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onsdag 4 mars 2015

Solusyklin vaiheitten progressio ja polyaminit ( putreskiini, spermidiini, spermiini ). Ornitiinin aineenvaihdunta

Polyaminit ja solusyklin vaiheittainen progressio . Ruotsalainen artikkeli vuodelta 1977 
Otan tästä ornitiinin aineenvaihdunnasta  jotain selventävää koska  sähkömagneettinen kenttä vaikuttaa siihen.  STUK, Sähkömagneettiset kentät. Sivu 197.


  SITAATTI:  Proliferaatioon liittyvät myös ne tutkimukset, joissa on mitattu polyamiinien biosynteesin ja solunjakautumisen säätelyyn liittyvän ornitiinidekarboksylaasientsyymin (ODC) aktiivisuutta. ODC:tä voidaan pitää solukasvun osoittimena; se on yleensä koholla nopeasti kasvavissa soluissa kuten esim. syöpäsolukossa. Monessa yksittäisessä tutkimuksessa on todettu ODC:n aktiivisuuden nousseen sähkö- ja magneettikenttäaltistuksessa. (STUK)
 
Putrescine synthesis inhibition

http://www.pnas.org/content/75/2/1039.full.pdf

Proc.Natl.Acad.Sci.USAVol.75,No.2,pp.1039-1042,February
1978PhysiologicalSciences
Inhibition of putrescine synthesis blocks development of the polychete Ophryot rocha labronica at gastrulation
[a-methylornithine/methylglyoxal bis(guanylhydrazone)/polyamines/embryogenesis]
HADAR EMANUELSSON And OLLE HEBY
Department of Zoophysiology, University of Lund, Helgonavigen
3, S-223 62 Lund, Sweden
Communicated by Ake Gustafsson, December 8, 1977

ABSTRACT


Developing eggs of the polychete Ophryotrocha labronica were analyzed for polyamines during the first 6 days after fertilization.
The spermine content dominated initially, but gradually decreased.
It was surpassed by putrescine, which rapidly increased to a maximum on the 3rd day, i.e., at the inception of gastrulation.
The spermidine content was low during the entire period.
Treatment of eggs with the putrescine synthesis inhibitor
a-methylornithine from the onset of development led to developmental arrest at gastrulation and to an normally low content of putrescine in the treated embryos.
Methylglyoxal bis(guanylhydrazone), an inhibitor of spermine and spermidine synthesis, had no visible effect on development.

Our observations strongly suggest that putrescine synthesis is indispensable in early embryonic development of Ophryotrocha.
The polyamines putrescine, spermidine, and spermine
are essential components of prokaryotic and eukaryotic cells as well as of virusparticles
(1).
When added to cell-free or cells in culture, the polyamines have been found to stimulate the synthesis of DNA, RNA, and protein.
This multifaceted action may be due to interaction with nucleicacids or nucleic acid- containing structures, such as chromatin and ribosomes,
for which the polyamines exhibit high affinity.

A finding of paramount importance has been that stimulation of cellular polyamine synthesis is associated with a shift from aquiescent
to a proliferating state(1-3).

In fact, the rate of polyamine synthesis has been shown to exhibit a high positive correlation with the rate of cell proliferation both in vitro (4) and in vivo (5).
In continuously dividing cells, polyamines are synthesized in a biphasic pattern (6). The fact that polyamine synthesis increases prior to DNA synthesis as well as cell division suggests a possible involvement of the polyamines in the progression through these phases of the cell cycle.

Recent experiments with polyamine auxotrophs of Escherichia coli (7-9) and inhibitors of polyamine synthesis (10-14) emphasize the importance of the polyamines in cell growth and division, and lend further support for the contention that polyaminesplay an important role in nucleic acid and protein synthesis in the cell.
The polyamine synthesis inhibitors used in the latter studies
were a-methylornithine (Me-Orn), a competitive inhibitor of L-ornithine decarboxylase (putrescine synthesis), the
initial enzyme in polyamine synthesis, and methylglyoxal bis(guanylhydrazone) (MeGAG), a potent inhibitor of S-adenosyl-L-methionine decarboxylase, an enzyme involved in spermidine and spermine synthesis. Both inhibitors caused a partial depletion
of the cellular polyamine content, a condition that perturbed the traverse of the cell cycle (10- 14).



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