At the cellular level, numerous structural modifications have been documented that are likely to contribute to light scattering.
It has been documented that endogenous cellular polyamine level is dependent upon several interconnected pathways, such as de novo synthesis, degradation and conjugation, but the exact contribution of an individual pathway is not yet identified.
It has been documented that miRNAs participate in cellular proliferation, differentiation, migration, and apoptosis [ 10– 10].
It has also been documented that NPs can instigate oxidative stress and cellular toxicity in various types of cells [8], [19].
It has been documented that vitamin D has functional roles in cellular proliferation, including different stages of the cell cycle, differentiation, and apoptosis [ 17, 18] that could have impact on normal angiogenesis and endothelial cell differentiation [ 19].
It has been documented that C-PC evades oxidative stress and related cellular damages by scavenging the free radicals and chelating metal ions [41].
It has been documented that multipotent MSCs synthesize a wide variety of growth factors and cytokines, exerting a paracrine effect on local cellular dynamics [ 42].
It is documented that the type-1 cellular immune response is impaired during the course of HIV infection [ 17].
It is documented that Pb prohibits the nutrient uptake, net photosynthetic rate, and cellular respiration and causes damage to cell membrane [ 7].
Secondly, although it is widely documented that cellular senescence is irreversible (Hayflick, 1965), other data refute this (Beauséjour et al, 2003; Rajaraman et al, 2006).
