Sodium μ2-Dithiosulphate-Tetranitrosyl Diferrate Tetrahydrate Prevents Heat Shock-Induced Mitochondria Dysfunction

The possibility of using the NO sodium μ2-dithiosulfato-tetranitrosyldiferrate tetrahydrate (TNIC-thio) as a drug preventing mitochondrial dysfunction under stress was studied. The properties of TNIC-thio were studied on the mitochondria of 5-day-old etiolated pea seedlings. The functional state of mitochondria was determined under conditions of heat shock (HS) and treatment of seedlings with TNIC-thio. Heat shock activated lipid peroxidation and led to swelling of mitochondria and changes in the content of C18 fatty acids (FAs): the C18 FA unsaturation index in mitochondrial membranes decreased from 1.42 ± 0.01 to 1.22 ± 0.01. Changes also took place in the C20 FA content: the 20:3ω6 content decreased by almost 43.6%, and the 20:0 content decreased by 1.3 times. The change in the pool of unsaturated FAs affected the bioenergetic characteristics of mitochondria: an almost 1.5-fold drop in the rates of oxidation of NAD-dependent oxidation substrates was shown. Treatment of pea seeds with 10 –6 M TNIC-thio was accompanied by prevention of lipid peroxidation (LPO), prevention of changes in the composition of FA membranes and mitochondrial morphology, and restoration of the bioenergetic characteristics of these organelles. The drug could help maintain the functional state of mitochondria under stress by preventing LPO. It perhaps resulted in the preservation of the efficiency of energy processes in the cell, which probably increased the organism’s resistance to changing environmental conditions.