Abstract
Vitamin E (α-tocopherol) is a known biological anti-oxidant able to quench the lipid peroxidation chain and to protect the cellular structures (e.g., plasma membranes) from the attack of free radicals which are reported to play a primary role in aging. To assess whether the absence of α- tocopherol from the diet of young laboratory animals may be considered a reliable model of precocious brain aging, intracellular ionic content of brain cortex pyramidal cells, ultrastructural features of synaptic contact zones, synaptic mitochondria and perykarial mitochondria positive to the succinic dehydrogenase (SDH) histochemical reaction with copper ferrocyanida have been investigated by X-ray microanalysis and computer-assisted morphometry in young, adult, old and 11-month-old vitamin E deficient rats. Our data document significant alterations of intracellular ionic content, synaptic contact areas and synaptic and perykarial mitochondria in aging. Vitamin E deficiency caused similar alterations in adult animals. Taking into account the known role of α-tocopherol in protecting the cellular membrane structure, we support that the common process underlying the changes found in aging and vitamin E deficiency is an excessive deterioration of the neuronal membrane.
Original language | English |
---|---|
Pages (from-to) | 289-302 |
Number of pages | 14 |
Journal | Scanning Microscopy |
Volume | 9 |
Issue number | 1 |
Publication status | Published - 1995 |
Keywords
- aging of synaptic membranes
- brain aging
- free radicals and aging
- mitochondrial aging
- morphometry
- perykarial mitochondria
- succinic dehydrogenase activity
- synaptic mitochondria
- vitamin E deficiency
- X-ray microanalysis
ASJC Scopus subject areas
- Instrumentation