Silent Superbug Revisited Apr 3, 2012 3:22:41 GMT -5
Post by skyship on Apr 3, 2012 3:22:41 GMT -5
Chitin is from insect cells, in the baculovirus, used in human vaccines.
Fungi in the sense of rhizoids, mycelias, not reg fungi, these are small and need blue light.
photolyase....these are in these notice the change here: from native dna to dimers etc. they say is from UV light, however, it is not.
this creates the dimer .....not the UV. The UV makes the dimer come alive!
Chlorella pyrenoidosa is a freshwater green alga and belongs to class Chlorophyceae, order Chlorellales and family Chlorellaceae. CPD photolyase is an enzyme found in Chlrella pyrnoidosa and responsible for repairing of DNA damages caused by UV radiations.
The cyclobutane pyrimidine dimmer (CPDs) and 6-4 pyrimidone photoproducts (6-4 PPs) are major form of DNA damages and these damages are caused by various physical and chemical agents occurs in the environment such as UV and ionizing radiations, chemical mutagens fungal and bacterial toxins, and free radicals or alkalizing agents produced by metabolism.
This cyclobutane pyrimidine dimer CPD and the 6-4 pyrimidone photoproducts ARE REPAIR SUBUNITS This two were created.
This went inside the dna and created the dimer. lesion in the dna itself.
We are being effected by these repair units.
now what happens is the repair CPD, cyclobutane pyrimidine dimer,
"This diagram depicts how the Photolyase by using light radiation energy, breaks such bonds to restore the dimers into monomers, which facilitates the normal replication and even transcription. FADH provides electrons to cyclobutane rings for splitting the bonds.
The diagram .. shows how the Photolyase uses light energy and transfers the light energy to Cyclobutane rings to open up to generate individual nucleotide free to base pair with their normal bases. Before they execute repair functions they flip the dimers towards enzyme surface, then perform reaction.
So, when sun heats them up, they come out, these dimers are made of some kind of monomer? So what makes the dimers in the first place?
It is those dimers that are coming out. these are protofibrils as well.
So, this is inside of us already. What makes the monomer?
Cyclobutane rings? these themselves are toxic.
When gets down to monomer level it begins to mutate again instead of being expelled out of skin.
Here shows they are toxic.
H-NMR Studies of Duplex DNA Decamer Containing a Uracil Cyclobutane Dimer: Implications Regarding the High UV Mutagenecity of CC Photolesions,
PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2002
To determine the origin of the UV-specific CC to TT tandem mutation at the CC site, we made a duplex DNA decamer containing a uracil cis,syn cyclobutane dimer (CBD) as the deaminated model of a cytosine dimer. Two-dimensional 1H-NMR spectroscopy studies were performed on this sequence where two adenines (Ade) were opposite to the uracil dimer.
Two imino protons of the uracil dimer were found to retain Watson,Crick hydrogen bonding with the opposite Ade, although the 5,-U(NH) of the dimer site showed unusual upfield shift like that of the 5,-T(NH) of the TT dimer, which seemed to be associated with deshielding by the flanking base rather than with reduced hydrogen bonding. (McAteer et al. 1998, J. Mol. Biol. 282:1013,1032). Hydrogen bondings at the dimer site were also supported by detecting typical strong nuclear Overhauser effects (NOE) between two imino protons and the opposite Ade H2 or NH2.
But sequential NOE interactions of base protons with sugar protons were absent at the two flanking nucleotides of the 5, side of the uracil dimer and at the intradimer site, contrasting with its thymine analog where sequential NOE was absent only at the A4,T5 step. In addition, NOE cross peak for U5(NH) , A4(H2) was detected, although the NOE interactions of U6(NH) with A7(H2) and A17(H2) were not observed in contrast to the thymine dimer duplex.
This different local structural alteration may be affected by the induced right-hand twisted puckering mode of cis,syn cyclobutane ring of the uracil dimer in the B-DNA duplex, even though the isolated uracil dimer had left-hand twisted puckering rigidly. In parallel, these observations may be correlated with observed differences in mutagenic properties between cis,syn UU dimer and cis,syn TT dimer. [source]
Cyclobutane photodimers ("CPD's") are formed by photochemical reactions that result in the coupling of the C=C double bonds of pyrimidines. T-T dimers thymine dimers formed in between two thymines are the most abundant of the CPD's. CPD's are readily repaired by nucleotide excision repair enzymes. In most organisms they can also be repaired by photolyases, a light-dependent family of enzymes. Xeroderma pigmentosum is a genetic disease where this damage can not be repaired,