[Peroxidative vulnerability of synaptosomal high affinity Ca++-ATPase and pharmacologic effects].
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| Abstract |
The high affinity Ca++-ATPase participates essentially in the regulation of intrasynaptosomal calcium homeostasis. Related to posthypoxically restricted transmitter release, we examined the influence of newly-generated free radicals (ascorbic acid-ferric salt mixture) or sodium dodecyl sulfate in vitro and of a mild hypobaric hypoxia in vivo on the activity of synaptosomal high affinity Ca++-ATPase. Moreover we tested the effectiveness of piracetam, meclofenoxate hydrochloride, pyritinol and verapamil on the changed enzyme activity subsequent to a hypoxic exposure. The activity of synaptosomal high affinity Ca++-ATPase (1.04 +/- 0.03 mumol Pi/mg.h) is reduced by not more than 40% depending on the concentration of the ascorbic acid-ferric salt mixture used but is nearly totally inhibited by sodium dodecyl sulfate (0.2 mg/ml). Hypobaric hypoxia (18 h, 8.7 kPa) decreases the enzyme activity to 0.79 +/- 0.03 mumol Pi/mg.h. Piracetam, meclofenoxate hydrochloride and pyritinol are protectively effective on the decrease of enzyme activity induced by hypoxia. The results emphasize the importance of intact protein-phospholipid interactions for the enzyme activity and support relations between synaptosomal high affinity Ca++-ATPase and transmitter release.
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| Authors | M Blaschke, H D Fischer, J Schmidt |
| Journal | Biomedica biochimica acta (Biomed Biochim Acta) Vol. 47 Issue 9 Pg. 887-93 ( 1988) ISSN: 0232-766X [Print] Germany |
| Vernacular Title | Zur peroxidativen Schädigung der synaptosomalen hochaffinen Ca++-ATPase und ihrer pharmakologischen Beeinflussbarkeit. |
| PMID | 2977726 (Publication Type: Journal Article) |
| Chemical References |
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