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Diversity of abnormal half-life for specific RNA molecules may cause the development of diseases.
It is important to realize that the attachment of large targeting molecules may cause a decrease in their targeting efficiency due to conformational changes [ 56– 58].
However, unprovoked activation of immune responses can be harmful because production of very potent biological effector molecules may cause damage to host tissues.
Given the above considerations, it is clear that the interaction between NPs and other biological molecules may cause a modification of both, with consequences for human health that are not yet easy to predict.
Fewer Cdc20 molecules could provide an opportunity for one of the earlier models to emerge as appropriate, whereas more Cdc20 molecules may cause even the indirect inhibition to fail.
On the other hand, the possible role of the cysteinyl leukotrienes has been proposed; in addition to constituting one of the principal inflammatory mediators of asthma, these molecules may cause endothelial lesion or dysfunction [ 38].
Similar(54)
These toxic molecules readily react with adjacent membrane proteins or DNA molecules which may cause more hepatic complications and functional abnormalities.
Nevertheless, the Fe-S cluster may still be accessible to small molecules that may cause damage.
When these free radicals interact with biological molecules, it may cause cellular lipid peroxidation and DNA damage [ 9].
Several studies have described the release of harmful molecules that may cause endothelial damage from the placenta toward maternal circulation during this disease [ 104– 104].
One possible mechanism for the association might be the load of reactive free iron molecules which may cause DNA damage [ 23, 24], which may suppress the host defense cells and induce proliferation [ 25, 26], and which may convert nitric oxide from a proapoptotic to an antiapoptotic molecule [ 27].
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