Histatin-5 is a peptide secreted in the human saliva, which possesses powerful antifungal activity. Previous studies have shown that this peptide exerts its candidacidal activity, through the inhibition of both mitochondrial respiration and the formation of reactive oxygen species. The purpose of the present study was to investigate the biological consequences of histatin-5 action on mammalian mitochondria to verify if the toxic mechanism exerted on mitochondria from Candida albicans is an exclusive for fungal cells. Moreover, hypothesising that the damage exerted on mitochondria may induce programmed cellular death pathways, we evaluated two main markers of apoptosis: the mitochondrial membrane potential (DeltaPsi) and the release of cytochrome c. The results obtained show that exposure of isolated mammalian mitochondria to histatin-5 determines: (i) a large inhibition of the respiratory chain at the level of complex 1, (ii) a slight decrease in the mitochondrial membrane potential, and (iii) no release of cytochrome c. (C) 2003 Elsevier Inc. All rights reserved.

Petruzzelli, R., Clementi, M., Marini, S., Coletta, M., Di Stasio, E., Giardina, B., et al. (2003). Respiratory inhibition of isolated mammalian mitochondria by salivary antifungal peptide histatin-5. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 311(4), 1034-1040.

Respiratory inhibition of isolated mammalian mitochondria by salivary antifungal peptide histatin-5

MARINI, STEFANO;COLETTA, MASSIMILIANO;
2003-11-01

Abstract

Histatin-5 is a peptide secreted in the human saliva, which possesses powerful antifungal activity. Previous studies have shown that this peptide exerts its candidacidal activity, through the inhibition of both mitochondrial respiration and the formation of reactive oxygen species. The purpose of the present study was to investigate the biological consequences of histatin-5 action on mammalian mitochondria to verify if the toxic mechanism exerted on mitochondria from Candida albicans is an exclusive for fungal cells. Moreover, hypothesising that the damage exerted on mitochondria may induce programmed cellular death pathways, we evaluated two main markers of apoptosis: the mitochondrial membrane potential (DeltaPsi) and the release of cytochrome c. The results obtained show that exposure of isolated mammalian mitochondria to histatin-5 determines: (i) a large inhibition of the respiratory chain at the level of complex 1, (ii) a slight decrease in the mitochondrial membrane potential, and (iii) no release of cytochrome c. (C) 2003 Elsevier Inc. All rights reserved.
nov-2003
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10 - BIOCHIMICA
English
Con Impact Factor ISI
Apoptosis; Histatin-5; Mitochondria; Salivary peptides
Petruzzelli, R., Clementi, M., Marini, S., Coletta, M., Di Stasio, E., Giardina, B., et al. (2003). Respiratory inhibition of isolated mammalian mitochondria by salivary antifungal peptide histatin-5. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 311(4), 1034-1040.
Petruzzelli, R; Clementi, M; Marini, S; Coletta, M; Di Stasio, E; Giardina, B; Misiti, F
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/53106
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