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Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay
05:53

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

Age-related alterations in Ca2+ signals and mitochondrial membrane potential in exocrine cells are prevented by

Cristina Camello-Almaraz1, Pedro J Gomez-Pinilla, Maria J Pozo

  • 1Department of Physiology, Faculty of Veterinary Science, Nursing School and RETICEF, University of Extremadura, Caceres, Spain.

Journal of Pineal Research
|March 6, 2008
PubMed

Insights

Melatonin supplementation improved calcium (Ca2+) signaling and mitochondrial function in aged pancreatic cells, restoring normal secretory responses. This suggests melatonin can counteract age-related cellular dysfunction in exocrine cells.

Area of Science:

  • Cellular Biology
  • Gerontology
  • Endocrinology

Background:

  • Age-related decline in calcium (Ca2+) signaling and mitochondrial potential affects nonexcitable cells.
  • Limited understanding of melatonin's role in mitigating aging effects on Ca2+ homeostasis and mitochondrial function.

Purpose of the Study:

  • To investigate melatonin's efficacy in preventing age-associated alterations in intracellular Ca2+ homeostasis and mitochondrial potential in pancreatic exocrine cells.
  • To assess the impact of aging and melatonin treatment on pancreatic acinar cell secretory function.

Main Methods:

  • Pancreatic acinar cells isolated from adult and aged mice.
  • Measurement of Ca2+ signals, in situ mitochondrial potential, and in vitro amylase secretion.
  • Assessment of calcium pools and capacitative calcium entry using ionomycin and thapsigargin.

Main Results:

  • Aged pancreatic acini exhibited impaired secretion, reduced Ca2+ signal amplitude and oscillation patterns, diminished calcium pools, and reduced capacitative calcium entry.
  • Aging was associated with mitochondrial depolarization in pancreatic acinar cells.
  • Melatonin treatment in aged mice restored secretory function, normalized Ca2+ signaling dynamics, replenished calcium pools, enhanced capacitative calcium entry, and improved mitochondrial potential.

Conclusions:

  • Aging significantly disrupts Ca2+ homeostasis and mitochondrial function in pancreatic exocrine cells, leading to impaired secretory capacity.
  • Melatonin effectively reverses age-induced deficits in Ca2+ signaling, mitochondrial potential, and secretory function in pancreatic acinar cells.
  • Melatonin shows potential as a therapeutic agent to combat age-related cellular dysfunction in exocrine tissues.

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