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Z A Medvedev

Publications and source records attributed to Z A Medvedev.

At least 19 recordsLinked to original sources
PubMed1990

Age-related changes of the H1 and H1(0) histone variants in murine tissues.

The relative proportion of the histone H1(0) which is present in chromatin of nondividing and terminally differentiated cells is shown to increase with age. CNBr nonenzymatic cleavage and SDS-polyacrylamide gel electrophoresis of H1(0) extracted from liver chromatin of young and old mice and from age-related hepatocarcinomas showed that H1(0) consists of two variants, one contains methionine the other is methionine-free. The ratio between these two H1(0) variants also changes with age. The relative amounts of specific minor H1 and H1(0) histone fractions which are more loosely bound in chromatin and are extractable with 0.35 M NaCl, together with the HMG nonhistone proteins decrease in ageing mouse tissues. The age-related alteration of the ratio between H1(0) variants probably represents the chromatin repair process, whereas the age-related replacement of H1A and H1B subfractions by H1(0) histones may reflect the continuing process of differentiation.

Aging↗
PubMed1988

Age related variations of hepatocarcinogenic effect of azo dye (3'-MDAB) as linked to the level of hepatocyte polyploidization.

Four-week-old CBA mice fed a diet containing the hepatocarcinogenic azo dye 3'-MDAB showed a rapid polyploidization of hepatocytes, a sharp increase of two liver-specific acid soluble non-histone proteins (LSP 1 and 2) and induction of hepatomas between 44 and 52 weeks of the regimen. More mature 18-week-old mice fed the same diet did not develop induced hepatocarcinogenesis after 55 weeks of the regimen. Interruption of the azo dye regimen showed that the increase of LSP 1 and 2 was reversible, whereas the carcinogenic effect and polyploidization were irreversible. Sprague-Dawley rats were more sensitive to the carcinogenic effect of the azo dye regimen. It is suggested that the higher resistance of older mice to the carcinogenic effect could be linked to the higher level of hepatocyte polyploidization and that the increase of LSP 1 and 2 is relevant to the toxic effect of the azo dye.

Aging↗
PubMed1984

Age-related changes of the pattern of non-histone proteins in active and condensed fractions of mouse liver chromatin and hepatocarcinoma.

Electrophoretic analysis of histones and non-histone acid-soluble proteins in active (nuclease sensitive) and inactive chromatin from liver of young and old CBA mice and in age-related hepatocarcinomas showed a higher ratio of NHP:histones in active chromatin in old cells. Some liver- and hepatoma-specific fractions of non-histone proteins have been identified as chromatin matrix proteins.

Aging↗
PubMed1984

Age changes of chromatin. A review.

The age-related studies of chromatin and DNA has attracted significant interest in recent years. However, individual works describe only some and a few of the many changes of chromatin. It is often difficult to decide whether these changes have secondary or primary nature. The overview of these studies makes it possible to realize how many very complex and interdependent changes occur in chromatin during ageing. Chromatin is the most complex among self-reproducible parts of the cell. A very sophisticated structure of chromatin makes possible the differential transcription of a genetic programme which supports the accurate specialized functions of each cell in interphase and also provides a mechanism for perfect reproduction of this complex machinery of genetic information during cell division. It is known that chromatin proteins, more than chromatin DNA show tissue specificity and developmental changes. There are many theories of cellular ageing which select some special types of DNA, RNA or protein changes and to promote them as the main or primary causes of cellular senescence. However, if these changes are considered within the more comprehensive picture of functional structure of chromatin the results show the interdependence of individual alterations and their proper place in the complex, multichannel, species and tissue-specific character of actual ageing. An attempt to summarize the basic facts and theories about age changes of the two main parts of chromatin structure, proteins and DNA is being made in this review. At the same time the author tried to develop a concept of non-random distribution of the age changes in chromatin and a possible higher rate of accumulation of different alteration and lesions in the transcribed and functionally active parts of chromatin.

Aging↗
PubMed1983

Developmental switches in reiterated genes may reduce the rate of age changes in DNA.

The possible role of the redundancy of genetic information in the regulation of the ageing rate has been discussed in several works. However, it was shown recently that the gene reiteration in most cases is represented by families of similar, but not identical genes. Their expression usually related to the different stages of development and when "early" embryonic or fetal genes are active, the "late" or adult genes are repressed. It is known that the DNA repair needs double stranded structure of DNA which is usual for inactive genes. Genes which are being transcribed and active are repressed by unwound, relaxed DNA which is less protected by the DNA repair enzymes. Aging of genetic information in somatic cells can be, therefore, considered as stage specific and alterations of "early" embryonic and fetal genes do not constitute the genetic load which influences the ageing rate of differentiated cells.

Aging↗
PubMed1982

The characterization of non-histone proteins whose amounts increase in chromatin from mouse hepatocarcinomas.

A fraction containing liver- and hepatoma-specific non-histone proteins has been isolated from the chromatin of mice. Amino acid analysis of this fraction shows that it contains 16 mol of glutamic acid, 10 mol aspartic acid, 7 mol of both arginine and lysine per 100 mol and contains no cysteine or tyrosine. The proteins in this fraction are strongly associated with DNA and are co-extracted with histones from chromatin with 0.25 M HCl. In chromatin from age-related hepatomas, the amount of this fraction increased six-fold. This increase in concentrations of these chromatin proteins may be associated with changes of chromatin structure necessary to initiate malignant growth in liver cells.

Amino Acids↗
PubMed1981

On the immortality of the germ line: genetic and biochemical mechanism. A review.

The nature of the differences between mortal somatic cells and immortal germ cell lines constitutes a major area of theoretical gerontology which has not yet received adequate attention. Weismann's theory, first stated almost exactly a century ago, was recently reconsidered by Kirkwood and Holliday. They applied modern concepts and findings on the factors regulating the accuracy of synthesis of macromolecules to explain germ line immortality. In the present paper, evidence on ageing of reproductive cells and the relationship of cytomorphogenetic events to periodic rejuvenation of germ cell lines is summarized and evaluated. Key events include the elimination or reversal of some DNA changes in germ cells through recombination and meiotic haploidization, cyclic regeneration of transcriptional and translational systems during gametogenesis and early development, and the selection of stable, viable genomes at various stages of the reproductive cycle. These rejuvenatory processes are compared and related to molecular events which differentiated somatic cells are unable to carry out.

Aging↗