Size and surface charge of gold nanoparticles determine absorption across intestinal barriers and accumulation in secondary target organs after oral administration

Figures & data

Table I. Characteristics of the applied ¹⁹⁸Au NP suspensions.

	1.4 nm	5 nm	18 nm	80 nm	200 nm	2.8 nm Carboxyl	2.8 nm Amine
Applied radioactivity [kBq]	76.0 ± 33.3	130.2 ± 10.3	73.5 ± 2.3	297.1 ± 5.1	219.5 ± 2.	21.8 ± 0.1	90.6 ± 5.8
Applied mass [μg]	1.0 ± 0.5	27.4 ± 2.2	2.4 ± 0.1	19.9 ± 0.3	19.0 ± 0.2	1.4 ± 0.1	16.4 ± 1.1
Applied number	3.8 ± 1.7 × 10^13	2.2 ± 0.2 × 10^13	4.1 ± 0.1 × 10^10	3.9 ± 0.1 × 10^9	3.8 ± 0.0 × 10^8	6.3 ± 0.2 × 10^12	7.5 ± 0.5 × 10^13
Applied surface area [cm^2]	2.4 ± 1.0	17.3 ± 1.4	0.4 ± 0.0	0.8 ± 0.0	0.1 ± 0.0	1.2 ± 0.1	14.5 ± 1.0

Table II. Characteristics of the applied gold NPs.

Core diameter [nm]	Hydrodynamic diameter [nm]	Polydispersity Index (PdI)	Ligand (Charged surface group)	ζ-potential [mV]
1.4	2.9*	ND	TPPMS (SO3 ^-)	−20.6 ± 0.5
5	12.1^#	0.19	TPPMS (SO3 ^-)	−21.1 ± 1.4
18	21^§	0.10	TPPMS (SO3 ^-)	−22.8 ± 3.1
80	85^#	0.12	TPPMS (SO3 ^-)	−22.3 ± 1.6
200	205^#	0.05	TPPMS (SO3 ^-)	−41.3 ± 4.5
2.8	ND	ND	TGA (COO^-)	Negative
2.8	ND	ND	CA (NH3 ^+)	Positive

*As determined earlier (Tominaga et al. 1996); ^#DLS measurement using Malvern HPPS5001, Herrenberg, Germany; ^§DLS measurement using Malvern Zetasizer, Herrenberg, Germany. TPPMS, triphenylphosphine m-monosulfonate; TGA, thioglycolic acid (mercaptoacetic acid); CA, cysteamine (2-aminoethanethiol); ND, Not determined.

Table III. NP content in the gastro-intestinal tract (GIT).

	Particle retention [%]
Particle type	GIT with internal feces	Excreted feces	GIT+feces
1.4 nm	17.2 ± 4.0	82.4 ± 4.0	99.63 ± 0.10
5 nm	74.1 ± 14.0	25.9 ± 14.0	99.95 ± 0.01
18 nm	29.7 ± 6.7	70.3 ± 6.7	99.88 ± 0.02
80 nm	22.3 ± 7.3	77.7 ± 7.3	99.97 ± 0.01
200 nm	34.9 ± 7.1	65.1 ± 7.1	99.99 ± 0.00
2.8 nm COO^-	54.2 ± 4.5	45.4 ± 4.5	99.63 ± 0.02
2.8 nm NH3 ^+	64.8 ± 11.8	35.0 ± 11.8	99.86 ± 0.02

NP content in the gastro-intestinal tract (including internal feces) and excreted feces after intra-oesophageal application in % of administered particle-amount.

Figure 1. NP content which reached the circulation after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals.

Figure 2. NP content which accumulated in secondary organs, the remainder, as well as the urine after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals. *p < 0.05; ***p < 0.001; nd, not detected.

Figure 3. NP content which reached the circulation after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals.

Figure 4. NP content which accumulated the blood (A), reticulo endothelial system (RES; liver plus spleen), (B), kidney (C), as well as urine (D) after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals.

Figure 5. NP content which accumulated the heart (A), and brain (B) after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals.

Figure 6. NP content which accumulated in the remaining carcass after intra-oesophageal application in % of administered particle-amount. Given is the mean ± standard error of the mean of four animals.

Tominaga T, Tenma S, Watanabe H, Giebel U, Schmid G. 1996. Tracer diffusion of a ligand-stabilized two-shell gold cluster. Chem Lett (12):1033–1034.

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