By M. S. Kanungo
This e-book reports the molecular biology of the gene when it comes to getting older. the writer offers simple details on eukaryotic genes and follows this with information of the alterations that happen of their constitution and serve as in the course of getting older. He studies the newest reports being performed in numerous laboratories, outlines the gaps and deficiencies in our current wisdom, and indicates the main ecocnomic destiny components of study.
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Example text
Taking into account the above deficiencies in the studies on agerelated changes in enzymes it is seen that no comparable data on all enzymes of even one metabolic path are available for any organism as a function of its age. Especially, data on the levels of regulatory enzymes of a metabolic path at different ages may be of greater significance than those of constitutive enzymes. For example, the study of the levels of the glycolytic enzymes, glucokinase, phosphofructokinase (PFK), and pyruvate kinase and the gluconeogenic enzymes, pyruvate carboxylase, fructose 1,6-diphosphatase (F-l,6-diPase), and glucose-6-phosphatase 24 Phenotypic changes during aging (G-6-Pase), which are the key regulatory enzymes for glucose metabolism, would be of much value for understanding how glucose metabolism changes during aging.
Is this process programmed, just as the process of development is believed to be? Is there a single The science of aging 19 universal cause of aging? Or does the cause differ with the organization of the system? Answers to the above questions may help in devising methods for postponing the onset of the aging process and for the control of aging. These measures could conceivably prolong the active and youthful period from age 20 to 40 years to say 20 to 60 years or more. This will also greatly increase the period of work output in humans, besides giving them the psychological satisfaction of being youthful longer.
To verify this, homogenates of the cerebral hemisphere of 7-, 44-, and 108-week-old ovariectomized rats were incubated with 3H-estradiol, and the estradiolbinding protein was assayed (Kanungo, Patnaik & Koul, 1975). It was found that the affinity of this protein for 17p-estradiol is the highest in the cerebral hemisphere of immature rats in which the induction of AChE is also the highest. The affinity is lower in old rats. 3. Mechanism of action of steroid hormone. in the brain of old rats appears to be a decrease in the estradiol-binding protein.