ahlok2002
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complex in inhibition of gene expression!
how possible the metal complex(transition metal of amino acid complex) act as the inhibitor/enzyme mimic to cleave the dna sequences hence retarding
the cell growth and finally cause the cell to die?
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chemoleo
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Sorry I don't understand what you mean. Would you care to give a better description of the question/problem?
Transition metal of amino acid complex? Huh? inhibitor mimic of what?
Never Stop to Begin, and Never Begin to Stop...
Tolerance is good. But not with the intolerant! (Wilhelm Busch)
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ahlok2002
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sorry.
now i'm going to explan my question.
actually i'm with the anticancer property of peptide complexes of different metal that more concentrate in the transition metals in my project
work.
i'm just to complete my dregree and now involved in some research work with my Prof in cancer drug.
now, we want to test the copper(II) peptide complexes [Co(DMG)2] that may belive to have the porperty to inactivated of the gene expression afther the
coordination of the copper(II) peptide complexes into the DNA stucture by alter the normal funtion. Or we belive the copper(II) peptide complexes may
have the ability to cleave the DNA sequence( act as 'mimic' of the nuclease) so able to stop the replication of the tumor cell.
so my question is whether is any complexes that discoved to have the same porperty( cleave DNA or only cleave tumor DNA) of peptide complexes.
and the causes of this...i belive that the charge of the complex and the lability of the peptide ligand cause the different porperty..and what other
factor what can i look for beside those.
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chemoleo
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Hmmm
I am not sure whether I understand your question correctly. For one thing, it is probably Cu(DMG)2, not Co. Co is Cobalt, Cu is
copper.
Now what is DMG? I checked, there are three possibilities:
1) Dimethylglyoxime (probably H3C(C=NOH)(C=NOH)CH3 ?) or
2) a degraded D-manno-D-glucan from Microellobosporia grisea, which has known antitumour properties.
3) DMG-DMDOT/MINO which are two semisynthetic tetracyclines called glycylcyclines (and tetracyclines are antibiotics, which per definition work
against prokarya - which don't work with eukarya and thus tumours.
Regardless what DMG is, it's definitely possible that one or more of the above interacts (non) covalently with DNA, and thus halts or retards
DNA replication. Alternatitvley they may induce mutations, which wouldnt be quite so desired.
I doubt, however, that the DNA is easily cleaved. Do you have a publication you'd like to point to? Is the cleavage single or double strand? As
you probably know, single strand cleavage is easily repaired, while d.s. cleavage is not.
To ask for compounds that specifically cleave 'tumour DNA' is ludicrous, as 'tumour DNA' is chemically the same as non-tumour DNA,
except for certain mutations in the right (wrong) places. There isn't a single chemical that would be able to pick those out specifically.
You'd need specific recognition proteins.... Good luck designing them  .
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and the causes of this...i belive that the charge of the complex and the lability of the peptide ligand cause the different porperty..and what other
factor what can i look for beside those. |
What properties are you talking of? what factors?
By the way, I am sure you have tried to search for your quest, PubMed ( http://www.ncbi.nlm.nih.gov/entrez/query.fcgi )is a good start.
[Edited on 23-2-2004 by chemoleo]
Never Stop to Begin, and Never Begin to Stop...
Tolerance is good. But not with the intolerant! (Wilhelm Busch)
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Lugh
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"To ask for compounds that specifically cleave 'tumour DNA' is ludicrous"
This may be true, but it might be possible to give doses of a toxic substance which is small enough not to damage healthy cells but are taken up and
used by rapidly dividing cells i.e. Tumours.
As far as I know this method is used in some chemotherapies.
Maybe by targeting replicating DNA or say transcription enzymes you could preferentially target tumour cells. But then you also have to consider the
horrible side effects - other rapidly dividing cells like T and B cells would also be affected.
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ahlok2002
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thanks!
sorry for the confusing of copper(Cu) and cobalt(Co).
DMG (Dimethylglycine) that i used as the ligand in the Cu(DMG)2 this experiment.
i think i haven't found any publicaton on this Cu(DMG)2.
this maybe new because is part of my prof current research work and if can soon he will publish on the topic (that depent on how fast i can finish my
work)
and besides the interaction of the anticancer drug with the DNA, what other common mechanism of the drug carry out in oder to stop repication of
cancer cell/ kill the cell.
is that posible the drug stop poliferation of membrane pores thus stop the substances to pass through?
since we don't have the specific drug that kill only cancer cell, i think maybe we can activate the drug only afther the drug enter into the
cancer cells. like some drug need ascobic acid. H2O2..to activate. so we can infect the cancer cells with certain gene so that produce the activator
in the cancer cell? is that what they done in gene therapy in cancer to boost the chemotherapy with the combination of the gene therapy?
if i'm wrong please correct me.
always ready to learn.
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