration and Communication Group Co-Chair 2013–2014, Chair 2014–2015
South Central Regional Chapter 2002–present, Presidential Chain 2002–2006
Clinical and Translational Toxicology Specialty Section Founding Member 2011–present, Presidential chain 2011–2016
Mechanisms Specialty Section 1984–present
Awards and Honors
Kenneth Morgareidge Award in Toxicology, ILSI 1988
Fellow, American Academy of Clinical Toxicology 2009
Chair, Board of Scientific Counselors of the National Toxicology Program 2016-19
Society of Toxicology Translational Impact Award 2010
Distinguished Service Award, American Academy of Clinical Toxicology 2018
Member of numerous special emphasis panels and study sections for NIH, as well as review panels for NTP-CERHR, WHO (IPCS), US EPA, ATSDR, and NTP-ROC Expert Panels
Research Interests
As I tell students, I want to understand why something is poisonous – and by knowing this, we can then design improved therapies for the poisonings. My research focuses on determining the mechanism by which a substance is toxic because this is critical to develop antidotes for clinical toxicants. In my early studies, we showed in experimental methanol poisonings that formic acid has a causative role in the severe metabolic acidosis and the ocular toxicity observed for these intoxications. Subsequently, we worked with collaborating laboratories to develop new treatment modalities to block methanol metabolism. This effort culminated in the commercialization of an antidote – 4-methylpyrazole, now called fomepizole. The ensuing product development progressed through animal experimentation and then phase I-phase III clinical trials. Importantly, fomepizole is now utilized worldwide and has become the standard of care for both ethylene glycol and methanol poisonings.
In recent years, I have conducted mechanistic experimental studies on the pathogenesis of the renal toxicity of glycols, again with the goal of improving therapies. One project began as a study of why ethylene glycol (antifreeze) produces acute renal failure, but evolved to impact on kidney stone disease, because we have shown that kidney damage results from renal accumulation of calcium oxalate crystals. Oxalate crystals are endocytosed by renal tubular cells in which they produce mitochondrial dysfunction and cell death. Calcium oxalate crystals also accumulate in kidney stone disease and current therapy does not target the adherence of crystals to tubular cells. We have shown that aluminum citrate, uniquely among citrate salts, blocks the toxicity of calcium oxalate by preventing attachment to the tubular cell membrane. We have also shown that aluminum citrate, by itself, minimizes the kidney damage from acute EG poisoning. Thus it or a suitable alternative may be useful in minimizing calcium oxalate-induced kidney damage, either from ethylene glycol poisoning or in kidney stone disease.
A second project has examined the toxicity of diethylene glycol (DEG), which has led to many mass poisonings world-wide when it has been mistakenly used in liquid drug formulations. DEG produces severe kidney damage, moderate hepatotoxicity and a peripheral neuropathy. The mechanism by which DEG produces organ damage is not known and there is no accepted treatment. Our studies have demonstrated that DEG must be metabolized to produce toxicity and that a heretofore unknown metabolite of DEG, diglycolic acid (DGA), is the likely metabolite responsible for damaging the kidney, liver and neurons. Following up on this observation, we have shown that DGA accumulates in the kidney and likely other tissues because it is a substrate for the uptake transporter sodium dicarboxylate transporter-1. Because pharmacological inhibition and genetic knock down of this transporter reduces the uptake and toxicity of DGA, a small molecule inhibitor may be a useful therapeutic to reduce the organ toxicity from DEG.
Presentation Topics
“Mechanism-based translational studies on alcohol and glycol toxicity – from one carbon to four”
Such a talk will focus on how studies on the mechanism of toxicity of one carbon (methanol) led to similar studies on the toxic mechanisms of two carbons (ethylene glycol) and eventually to four carbons (diethylene glycol). Most of the talk will focus on how these studies that focus on mechanisms can lead to new molecular targets for antidotal therapy.
“The trials and tribulations of an academic toxicologist doing antidotal drug development”
Such a talk will discuss the unique problems faced by academic scientists, in particular toxicologists, face when discovering a possible therapeutic. The talk will go over the many steps by which an academic can promote drug development and can interact with drug companies to bring their ideas/drugs to the market.
“Career development for academic toxicologists”
This talk will discuss the importance on the role of mentors in creating a path for advancement, but also in how serendipity plays a role in scientific advancement.