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Cells are in a constant state of generating oxidative molecules, clearing those molecules via the use of antioxidant proteins, and repairing the damage caused by oxidative reactions. Researchers here show that aging is accompanied by declining amounts of the natural antioxidants involved in clearing oxidizing molecules from cells, preventing them from reacting with cellular machinery to cause damage. This is an unfortunate downstream consequence of the underlying causes of aging, one that will cause further dysfunction in cells. Exactly how and why this is a feature of aging, the exact chain of cause and effect that leads from the underlying damage to this result, remains to be determined. At the present time, the fastest approach to answering that sort of inquiry is likely to build rejuvenation biotechnologies that can repair specific forms of molecular damage thought to cause aging, and then see what happens when the therapies are applied in animal studies.
An integral part of aerobic metabolism is reactive oxygen species (ROS) generation which should be analyzed according to its two main functions. On the one hand, ROS plays an important role in biomodulating and regulating many cellular functions, such as defense against pathogens, signal transduction processes during transmission of intercellular information, and activation of specific transcription factors. On the other hand, an excessive quantity of ROS has a deleterious effect on cells, reacting with a variety of molecules and thereby interfering with cellular functions. To cope with the elevated generation of ROS, ROS-scavenging biochemical pathways have been developed in aerobic cells.
In recent years there have been a lot of studies supporting the role of ROS in molecular aging mechanisms. The confirmation of oxidative stress increase with age of diverse organisms, and the generation of transgenic invertebrates overexpressing the antioxidant enzymes with increased lifespan were among the most important results of these studies. Nevertheless, there were no alterations in the lifespan in most of the examined mouse models, which under- or overexpressed a wide variety of genes coding for antioxidant enzymes. Thus, the role of oxidative stress in aging mammals is not fully understood and still demands further inquiries.
In this study, analysis of antioxidant defense was performed on the blood samples from 184 “aged” individuals aged 65-90+ years, and compared to the blood samples of 37 individuals just about at the beginning of aging, aged 55-59 years. Statistically significant decreases of Zn,Cu-superoxide dismutase (SOD-1), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were observed in elderly people in comparison with the control group. Moreover, an inverse correlation between the activities of SOD-1, CAT, and GSH-Px and the age of the examined persons was found. No age-related changes in glutathione reductase activities and malondialdehyde concentrations were observed. These lower activities of fundamental antioxidant enzymes indicate the impairment of antioxidant defense in the erythrocytes of elderly people.
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