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  • Rodney C. Baker, PhD

    Office: R413
    Phone: (601) 984-1620
    E-mail: rbaker@umc.edu

    Current research

    I am interested in the mechanisms by which disruption of phosphatidic acid metabolism contributes to the pathophysiology of ethanol. Chronic ethanol is linked with a number of disease states including; cancer, cardiovascular disease, liver disease and brain damage. The specific metabolic and morphological consequences of chronic ethanol use are diverse and are dependent on the organ affected, but studies in this laboratory suggest that cell signaling mechanisms common to a variety of cell types may be compromised by chronic ethanol exposure.

    We have shown that unique phospholipase D product, phosphatidylethanol; which is produced in the presence of ethanol, at the expense of phosphatidic acid, induces apoptosis in lymphocytes, inhibits DNA synthesis in brain cells, and accelerates cell differentiation in lymphoid cells.Inhibiting the synthesis of phosphatidic acid prevents a number of cell functions that require cell membrane fusion such as phagocytosis, cell division and cell movement, all functions that are linked to chronic ethanol use or treatment.

    Selected publications

    • Kyle PB, Smith SV, Baker RC, Kramer RE. Mass spectrometric detection of CYP450 adducts following oxidative desulfuration of methyl parathion. J Appl Toxicol. 2012 .
    • Quan Z, Purser C, Baker RC, Dwyer T, Bhagat R, Sheng Y, Leszczynski JR.Determination of derivatized urea in exhaled breath condensate by LC-MS. J Chromatogr Sci. 2010 48: 140-144, 2010. PMID: 20109293
    • Kyle P Kyle PB, Adcock KG, Kramer RE, Baker RC. Use of liquid chromatography-tandem mass spectrometry for the analysis of pentoxifylline and lisofylline in plasma.Biomed Chromatogr. 19: 231-236, 2005. PMID: 15627284
    • P Kramer RE, Wellman SE, Rockhold RW, Baker RC.Pharmacokinetics of methyl parathion: a comparison following single intravenous, oral or dermal administration. J Biomed Sci. 9: 311-320, 2002. PMID: 12145528