We have investigated the enzymatic reduction and accumulation of vitamin C in HaCaT epithelial cells. The subcellular localization and the activities of ascorbyl free radical reductase and dehydroascorbate reductase showed that mitochondrial, microsomal and plasma membranes fractions express high levels of ascorbyl free radical reductase activity, whereas dehydroascorbate reductase activity was found at low levels only in the post microsomal supernatant. We have also investigated cell proliferation and vitamin C accumulation induced by ascorbic acid 2-phosphate. This derivative caused no inhibition of cell growth, was uptaken from the extracellular medium and accumulated as ascorbic acid in mM concentrations. These results show that HaCaT cells possess very efficient systems to maintain high levels of both intracellular and extracellular ascorbic acid. The regeneration and uptake of ascorbic acid from extracellular medium contributes to the intracellular antioxidant capacity, as evaluated by 2',7'-dihydrodichlorofluorescein staining. Consequently, cells became more resistant to free radical generation and cell death induced by UV-B irradiation. (C) 1999 Elsevier Science Inc.

Savini, I., D'Angelo, I., Ranalli, M., Melino, G., Avigliano, L. (1999). Ascorbic acid maintenance in HaCaT cells prevents radical formation and apoptosis by UV-B. FREE RADICAL BIOLOGY & MEDICINE, 26(2009/10/09 00:00:00.000), 1172-1180 [10.1016/S0891-5849(98)00311-6].

Ascorbic acid maintenance in HaCaT cells prevents radical formation and apoptosis by UV-B

SAVINI, ISABELLA;MELINO, GENNARO;AVIGLIANO, LUCIANA
1999-01-01

Abstract

We have investigated the enzymatic reduction and accumulation of vitamin C in HaCaT epithelial cells. The subcellular localization and the activities of ascorbyl free radical reductase and dehydroascorbate reductase showed that mitochondrial, microsomal and plasma membranes fractions express high levels of ascorbyl free radical reductase activity, whereas dehydroascorbate reductase activity was found at low levels only in the post microsomal supernatant. We have also investigated cell proliferation and vitamin C accumulation induced by ascorbic acid 2-phosphate. This derivative caused no inhibition of cell growth, was uptaken from the extracellular medium and accumulated as ascorbic acid in mM concentrations. These results show that HaCaT cells possess very efficient systems to maintain high levels of both intracellular and extracellular ascorbic acid. The regeneration and uptake of ascorbic acid from extracellular medium contributes to the intracellular antioxidant capacity, as evaluated by 2',7'-dihydrodichlorofluorescein staining. Consequently, cells became more resistant to free radical generation and cell death induced by UV-B irradiation. (C) 1999 Elsevier Science Inc.
1999
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/49 - SCIENZE TECNICHE DIETETICHE APPLICATE
English
Con Impact Factor ISI
ascorbate oxidase; ascorbic acid; apoptosis; article; cell proliferation; cellular distribution; controlled study; enzyme activity; enzyme localization; human; human cell; priority journal; ultraviolet b radiation; Antioxidants; Apoptosis; Ascorbic Acid; Cell Division; Cell Line; Free Radicals; Humans; Keratinocytes; Kinetics; NADH, NADPH Oxidoreductases; Oxidoreductases; Subcellular Fractions; Ultraviolet Rays
Savini, I., D'Angelo, I., Ranalli, M., Melino, G., Avigliano, L. (1999). Ascorbic acid maintenance in HaCaT cells prevents radical formation and apoptosis by UV-B. FREE RADICAL BIOLOGY & MEDICINE, 26(2009/10/09 00:00:00.000), 1172-1180 [10.1016/S0891-5849(98)00311-6].
Savini, I; D'Angelo, I; Ranalli, M; Melino, G; Avigliano, L
Articolo su rivista
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/51165
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 59
  • ???jsp.display-item.citation.isi??? 56
social impact