Nianqing Liu

Mapping technique for biodistribution of elements in a model organism, Caenorhabditis elegans, after exposure to copper nanoparticles with microbeam synchrotron radiation X-ray fluorescence

To investigate the toxicological effects of nanomaterials, experimental studies on the absorption and accumulation in organisms are of broad interest. In the present study, Caenorhabditis elegans (C. elegans) was used as a “model” organism to investigate the bioaccumulation and toxicological effects of engineered copper nanoparticles with a scanning technique of microbeam synchrotron radiation X-ray fluorescence (μ-SRXRF). The adult hermaphrodite is anatomically simple with 959 somatic cells and 1 mm in length. The mapping results of the whole organism indicate that the exposure to copper nanoparticles can result in an obvious elevation of Cu and K levels, and a change of bio-distribution of Cu in nematodes. Accumulation of Cu occurs in the head and at a location 1/3 of the way up the body from the tail compared to the un-exposed control. In contrast, a higher amount of Cu was detected in other portion of worm body, especially in its excretory cells and intestine when exposed to Cu2+. The results compared well with total Cu levels in nematodes, which were 4.10 ± 0.54, 12.32 ± 0.49 and 5.22 ± 0.63 μg g−1 dry weight for the PBS, Cu2+ and Cu nanoparticle groups, respectively, measured by ICP-MS. The nondestructive and multi-elemental μ-SRXRF provides an important tool for mapping the elemental distribution in the whole body of a single tiny nematode at lower levels.

Copper ions influence the toxicity of β-amyloid(1-42) in a concentration-dependent manner in a Caenorhabditis elegans model of Alzheimer's disease.

Abstractβ-amyloid (Aβ) and copper play important roles in the pathogenesis of Alzheimer’s disease (AD). However, the behavioral correlativity and molecular mechanisms of Aβ and copper toxicity have been investigated less often. In the present study, we investigated the interaction and toxicity of Aβ1–42 and copper in the Aβ1–42 transgenic Caenorhabditis elegans worm model CL2006. Our data show that the paralysis behavior of CL2006 worms significantly deteriorated after exposure to 10−3 mol L−1 copper ions. However, the paralysis behavior was dramatically attenuated with exposure to 10−4 mol L−1 copper ions. The exogenous copper treatment also partially changed the homeostatic balance of zinc, manganese, and iron. Our data suggest that the accumulation of reactive oxygen species (ROS) was responsible for the paralysis induced by Aβ and copper in CL2006. The ROS generation induced by Aβ and copper appear to be through sod-1, prdx-2, skn-1, hsp-60 and hsp-16.2 genes.

Ytterbium and trace element distribution in brain and organic tissues of offspring rats after prenatal and postnatal exposure to ytterbium

Lanthanides, because of their diversified physical and chemical effects, have been widely used in a number of fields. As a result, more and more lanthanides are entering the environment and eventually accumulating in the human body. Previous studies indicate that the impact of lanthanides on brain function cannot be neglected. Although neurological studies of trace elements are of paramount importance, up to now, little data are provided regarding the status of micronutritional elements in rats after prenatal and long-term exposure to lanthanide. The aim of this study is to determine the ytterbium (Yb) and trace elements distribution in brain and organic tissues of offspring rats after prenatal and long-term exposure to Yb. Wistar rats were exposed to Yb through oral administration at 0,0.1, 2, and 40 mg Yb/kg concentrations from gestation day 0 through 5 mo of age. Concentrations of Yb and other elements (Mg, Ca, Fe, Cu, Mn, and Zn) in the serum, liver, femur, and brain regions (cerebral cortex, hippocampus, cerebellum, and the rest) of offspring rats at the age of 0 d, 25 d, and 5 mo were analyzed by inductively coupled plasma-mass spectrometry. The accumulation of Yb in the brain, liver, and femur is observed; moreover, the levels of Fe, Cu, Mn, Zn, Ca, and Mg in the brain and organic tissues of offspring rats are also altered after Yb exposure. This disturbance of the homeostasis of trace elements might induce adverse effects on normal physiological functions of the brain and other organs.

Delayed changes in T1-weighted signal intensity in a rat model of 15-minute transient focal ischemia studied by magnetic resonance imaging/spectroscopy and synchrotron radiation X-ray fluorescence

Previous studies have found that rats subjected to 15‐min transient middle cerebral artery occlusion (MCAO) show neurodegeneration in the dorsolateral striatum only, and the resulting striatal lesion is associated with increased T1‐weighted (T1W) signal intensity (SI) and decreased T2‐weighted (T2W) SI at 2–8 weeks after the initial ischemia. It has been shown that the delayed increase in T1W SI in the ischemic region is associated with deposition of paramagnetic manganese ions. However, it has been suggested that other mechanisms, such as tissue calcification and lipid accumulation, also contribute to the relaxation time changes. To clarify this issue, we measured changes in relaxation times, lipid accumulation, and elemental distributions in the brain of rats subjected to 15‐min MCAO using MRI, in vivo 1H MR spectroscopy (MRS), and synchrotron radiation X‐ray fluorescence (SRXRF). The results show that a delayed (2 weeks after ischemia) increase in T1W SI in the ischemic striatum is associated with significant increases in manganese, calcium, and iron, but without evident accumulation of MRS‐visible lipids or hydroxyapatite precipitation. It was also found that 15‐min MCAO results in acutely reduced N‐acetylaspartate (NAA)/creatine (Cr) ratio in the ipsilateral striatum, which recovers to the control level at 2 weeks after ischemia. Magn Reson Med, 2006.

Effect of iodine supplement on iodine status and 5'-deiodinase activity in the brain of neonatal rats with iodine deficiency

The weanling Wistar rats of iodine deficiency were divided into three groups for supplementation of different levels of iodine (iodine-excessive [IE], iodine-adequate [IA], and iodine-deficient [ID]), with a control group (C). The iodine content in the thyroid was determined by epithermal neutron activation analysis. The activities of 5′-deiodinase and 5-deiodinase in the brains were assayed by determining the conversion ratios of T4 to T3 and rT3, respectively. The thyroid hormones levels in serum were also tested. The results indicated that the ID group had a goiter containing a small amount of iodine, but the IE group had a slightly swollen thyroid with rich iodine; the concentration of iodine per unit mass of thyroid was lower in group IE than in groups IA and C. The highest 5′-deiodinase and lowest 5-deiodinase activities in group ID and the lowest 5′-deiodinase activity in group IE were found. The iodine deficiency or excess resulted in a compensated hypothyroid state. The results suggest that the iodine status and the deiodinases activities would become normal for the rats of iodine deficiency if adequate iodine is supplemented soon after birth. Meanwhile, it is also critical to avoid excessive intake of iodine to reduce the risk for overcorrecting.