Abstract
The influence of some guanidine derivatives on the level of brain citrate, brain activities of aconitase and citrate synthase has been investigated in rats subjected to ischemia-reperfusion. Administration of N-[imino(1-piperidinyl)methyl]guanidine and N-[imino(4-morpholinyl)methyl]guanidine resulted in changes of specific activities of aconitase and citrate synthase towards control values. Under these conditions the citrate level considerably decreased versus rats with untreated ishemia-reperfusion. Treatment with these compounds also decreased the degree of DNA fragmentation markedly increased in rats with ischemia-reperfusion.
MeSH terms
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Aconitate Hydratase / metabolism*
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Animals
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Antioxidants / pharmacology*
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Brain / blood supply
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Brain / drug effects*
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Brain / metabolism
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Brain Ischemia / metabolism*
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Citrate (si)-Synthase / metabolism*
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Citric Acid / analysis
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Citric Acid / blood
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Citric Acid / metabolism
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DNA Fragmentation / drug effects
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Dose-Response Relationship, Drug
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Free Radicals / metabolism
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Male
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Methylguanidine / analogs & derivatives*
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Methylguanidine / pharmacology
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Morpholines / pharmacology*
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Neuroprotective Agents / metabolism
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Neuroprotective Agents / pharmacology
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Oxidation-Reduction / drug effects
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Oxidative Stress / drug effects
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Piperidines / pharmacology*
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Rats
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Reperfusion Injury / metabolism*
Substances
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Antioxidants
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Free Radicals
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Morpholines
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N-(imino(1-piperidinyl)methyl)guanidine
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N-(imino(4-morpholyl)methyl)guanidine
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Neuroprotective Agents
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Piperidines
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Citric Acid
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Methylguanidine
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Citrate (si)-Synthase
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Aconitate Hydratase