Radical initiated alpha-tocopherol depletion and lipid peroxidation in mitochondrial membranes.

The relationships between antioxidant status, lipid peroxidation and membrane protein integrity have been studied in an isolated mitochondrial membrane system. Tocopherol was shown to be present in both the outer and inner membrane of normal rat liver mitochondria; 77.3 and 22.3% of the total alpha-tocopherol was present in the outer and inner membranes, respectively. The endogenous alpha-tocopherol was depleted in a time-dependent manner by low levels of ferrous iron and by irradiation in the presence or absence of ferrous iron. This antioxidant depletion was followed by the appearance of lipid hydroperoxides. Fragmentation of monoamine oxidase, an integral outer membrane protein, was observed at irradiation doses that caused by antioxidant depletion and peroxide generation.

Mycosporine glycine protects biological systems against photodynamic damage by quenching singlet oxygen with a high efficiency.

This report concerns physiological function of mycosporine-like amino acids (MAA) as an active defense against the photooxidative effects of sunlight in marine organisms. Mycosporine glycine (MG) is a representative member of MAA family and was found to effectively suppress various detrimental effects of the Type-II photosensitization in biological systems, such as inactivation of mitochondrial electron transport, lipid peroxidation of microsomes, hemolysis of erythrocytes and growth inhibition of Escherichia coli. The presence of MG in solutions of eosin Y or methylene blue resulted in a marked decrease in the level of singlet oxygen (1O2) produced by the sensitizers under illumination. The rate constant of 1O2 quenching by MG was determined to be 5.6 x 10(7) M(-1) s(-1) by the time-resolved 1O2 luminescence decay method, which is higher than, or at least comparable to, the values for 1O2 reaction of well-known quenchers such as 1,4-diazabicyclo[2,2,2]octane and furfuryl alcohol. The results suggest that MG probably together with some other active MAA may play an important role in protecting marine organisms against sunlight damage by eliminating 1O2 generated from certain endogenous photosensitizers.

[Changes in the mitochondrial ATPase activity of liver cells after X-ray irradiation]. / Izmenenie aktivnosti mitokhondrial'noi ATFazy kletok pecheni posle rentgenovskogo oblucheniia.

24 h following total-body X-irradiation of rats with a dose of 7 Gy the growth of the ATPase activity diminished, with the addition of bicarbonate, by 2 times in the preparations of mitochondria and submitochondrial particles, and by 1.5 times, in preparations of a soluble enzyme. No changes were noted in the electrophoretic motility of soluble ATPase.

[Radiation modification of the ATPase properties of submitochondrial particles]. / Modifikstsiia radiatsiei svoistv ATFazy submitokhondrial'nykh chastits.

The appreciable changes in hydrophobic properties of ATPase of rat liver submitochondrial particles were discovered 3 days after whole-body X-irradiation with a dose of 7 Gy. The sensitivity of ATPase activity to stimulating anions decreased. The radiation damages to ATPase were detected and the ratio of concentrations of magnesium and ATP exceeded a unity.

Functional and molecular changes in FoF1 ATP-synthase of cardiac muscle during aging.

We have studied the functional and molecular changes of mitochondrial FoF1 ATP synthase of cardiac muscle during aging. ATP hydrolase activity was lower in sonic submitochondrial particles prepared from hearts of senescent rats (24 months) than in those prepared from hearts of adult rats (12 months). Oligomycin-sensitive proton conduction of cardiac submitochondrial particles was greater in senescent rats than in adult rats. The beta subunit of F1, detected immunologically in submitochondrial particles, was less in senescent rats than in adult rats. Exposure of cardiac submitochondrial particles from adult rats to free radicals, generated by 60Co, resulted in inactivation of ATP hydrolase activity and a decreased content of F1. The structural and functional alterations of mitochondrial FoF1 ATP synthase during aging may be expected to affect energy metabolism, and our results suggest that they could originate from the action of free radicals generated in the inner mitochondrial membrane.