Abstract
There are multiple determinants of PDT efficacy. An in vitro study showed that the head and neck tumor lines derived from patients with an HPV infection showed a substantial decrease in the degree of photokilling by PDT directed at ER/mitochondria. We previously reported that this was not correlated with altered photosensitizer uptake, sites of sub-cellular concentration, or rate of ROS formation. PDT targeted to the ER can lead to the initiation of parapotis, a death pathway associated with ER stress. This pathway appears to be operational even cell lines with an impaired apoptotic pathway and can lead to an apoptotic response. Impaired PDT-induced photokilling in HPV(+)line was associated with a decrease of both the paraptotic response to ER photodamage and the loss of mitochondrial membrane potential (ΔΨ<sub>m</sub>) after mitochondrial photodamage. This may explain, in part, the impaired response to PDT when BPD (benzoporphyrin derivative, Vidsudyne) was the photosensitizing agent.
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