Redox Biology Program

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Albert Girotti, PhD

Phone:  414-955-8432
Fax:      414-955-6510
Email:   agirotti@mcw.edu

 

Girotti Laboratory

Albert Girotti, PhD, has had a longstanding interest in the pathologic, as well as therapeutic effects of oxidative stress, including photodynamic stress used in anticancer photodynamic therapy (PDT). For quite some time, the special focus of his work has been on the generation, translocation, signaling action, and detoxification of lipid oxidation products, particularly lipid hydroperoxides (LOOHs).

His group, which includes visiting academic collaborators, postdoctoral fellows, and graduate students, has contributed steadily in these areas during the past 30 years with National Institutes of Health (National Cancer Institute) support.

In PDT-related aspects, he has studied various sensitizing agents (phthalocyanines, merocyanines, and tetrapyrroles, including ALA-generated PpIX) and oxidizable targets ranging from plasma membrane-mimetic liposomes to cultured tumor cells.

He served as program principal investigator on an National Cancer Institute P01 grant: Mechanisms of Merocyanine-Mediated Phototherapy from 1989 to 1996.

Much of his recent work has focused on biochemical factors that influence PDT effectiveness, e.g., effects of LOOH-detoxifying selenoperoxidases, and pro-oxidant vs. antioxidant effects of iron vs. nitric oxide (NO). Elucidation of cytoprotective signaling mechanisms that underlie photostress-induced upregulation of inducible nitric oxide synthase (iNOS) in tumor cells, a phenomenon recently discovered in his laboratory, is a major goal of his current research.

 

   
  Aerobic cells may experience oxidative stress damage if their enzymatic and nonenzymatic antioxidant defenses are overwhelmed by reactive oxygen species (ROS) generated by various endogenous and exogenous challenges.  Unsaturated lipids in cell membranes and lipoproteins are prominent targets of ROS attack, undergoing peroxidative degradation with numerous structurally and functionally disruptive effects. Above:  Examples of free radical and nonradical ROS.  

 

 

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