Previous studies have shown that Rhodamine 123 (Rh123) is an efficient
tumor targeting agent for argon laser photodynamic therapy in vitro.
Effective ness of this approach for cancer treatment in vivo will depe
nd on Rh123 tumor uptake kinetics and laser energy delivery via fibero
ptics to the tumor site. In the present study, tumor and normal cells
were exposed in vitro to 1 mu g/mL Rh123 until 10%, 50%, and 100% of m
aximum uptake was achieved. Laser treatment response was monitored by
trypan blue exclusion for tumor cell viability and by MTT tetrazolium
assays to measure mitochondrial dehydrogenase activity. TE671 fibrosar
coma cells were highly sensitive to argon laser phototherapy (514 nm,
5 W, 1 minute, Tmax = 8 degrees C), with mitochondrial inhibition seen
after Rh123 uptake of 12, 50, and 100 ng/million cells. P3 squamous c
ell carcinoma cells were inhibited 20% and 75% by the laser after Rh12
3 uptake of 13 or 30 ng/million cells, respectively. M26 melanoma cell
s were not sensitive to the laser after 15 ng/million cells Rh123 upta
ke but were inhibited 45% and 75% after Rh123 uptake of 80 and 160 ng/
million cells. Micro2 fibroblast mitochondrial activity was reduced le
ss than 25% by the laser after Rh123 uptake of 50 ng/million cells. Ce
ll viability after maximum Rh123 uptake and laser treatment was decrea
sed to 30%, 15%, and 2% for M26 melanoma, P3 squamous cell carcinoma,
and TE671 fibrosarcoma cells, but remained over 80% for Micro2 fibrobl
asts. The results suggest that Rh123 laser treatment response depends
on tumor type and drug uptake level, with normal cells being much less
sensitive to phototherapy.