Biomedical Engineering Reference
In-Depth Information
9.2.1 Oral Absorption
According to the literature, mice, rats, sheep, pigs, and cows can absorb NPs
from the GIT. Florence [6] observed that the ability of intact microparticles
and NPs to be absorbed through the gut walls was different. A literature
consensus mentioned that the absorption increases with decreasing particle
diameter. The uptake of inert NPs has been shown to occur transcellulary
through normal enterocytes and Peyer's patch (PP) via M cells and to lesser
extent across paracellular pathways [7]. The absorption can also occur by
a mechanism of persorption, which gave rise to contemporary studies of
particulate absorption NPs, such as polystyrene latex, that have been recog-
nized as a useful model because they do not easily degrade. This study con-
firmed that NPs ranging from 50 to 100 nm in diameter reached the maximal
absorption rate. However, NPs >1 μm are being trapped in the PP [8,9]. It
seems that at this size, NPs are not translocated to the systemic circulation.
Oral absorption is influenced by different characteristics related to the NPs
(e.g., diameter, surface chemistry, surface ligands, shape and elasticity, physi-
cal and chemical stability) [7]. In general, smaller particles lead to higher
absorption rates. NPs <1 μm have a limited absorption capability. Particles
>3 μm are phagocytes and stay sequestered in the GIT cells. This is what we
should observe in theory, but not necessarily the experimental observation.
For example, even for NPs, the surface charge might limit absorption com-
pared with nonionic NPs. Biological surfaces such as an epithelia-containing
receptor at the surface can express higher absorption rates. Shape and elas-
ticity facilitate the passage across the barrier [8].
In the GIT, it seems well established that the PP would be mostly implicated
in the process of particle uptake via specialized epithelial cells. However,
these specialized cells represent only approximately 10% of the cells covering
the dome of these patches. Florence [8] mentioned that these immunologic
cells have their analogues in the bronchus-, larynx-, and nose-associated
lymphoid tissue regions (referred to as BALT, LALT, and NALT, respectively).
It is not surprising that the PP part of the gut-associated lymphoid tissue
(GALT) structure of the GIT wall is, as part of the lymphoid tissue, adapted
for large range of phagocytes. The uptake of particles, microorganisms, and
macromolecules by M cells occurs through adsorptive endocytosis by an
approach of clathrin-coated pits and vesicle formation through endocyto-
sis and phagocytosis processes [10]. This absorption route has a limitation
because M cells (lymphoid tissues) occupy a relatively small region of the
total GIT surface area, which is not compensated for by enhanced affinities.
It has been shown that particulate systems can gain entry through normal
gut epithelial cells (enterocytes); however, this absorption rate is not signifi-
cant compared with the M cells. In addition, gastric mucus covers the entire
wall of the GIT. Some authors have reported that mucus might inhibit the
uptake of NPs through a dense structure in the viscous glycoprotein gel.
However, there is a thought that entrapment of NPs in mucus actually delays
