The Toxicologist - Society of Toxicology

seen rapid uptake in biological imaging applications. In this study, we have evaluated
the potential of commercially available CdSe/ZnS-based quantum dots
(Qdot® 655 ITK amino and Qdot® 655 ITK carboxyl) to induce cytotoxicity
and DNA damage in CHO-K1, V79, Hep, THP-1, and Caco-2 cells using
LDH release, trypan blue dye exclusion, and MTT vital stain methods and Comet
assay at concentrations of 15 nM to 500 nM. These quantum dots were also evaluated
in bacterial tryptophan reverse mutation assay (500 nM). Lastly, cell growth
rate was studied during subchronic exposure of the quantum dots to MRC-5 and
GM03440 cells (5-15 nM). At 3-, 24-, and 48-hour treatment points with LDH
release method, the relative toxicity range was from 0% to 50% at 15 nM to 500
nM quantum dots. In the MMT cell viability experiment, the cell viability ranged
from 100% to 25% at 15 nM to 500 nM quantum dots. In the trypan blue cell viability
experiment, the viability range was from 100% to 60% at 15 nM to 500 nM
of quantum dots. Quantum dots were not mutagenic with and without metabolic
activation. No statistically significant changes in cell growth, population doubling
or cell morphology were found for subchronic treatment of human primary skin or
lung fibroblast cell lines with various Qdot® nanoparticles. In the Comet assay, no
significant DNA damage was seen across all tested quantum dot types at 50 nM.
Some DNA damage was observed at 500 nM, but was far below methyl methanesulfonate
(MMS) control. Based on the study results described above, CdSe/ZnSbased
Qdot® nanoparticles are non-toxic at concentrations used for most biological
applications (10 nM).
2185 GLOBAL GENE EXPRESSION PROFILING ANALYSIS OF
FOOD DEPRIVED MATERNAL AND FETAL MICE
LIVERS.
T. Ogawa 1, 2 , R. Rakwal 1, 2 , J. Shibato 2 , C. Sawa 1, 2 , T. Saito 1 , A. Murayama 1 ,
M. Kuwagata 2, 3 and S. Shioda 1, 2 . 1 Anti-aging Medicine, Showa University, Tokyo,
Japan, 2 Anatomy, Showa Unversity, Tokyo, Japan and 3 Laboratory of Pathology, Food
and Drug Safety Center, Kanagawa, Japan.
Accumulated human epidemiological evidence has led scientists to theorize that
undernutrition during gestation is an important early origin of adult diseases.
Animal models have successfully demonstrated that maternal diet could contribute
to some of adult diseases. Nevertheless, the mechanisms by which maternal diet
causes these long-term impacts remain poorly understood. Although undernutrition
is harmful in pregnant women, calorie restriction is a strategy proven to extend
healthy and maximum life span in adult. This opposite effect of nutritional condition
might provide us a hint to understand the mechanisms. In this direction, we
have initiated a study on global gene expression profiling (via DNA microarray) following
undernutrition, between adult and fetal tissues. Pregnant mice (C57BL/6J)
were exposed to food deprivation (FD) on gestation day (GD) 17, and caesarean
section was performed on GD18. Control mice were supplied with chow ad libitum
till sacrifice on GD18. Liver was collected from five control and six FD mothers.
Fetal liver was collected from two fetuses from each mother. Total RNA extracted
from mother and fetal livers for each control and treatment (FD) was
pooled in each group (control and FD), prior to DNA microarray analysis (Agilent
mouse whole genome 4 x 44K). Results revealed 3058 & 3126 up (>1.5 fold)- and
down (