Enhanced Responsiveness to Photodynamic Therapy-Induced Apoptosis after Mitochondrial DNA Depletion
Corresponding Author
David Kessel
Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, Ml, USA
*Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. Fax: 313–577–6739; e-mail:[email protected]Search for more papers by this authorHai Hao Sun
Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, Ml, USA
Search for more papers by this authorCorresponding Author
David Kessel
Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, Ml, USA
*Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. Fax: 313–577–6739; e-mail:[email protected]Search for more papers by this authorHai Hao Sun
Departments of Pharmacology and Medicine, Wayne State University School of Medicine, Detroit, Ml, USA
Search for more papers by this authorAbstract
Several lines of evidence indicate that mitochondria are an especially sensitive target for photodamage. Reports of cross resistance between photodynamic therapy (PDT) and the drug cisplatin, along with evidence that depletion of mitochondrial DNA (mtDNA) sensitized cells to cisplatin suggested a study of the photodynamic responsiveness of murine leukemia control L1210 cells versus cells depleted of mtDNA. Loss of mtDNA led to an increased sensitivity to mitochondrial photodamage, while the cytotoxic effects of lysosomal photodamage were not affected. Cells depleted of mtDNA showed an enhanced ap-optotic response to PDT involving a mitochondrial target, compared with control cells.
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