[Comparative-physiological study of leukocyte participation in initiation of lipid peroxidation during nitrite intoxication in rats and muskrats].
The study is carried out on Wistar white rats non-adapted to oxygen deficit and on semiaquatic rodents muskrats adapted to periodic arrest of respiration during diving under conditions of Nembutal narcosis. It has been revealed that 1 h after a subcutaneous injection of sodium nitrite (3 mg/100 g body mass), intensification of lipid peroxidation (LPO) in the muskrat brain is absent, the activity of the antioxidant enzyme catalase increasing 16 times (p < 0/01) as compared with control injected with equivalent saline volume. In heart and liver, a statistically significant decrease of the content of LPO products active in the test with 2-thionarbituric acid; in the femoral muscle tissue, the LPO intensity does not change. In rats, unlike muskrats, after injection of sodium nitrite, an increase of LPO is recorded in brain, while a decrease of the LPO product content in the femoral muscle; in liver the LPO intensity did not change. In muskrats, the sodium nitrite administration leads to a decrease of the leukocyte spontaneous mobility, of lymphocyte cytokine-producing activity, and ofneutrophil bactericidal activity (by the content of cationic proteins in neutrophilic phagocytes), whereas in rats the leukocyte mobility does not change, only the blood neutrophil bactericidal activity decreases. The ability of neutrophils to produce the superoxide anion during the nitrite intoxication does not change both in rats and in muskrats. The obtained data allow concluding that under conditions of Nembutal narcosis the leukocyte functional activity on the background of nitrite intoxication is suppressed to the greater degree in the muskrats genotypically adapted to oxygen deficit than in immunocompetent cell of the rodents not adapted to hypoxia.
Tsoĭ
E M
EM
Kovalenko
R I
RI
Kuz'min
D A
DA