Biomedical Engineering Reference
In-Depth Information
Fig. 3. There is no cytotoxicity for the cells.
2.3 Neurotoxic effects
Several studies revealed neurotoxic effects as well as ataxi and muscle weakness caused by
biomaterials on humans and on laboratory animals. It has been suggested that they cause
axonal degeneration in central and peripheric nervous system (Barber et al., 2001).
Astrocytes are the stellate glial cells in the central nervous system, which play a major role
in supporting neurons, scar formation and development and maintenance of the blood-brain
barrier. The physiological and metabolic properties of astrocytes indicate that those cells are
involved in the regulation of water, ions, neurotransmitters, and pH of the neuronal milieu
(Montgomery 1994). They are also implicated in protection against toxic insults such as
excitotoxicity and oxidative stress (Lamigeon et al., 2001). Glial fibrillary acidic protein
(GFAP) is an intermediate filament protein found predominantly in astrocytes (McLendon
1994). Therefore it is important to determine the glial fibrillary acidic protein (GFAP)
immunoreactivity in astrocytes for the evaluation of biomateials.
In our study, immunolocalization of glial fibrillary acidic protein (GFAP) was determined,
and it was evaluated by using semi-quantitative morphometrical techniques (Unver
Saraydin et al., 2011). GFAP immunoreactivity was found to be very strong in the
methacrylamide, N-isopropylacrilamid, ethylene glycol and N-vinyl pyrrolidine application
groups whereas it was weak in acrylic acid, acrylamide and 2-hydroxyethyl metacrylad
applied groups (Table 1, Figure 4-10). Changes in GFAP immunoreactivity could be due to
following conditions; astrocyte dysfunction, astrocyte loss accompanied by astroglial cell
proliferation, de-differentiation, and changes in functional state of neuronal cell types, thus
altering the neuron-glial homeostasis. The over-expression of GFAP could probably indicate
the protective strategy of these tissues.
Although the neurotoxicity of acrylamide and many monomers has been known since 1950s,
its' mechanisms have remained obscure (Lee et al., 2005, Gold and Schaumburg, 2000).
Acrylamide increases p53 protein (Okuno et al., 2006), recent studies indicate that it plays a
role in apoptotic cell death in neurons (Morrison et al., 2003). Acrylamide can activate
caspase- 3 and cause apoptosis in neuronal cells (Sumizawa and Igisu, 2007). The cellular
process of apoptosis is an important component of tissue and organ development as well as
the natural response to disease and injury (David et al., 2003). DNA fragmentation in
neurons was characterized by double staining with terminal deoxynucleotidyl transferase-
mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) (Bao and Liu, 2004).
To our knowledge, however, it has not been determined whether acrylamide and other
