[The influense of guanidine derivatives on free radical oxidation intensity and aconitase activity at development of brain ischemia-reperfusion at rats].
The study of some guanidine derivatives influence on free radical oxidation intensity and aconitase activity during the development of brain ischemia-reperfusion at rats has been carried out. The biochemiluminescence parameters increasing at the brain pathology changed toward normal values under the influence of N-[4-(chlorbenzoyl)benztiazol-2-yl]guanidine, N-[imino(1-piperidinyl)methyl]guanidine and N-[imino(4-morpholinyl)methyl]guanidine. The aconitase specific activity decreased in brain and blood of animals with ischemia-reperfusion. Administration of guanidine derivatives during brain ischemia-reperfusion development increased aconitase specific activity. These results suggest that investigated substances can play a role of neuroprotectors, preventing free radical oxidation development.
Makeeva
A V
AV
Popova
T N
TN
Slivkin
A I
AI
Kryl'skiĭ
D V
DV
D000154:Aconitate Hydratase / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D005609:Free Radicals / Q000378:metabolism*; D019791:Guanidine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010084:Oxidation-Reduction / Q000187:drug effects; D051381:Rats; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism*
D005609:Free Radicals; D018696:Neuroprotective Agents; D000154:Aconitate Hydratase; D019791:Guanidine