The hypothesis that age-associated impairment of cognitive and motor functions is due to oxidative molecular damage was tested in the mouse. In a blind study, senescent mice (aged 22 months) were subjected to a battery of behavioral tests for motor and cognitive functions and subsequently assayed for oxidative molecular damage as assessed by protein carbonyl concentration in different regions of the brain. The degree of age-related impairment in each mouse was determined by comparison to a reference group of young mice (aged 4 months) tested concurrently on the behavioral battery. The age-related loss of ability to perform a spatial swim maze task was found to be positively correlated with oxidative molecular damage in the cerebral cortex, whereas age-related loss of motor coordination was correlated with oxidative molecular damage within the cerebellum. These results support the view that oxidative stress is a causal factor in brain senescence. Furthermore, the findings suggest that age-related declines of cognitive and motor performance progress independently, and involve oxidative molecular damage within different regions of the brain.Age-related impairments of cognitive and motor capacity have been linked to a number of deleterious morphologic and functional changes involving different parts of the brain that are normally associated with such functions (1-4). However, the nature of the causal factors responsible for these deleterious changes is poorly understood. Oxidative damage was considered as a likely cause of age-associated brain dysfunction because the brain is believed to be particularly vulnerable to oxidative stress due to a relatively high rate of oxygen free radical generation without commensurate levels of antioxidative defenses (5-8). Indeed, there is a progressive increase in the steady-state concentration of oxidatively modified DNA and proteins in the brain during aging (9-12). This increase would appear to be region specific, as indicated by the variations in levels of protein oxidative damage within different areas of the brain in aged mice (13).In the current experiments, the hypothesis that regionspecific oxidative molecular damage in the brain is linked to the senescent loss of cognitive and motor functions was tested by using aged mice as a model system. The approach used was based upon the general observation that individuals of similar advanced chronological age frequently show varying degrees of cognitive and/or motor impairment, with some exhibiting little or no age-associated loss and others showing marked dysfunction (14). If the hypothesis were valid, then variations in the degree of cognitive or motor impairments within a group of old mice should be correlated with oxidative damage in appropriate regions of the brain. This prediction was tested by first screening individual aged mice for their degree of impairment on a behavioral test battery developed specifically for the measurement of age-impaired cognitive, locomotor, and motor coordination skills (15-18). Following...

The objective of this study was to test some of the predictions of the oxidative-stress hypothesis of aging, which postulates that aging is causally associated with the molecular damage inflicted by reactive oxygen species. Protein carbonyl content was used as an index of molecular oxidative modifications. The carbonyl content was found to be associated with the physiological age or life expectancy of flies rather than with their chronological age. Exposure of flies to sublethal hyperoxia (100% oxygen) irreversibly enhanced the carbonyl content of the flies and decreased their rate of oxygen consumption. Results of this study indicate that protein carbonyl content may be a biomarker of aging and support the general concept that oxidative stress may be a causal factor in the aging process.

No abstract

Background: In the present study, different methods for preparation of platelet-rich plasma (PRP) are investigated in order to standardize the component in terms of growth factor content. The effects of concentration technique and storage duration are also analyzed. Methods: PRP was collected from 40 donors by plateletpheresis as well as by the buffy coat and tube method. Concentration of growth factors was performed using double freeze thaw- and CaCl₂-induced degranulation techniques. Growth factor estimation was performed using ELISA. Results: The levels of growth factors were highest in PRP from buffy coat, moderately lower in plasma gained by plateletpheresis and lowest in that obtained by the tube method. Mean levels of platelet-derived growth factors (PDGF) AB and BB are significantly higher when CaCl₂ was used for concentrating the growth factors. The mean levels of transforming growth factor β1 and insulin-like growth factor I were higher when applying the double freeze thaw technique. There was a substantial decline in the levels of growth factors during storage. Conclusion: The buffy coat method is suitable as preparation method for PRP in most settings. The double freeze thaw technique is better suited as concentration technique as it causes lysis of both platelets and white blood cells for releasing growth factors and is easier to perform. Growth factors are not stable in plasma, thus PRP should be frozen immediately after preparation.