Significant decrease in the level of lipid antioxidants (measured from the kinetics of the induced chemiluminescence in brain homogenate) and of the hydrophilic antioxidant carnosine as well was observed in the brain of 14-16-month-old mice of SAMP1 line, which is characterized by accelerated accumulation of senile features, in comparison with the control line SAMR1. In the brain of SAMP1 animals the activity of cytosolic Cu/Zn-containing superoxide dismutase (SOD) was reduced, while the activity of membrane-bound Mn-SOD was at an extremely low level. The activity of glutathione-dependent enzymes (glutathione peroxidase, glutathione reductase, and glutathione transferase) did not differ in the brain of SAMP1 and SAMR1 animals, and catalase activity was similarly low in both cases. At the same time, excess concentration of excitotoxic compounds, significantly exceeding that for the control line, was determined in the brain and blood of SAMP1 animals. The activity of glutathione enzymes in liver and heart as well as the activity of cytosolic Cu/Zn-SOD in liver did not differ in the two studied lines, while the activity of erythrocyte glutathione peroxidase was slightly increased, and the activity of liver catalase and erythrocyte Cu/Zn-SOD was significantly decreased for SAMP1 compared with SAMR1. The results demonstrate that the accelerated ageing of SAMP1 animals is connected to a significant extent with the decreased efficiency of the systems utilizing reactive oxygen species (ROS) in tissues.
Natural hydrophilic antioxidant carnosine protects cerebral cytosolic Cu,Zn-superoxide dismutase (SOD) under conditions of oxidative stress in various in vivo models: short-term hypobaric hypoxia in rats and accumulation of age-related changes in senescence-accelerated mice (SAMP). Administration of carnosine preventing Cu,Zn-SOD inactivation reduced mortality in rats and prolonged average life span in SAMP-mice.
Editor's Note: The SAM (senescence accelerated mouse) model has been used in various aspects of aging research and JAAM has published work on this area previously (see HosoL·wa et al., l:l;[27][28][29][30][31][32][33][34][35][36][37]. The current study attempts to clarify some of the changes which occur in aging cells with the brain and liver of such a model. The particular approach here is to understand how enzymes which affect free radical metabolism alter over the lifespan of the aging animal. ABSTRACTThe comparative neurochemical characteristics of brain and liver membranes of senescenceaccelerated mice, prone (SAMPl) and senescence-accelerated mice, resistant (SAMR1) strains were evaluated using males and females of several ages. Abnormal N-methyl-D-aspartic acid (NMDA) binding and monoamine oxidase b activity in SAMP brain membranes may pro¬ mote increased accumulation of reactive oxygen species (ROS) in neurons. Na/K-adinosine triphosphatase (ATPase) and liver cytochrome P450 activities are greater in SAMPl neurons than in SAMR1 neurons, which may reflect an adaptive tissue response to ROS accumula¬ tion.Age changes in animal tissues are highly lar ROS generation remain obscure. Nonethecorrelated with an increased generation of less, we suggest that senescence-dependent reactive oxygen species (ROS).1'2 Senescence-ac-metabolic defects are induced by noncompencelerated mice (SAM), selected from the sis-sated intracellular ROS generation.2'4 We can¬ ter-brother mating of AKR/J strain mice,3 are not exclude such defects resulting from seccharacterized by ROS-induced accelerated ondary features of aging (i.e., resulting from senescence at earlier steps of normal develop-tissue adaptation.7 To elucidate the metabolic ment.4 These animals have aging changes in reactions providing the intracellular source of their tissues by 4 to 6 weeks after birth that are ROS and the primary targets for oxidative modaccompanied by increased ROS levels.5 This ification during aging, we studied the activity may be the major reason for accelerated senes-of specific brain and liver membrane systems in cence,5'6 although the precise sources of cellu-SAM animals at different developmental stages.
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