Dear Editor,
In a recent study, Hjelde and co-workers investigated thepossible effects of oxygen tension on photodynamic toxicity in a panel of established cell lines [1].The authors established that high levels of hyperoxia did not impact on the extent of toxicity of photodynamictherapy, relative to that determined under normoxic conditions, and that this contrasted with other experimentaland clinical studies [2-4]. They attributed the lack of hyperoxic effect on phototoxicity to either theabsence of a hypoxic component in their cell cultures or the availability of sufficient oxygen to compensatefor oxygen depletion during the photochemical reaction. It is clear that the main reason for the significantoxygen effect observed in the other studies is that illumination and oxygenation occurred simultaneously[2-4]. To test any possible interaction between agents, it is mandatory for the agents to co-exist. Atleast, the damaging process of the inducing agent (the illumination) should be in progress during theapplication of the modifier (hyperoxia). Therefore, to harness an oxygen effect the hyperoxic conditionhas to be prevalent to 'fix' the damage during the induction of the extremely short-lived free radicals[5]. This crucial requirement could not be achieved by these investigators given the experimental constraintof illuminating prior to hyperoxic treatment. The time window between these steps was not commented on.This is a very important detail since phototoxicity depends concurrently on the oxygen tension and photosensitiserconcentration, and the photochemical reaction is expected to cease immediately after the illumination.It is worth noting that the lifetime of a typical triplet state photosensitiser which is the longestand main determinant of the reaction rate is of the order of 0.5 milliseconds [6]. It is therefore notsurprising that hyperoxic treatment following illumination did not affect phototoxicity in the currentinvestigation. Also, it is not evident from these data that high oxygen tension interfered with the damagerepair mechanisms of the cell lines used. The current conclusions may change significantly if the experimentaldesign is modified to enable illumination of the cell cultures under hyperoxia.
Sincerely,
John M. Akudugu,Radiation Biophysics, iThemba LABS, P. O. Box 722, Somerset West 7129, South Africa, e-mail: [email protected]
References:
1.Hjelde A, Gederaas OA, Krokan HE, Brubakk AO: Lack of effect of hyperoxia on photodynamictherapy and lipid peroxidation in three different cancer cell lines. Med Sci Monit, 2005; 11(10): BR351-BR356
2.Maier A, Anegg U, Fell B et al: Hyperbaric oxygen and photodynamic therapy in treatment of advancedcarcinoma of the cardia and the esophagus. Lasers Surg Med, 2000; 26: 308-15
3.Maier A, Tomaselli F,Anegg U et al: Combined photodynamic therapy and hyperbaric oxygenation in carcinoma of the esophagusand the esophago-gastric junction. Eur J Cardiothorac Surg, 2000; 18: 649-54 4.Chen Q, Huang Z, ChenH et al: Improvement of tumor response by manipulation of tumor oxygenation during photodynamic therapy.Photochem Photobiol, 2002; 76: 197-203
5.Hall EJ: Radiobiology for the radiologist. 3(rd) ed. Philadephia:JB Lippincott Company, 1988
6.Leeds University Centre for Photobiology and Photodynamic Therapy. Thescience of PDT. Available from: URL:http//www.bmb.leeds.ac.uk/pdt/science.htm Received: 2005.10.25.

Keywords: Aerobiosis, Lipid Peroxidation - drug effects, Neoplasms - drug therapy, Oxygen - therapeutic use, Photochemotherapy