  Alcohol consumption interferes with the functioning of multiple organ
systems, causing changes in the chemistry, physiology and pathology of tissues
and cellular organelles. Although epigenetic modifications underlie the
development of cancer, exposure to carcinogenic chemicals, such as alcohol, can
also contribute to disease development. However, the effects of chronic
alcoholism on normal or pre-carcinogenic cells/tissues in different organelles
are not well understood. Therefore, we herein study the effect of alcohol
consumption on colonic nucleus using control and azoxymethane (AOM) and dextran
sulfate sodium (DSS) treated carcinogenic mice. Previous studies showed that
progression of carcinogenesis is associated with increase in the degree of
intranuclear nanoscale structural disorder. In the present work, we quantify
the degree of nanostructural disorder as a measure of carcinogenesis. To
accomplish this, transmission electron microscopy (TEM) imaging of respective
colonic epithelial cell nuclei are used to construct disordered optical
lattices, and the properties of nanoscale disorder are then studied by
analyzing the inverse participation ratio (IPR) of the spatially localized
eigenfunctions of these optical lattices. Nanoscale structural disorder
strength, as a marker of cancer progression, is measured in the length scale of
10 to 75 nm. Results show no significant visible effect in nanoscale structural
changes on colon cell nuclei from alcohol exposure. However, alcohol was found
to act as an enhancer of nanoscale disorder in precancerous cells and, hence,
carcinogenic processes. To the best of our knowledge, this is the first study
to quantify the effect of alcohol on early carcinogenic biological cells, using
mesoscopic condensed matter physics.
