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Inhibition of Proliferation of Human Fibroblast by δ-Aminolevulinic Acid (ALA) Derivatives through the Induction of Mitochondria Membrane Depolarization
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  • Journal title : KSBB Journal
  • Volume 30, Issue 6,  2015, pp.313-318
  • Publisher : Korean Society for Biotechnology and Bioengineering
  • DOI : 10.7841/ksbbj.2015.30.6.313
 Title & Authors
Inhibition of Proliferation of Human Fibroblast by δ-Aminolevulinic Acid (ALA) Derivatives through the Induction of Mitochondria Membrane Depolarization
Jun, Yong-woo; Han, Du-Gyeong; Lee, Jin-A; Jo, Su-Yeon; Jang, Deok-Jin;
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-Aminolevulinic acid (ALA) is an endogenous metabolite formed in the mitochondria from succinyl-CoA and glycine, and plays a key role in the living body as an intermediate of the compound in the porphyrin biosynthesis pathway. ALA has been commonly used in photodynamic therapy for several years, because ALA is of interest as a biodegradable mediator, a growth regulator, and an effective agent used in dermatology. Here, we determined which ALA derivatives were the most effective for the inhibition of the cell proliferation and growth of human fibroblast. As a result, we found that the treatment of ALA derivatives including ALA, ALAP (ALA phosphate salt), MAL (Methyl 5-aminolevulinate hydrochloride salt), PBGL (phophobilinogen lactam) and PBGH (phophobilinogen-HCl) could attenuate cell proliferation of human fibroblast cells. Among them, PBGH was the most effective derivative. In addition, PBGH treatment could induce mitochondrial membrane depolarization, leading to cell death of human fibroblast. These results suggest that mitochondrial membrane depolarization induced by ALA and PBGH treatment might be responsible for inhibition of cell proliferation and death. Taken together, our results propose the possibility that PBGH can be used as one of the effective drugs in human skin disease, psoriasis.
-Aminolevulinic acid;cell proliferation;mitochondria membrane depolarization;ALA derivatives;human fibroblast;HeLa;
 Cited by
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