Vitamin E deficiency impairs the modifications of mitochondrial membrane potential and mass in rat splenocytes stimulated to proliferate

Carlo Pieri, Fausto Moroni, Rina Recchioni

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10 Citations (Scopus)

Abstract

This study was designed to evaluate the time-dependent changes of mitochondrial membrane potential and mass during Con-A-induced proliferation of splenic lymphocytes from rat fed a normal or a vitamin E deficient diet. Rhodamine 123 and Nonyl Acridine Orange were used as specific probes to monitor the membrane potential and mass of mitochondria, respectively, by means of flow cytometry. The results demonstrate that the increase of Rh-123 and NAO uptake observed in cells from normally fed rats was prevented by vitamin E deficiency, at any time considered. After 72 h from Con A stimulation, 62% of cells from controls, as against 16% of cells from vitamin E deficient rats, showed hyperpolarized mitochondria. At the same time, in this last group, 60% of cells had depolarized organelles. The same pattern was observed considering the changes of mitochondrial mass, measured using NAO as a probe. These data support that mitogenic stimulation induced an increase of the respiratory activity of mitochondria with subsequent production of superoxide radicals. This resulted in depolarization and loss of mass of the organelles if the intracellular level of vitamin E is not adequate.

Original languageEnglish
Pages (from-to)661-665
Number of pages5
JournalFree Radical Biology and Medicine
Volume15
Issue number6
DOIs
Publication statusPublished - 1993

Fingerprint

Vitamin E Deficiency
Mitochondrial Membrane Potential
Vitamin E
Mitochondria
Rats
Membranes
Organelles
Rhodamine 123
Acridine Orange
Lymphocytes
Flow cytometry
Depolarization
Nutrition
Superoxides
Membrane Potentials
Flow Cytometry
Diet
10-N-nonylacridinium orange

Keywords

  • Free radicals
  • Lymphocyte proliferation
  • Membrane potential
  • Mitochondria
  • Mitochondrial mass
  • Vitamin E

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Medicine(all)
  • Toxicology

Cite this

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title = "Vitamin E deficiency impairs the modifications of mitochondrial membrane potential and mass in rat splenocytes stimulated to proliferate",
abstract = "This study was designed to evaluate the time-dependent changes of mitochondrial membrane potential and mass during Con-A-induced proliferation of splenic lymphocytes from rat fed a normal or a vitamin E deficient diet. Rhodamine 123 and Nonyl Acridine Orange were used as specific probes to monitor the membrane potential and mass of mitochondria, respectively, by means of flow cytometry. The results demonstrate that the increase of Rh-123 and NAO uptake observed in cells from normally fed rats was prevented by vitamin E deficiency, at any time considered. After 72 h from Con A stimulation, 62{\%} of cells from controls, as against 16{\%} of cells from vitamin E deficient rats, showed hyperpolarized mitochondria. At the same time, in this last group, 60{\%} of cells had depolarized organelles. The same pattern was observed considering the changes of mitochondrial mass, measured using NAO as a probe. These data support that mitogenic stimulation induced an increase of the respiratory activity of mitochondria with subsequent production of superoxide radicals. This resulted in depolarization and loss of mass of the organelles if the intracellular level of vitamin E is not adequate.",
keywords = "Free radicals, Lymphocyte proliferation, Membrane potential, Mitochondria, Mitochondrial mass, Vitamin E",
author = "Carlo Pieri and Fausto Moroni and Rina Recchioni",
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T1 - Vitamin E deficiency impairs the modifications of mitochondrial membrane potential and mass in rat splenocytes stimulated to proliferate

AU - Pieri, Carlo

AU - Moroni, Fausto

AU - Recchioni, Rina

PY - 1993

Y1 - 1993

N2 - This study was designed to evaluate the time-dependent changes of mitochondrial membrane potential and mass during Con-A-induced proliferation of splenic lymphocytes from rat fed a normal or a vitamin E deficient diet. Rhodamine 123 and Nonyl Acridine Orange were used as specific probes to monitor the membrane potential and mass of mitochondria, respectively, by means of flow cytometry. The results demonstrate that the increase of Rh-123 and NAO uptake observed in cells from normally fed rats was prevented by vitamin E deficiency, at any time considered. After 72 h from Con A stimulation, 62% of cells from controls, as against 16% of cells from vitamin E deficient rats, showed hyperpolarized mitochondria. At the same time, in this last group, 60% of cells had depolarized organelles. The same pattern was observed considering the changes of mitochondrial mass, measured using NAO as a probe. These data support that mitogenic stimulation induced an increase of the respiratory activity of mitochondria with subsequent production of superoxide radicals. This resulted in depolarization and loss of mass of the organelles if the intracellular level of vitamin E is not adequate.

AB - This study was designed to evaluate the time-dependent changes of mitochondrial membrane potential and mass during Con-A-induced proliferation of splenic lymphocytes from rat fed a normal or a vitamin E deficient diet. Rhodamine 123 and Nonyl Acridine Orange were used as specific probes to monitor the membrane potential and mass of mitochondria, respectively, by means of flow cytometry. The results demonstrate that the increase of Rh-123 and NAO uptake observed in cells from normally fed rats was prevented by vitamin E deficiency, at any time considered. After 72 h from Con A stimulation, 62% of cells from controls, as against 16% of cells from vitamin E deficient rats, showed hyperpolarized mitochondria. At the same time, in this last group, 60% of cells had depolarized organelles. The same pattern was observed considering the changes of mitochondrial mass, measured using NAO as a probe. These data support that mitogenic stimulation induced an increase of the respiratory activity of mitochondria with subsequent production of superoxide radicals. This resulted in depolarization and loss of mass of the organelles if the intracellular level of vitamin E is not adequate.

KW - Free radicals

KW - Lymphocyte proliferation

KW - Membrane potential

KW - Mitochondria

KW - Mitochondrial mass

KW - Vitamin E

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