G.A. Shakeel Ansari , Ph.D.

Affiliations: Department of Biochemistry & Molecular Biology, Department of Pathology
Tel: (409) 772-3107/3655
Fax: (409) 772-5102
sansari@utmb.edu
Route: 0645
514-B Basic Science Building

Publications (PubMed)

G.A. Shakeel Ansari , Ph.D.

GraphicMy research focuses on the elucidation of biochemical mechanisms of toxicity of halogenated hydrocarbons, amines, unsaturated hydrocarbons and aldehydes, and development of biological markers of chemical exposure.

We have shown that xenobiotics can covalently modify fatty acids. Those xenobiotics which are metabolized through free radicals, bind to the unsaturated part of fatty acids while xenobiotics which contain hydroxyl on amino groups conjugate at the carboxylic end of the fatty acids. These fatty acid conjugates cause selective organ toxicity which may be different form the parent compounds. The mechanisms of their formation, as well as of toxicity, is virtually unknown. We have shown that the formation of fatty acid conjugates is an enzymatic process. The most active organs for the synthesis are liver and pancreas where the enzymes are localized in the endoplamic reticulum. We have purified and characterized enzymes responsible of the synthesis fatty acid conjugates from the liver and pancreatic enzyme is being characterized.

The second major emphasis in my laboratory is to develop biological markers of chemical exposure which could provide more reliable exposure data than obtained by environmental monitoring. Over the years, we have shown that proteins and enzymes such as hemoglobin, albumin and 1-antiproteinase inhibitors, glutathione S- transferase as well as small excretory molecules such as mercapturic acids, can be used as a biological marker of chemical exposure. After thorough characterization of chemically modified proteins, we are currently directing our efforts to develop enzyme-linked immunosorbent assays to measure chemical exposure.

Other projects at the beginning stages in our laboratory are: initiation and/or acceleration of autoimmune diseases by environmental chemicals; oxidative stress and environmental chemicals.