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Photodynamic stimulation causes sustained increase in intracellular calcium concentration in cells of small cell lung carcinoma

Authors
Publisher
The Graduate School of Veterinary Medicine
Publication Date
Keywords
  • [Ca^<2+>]_I
  • Cell Injury
  • Chloro-Aluminum Phthalocyanine Sulphonate (Alpcs_4)
  • Methacholine
  • 649
Disciplines
  • Biology
  • Physics

Abstract

Photodynamic agents, due to their selective uptake by tumor cells and photon-dependent selective activation, have immense implications for cancer treatment. The present study provided direct evidence that the photon activation of chloro-aluminum phthalocyanine sulphonate (AlPcS_4) in the presence of extracellular Ca^<2+> caused a rapid increase followed by a sustained increase in intracellular concentration of calcium ion ([Ca^<2+>]_i) in a small cell lung carcinoma (SCLC) cell line, SBC-3. The [Ca^<2+>]_i increase by photodynamic stimulation was completely inhibited by the removal of extracellular Ca^<2+> and reintroduction of extracellular Ca^<2+> immediately led to a rapid elevation of [Ca^<2+>]_i. However, the increase was not inhibited by application of Ni^<2+>, nifedipine, or SK&F 96365,a receptor-mediated and voltage-dependent Ca^<2+> entry blocker. The photosensitizer AlPcS_4 alone or light alone (4 min) had no effect on [Ca^<2+>]_i. Cytotoxicity examination by trypan blue exclusion test, however, suggested photodynamic stimulation-induced cell injury which was observed in both the presence and the absence of extracellular Ca^<2+>. These results indicate that [Ca^<2+>]_i increase may not be mandatory for photodynamic stimulation-induced cell injury. Whether [Ca^<2+>]_i increase can accelerate, at least in part, cell death under the physiological condition, whether the mechanism(s) of cell death can be different in the presence and the absence of extracellular Ca^<2+>, and whether [Ca^<2+>]_i increase can be totally unrelated to cell death await further work.

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