Sandbox Reserved 192: Difference between revisions

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=='''Medical Implications'''==
=='''Medical Implications'''==


''Inhibition of Metastasis'': A recent study published in 2010 discusses the possibility of using the degradation capabilities of RNase A and a similar protein DNase I to treat tumors. Tumor propagation is associated with an imbalance in the level of nucleic acid degradation. This is shown by increased levels of nucleic acids and decreased levels of nuclease activity in the blood of patients. The high levels of nucleic acids are caused by the unregulated expression and the secretion of a specific tumor-derived miRNA and DNA. It was found that the combined treatment with the RNase A and the DNase produced the best results by slowing the growth rate of the tumor. But both the ribonucleases are toxic at high levels; thus, only low levels can be administered to prevent adverse effects.
''Inhibition of Metastasis'': A recent study published in 2010 revealed that tumor propagation is associated with an imbalance in nucleic acid metabolism. In the blood plasma of patients, there are increased levels of circulating nucleic acids and decreased nuclease activity. The abnormally high levels of circulating nucleic acids is associated with the increased expression and secretion of tumor-derived miRNA and DNA. With increased expression the tumor progresses and the patient has a bad prognosis.
RNase A and DNase I inhibit metastasis by catalyzing metastasis pathomorphosis which is apoptosis, necrosis and destruction of oncocytes (epithelial cells with large amounts of mitochondira). This capability retards the primary tumor growth by 30-40%. The tumor bearing mice received doses of RNase A, DNase I or a mixture of the two and the most significant effect observed was in the mice treated with both enzymes simultaneously. Thus the simultaneous administration of RNase A and DNase I lead to an anti-metastatic effect and results in an almost complete absence in the metastases of the tumor. Further observations suggest that RNase A and DNase I are toxic at high levels. So for effective treatment ultra low doses are required to stay below the level of toxicity.  


''Radicalization of RNase A'': Tandem radical damage is a degenerative process where the radicalization of one molecule leads to a number of adverse biological effects. Methionine (Met) residues are transformed to alpha-aminobutyric acid (Aba) with a methanethiyl radical byproduct when bombarded  with H*. When cysteine residues are radicalized, they are transformed to Alanine releasing sulfur radicals. This byproduct radical interact with the cis double bond in phospholipid fatty acids causing the conformational shift to the trans isomer. This switch from cis to trans causes many serious unfavorable biological diseases. Further studies into radical stresses on RNase A will help to better understand cellular degradation associated with aging and such degenerative pathologies.


<Structure load='7RSA' size='300' frame='true' align='left' caption='Insert caption here' scene='Insert optional scene name here' />
<Structure load='7RSA' size='300' frame='true' align='left' caption='Insert caption here' scene='Insert optional scene name here' />
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