Peroxidative stress during rat splenocyte proliferation may result in damage to mitochondria

C. Pieri, M. Marra, F. Moroni, F. Marcheselli, R. Recchioni, C. Benatti

Research output: Contribution to journalArticle

Abstract

We have investigated the time-dependent changes of mitochondria! membrane potential and mass on splenocytes from young, adult and old normally fed animals as well as on adult rats fed a vitamin E deficient diet. Rhodamine-123 (Rh-123) and Nonyl Acridine Orange (NAO) were used as specific vital probes to monitor the membrane potential and mass of mitochondria, respectively, by means of flow cytometry Rh-123 uptake was high in an increasing number of cells from young and adult normally fed animals during the three-day culture period On the contrary, splenocytes from old and vitamin E deficient animals showed a biphasic pattern. The number of cells showing a high uptake of Rh-123 increased after 24 hrs. from mitogenic stimulation, then it decreased at the two other time points considered In parallel, a continuous increase of the number of cells with depolarised organelles (more than 50% by 72 hrs) has been observed in cell from both old and vitamin E deficient animals These age- and diet-dependent alterations were fully prevented adding reduced glutathione into the culture medium. These data support that the increase of respiration elicited by mitogenic stimulation results in free radical production which damages the mitochondria if the antioxidant defence system of the cell is not efficient, like during aging and in vitamin E deficiency.

Original languageEnglish
JournalBiochemical Society Transactions
Volume24
Issue number4
Publication statusPublished - 1996

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Mitochondria
Rhodamine 123
Vitamin E
Rats
Animals
Cell Count
Nutrition
Membrane Potentials
Young Adult
Vitamin E Deficiency
Diet
Membranes
Acridine Orange
Flow cytometry
Organelles
Free Radicals
Glutathione
Culture Media
Flow Cytometry
Respiration

ASJC Scopus subject areas

  • Biochemistry

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Peroxidative stress during rat splenocyte proliferation may result in damage to mitochondria. / Pieri, C.; Marra, M.; Moroni, F.; Marcheselli, F.; Recchioni, R.; Benatti, C.

In: Biochemical Society Transactions, Vol. 24, No. 4, 1996.

Research output: Contribution to journalArticle

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