Melatonin is able to delay endoplasmic reticulum stress-induced apoptosis in leukocytes from elderly humans

Javier Espino, Ignacio Bejarano, Sergio D. Paredes, Carmen Barriga, Russel J. Reiter, José A. Pariente, Ana B. Rodríguez

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

The mechanisms regulating neutrophil apoptosis are basically unaffected by the aging process. However, a significant impairment of cell survival occurs in elderly individuals following neutrophil challenge with pro-inflammatory stimuli, such as granulocyte-macrophage colony-stimulating factor (GM-CSF). The goal of the present study was to prove the effects of melatonin supplementation on apoptosis induced by calcium signaling in human leukocytes from elderly volunteers. Treatments with the specific inhibitor of cytosolic calcium re-uptake, thapsigargin, and/or the calcium mobilizing agonist, N-formyl-methionyl-leucyl-phenylalanine (fMLP), induced mitochondrial membrane depolarization, caspase activation, phosphatidylserine (PS) externalization, and DNA fragmentation in leukocytes from both young and elderly volunteers, although such effects were much more evident in aged leukocytes. Importantly, melatonin treatment substantially preserved mitochondrial membrane potential, reversed caspase activation, reduced PS exposure and forestalled DNA fragmentation in leukocytes from both age groups. In conclusion, melatonin is able to delay endoplasmic reticulum stress-induced apoptosis in aged leukocytes and may counteract, at the cellular level, age-related degenerative phenomena linked to oxidative stress.

Original languageEnglish (US)
Pages (from-to)497-507
Number of pages11
JournalAGE
Volume33
Issue number4
DOIs
StatePublished - Dec 1 2011

Keywords

  • Aging
  • Apoptosis
  • Leukocytes
  • Melatonin

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

Fingerprint Dive into the research topics of 'Melatonin is able to delay endoplasmic reticulum stress-induced apoptosis in leukocytes from elderly humans'. Together they form a unique fingerprint.

Cite this