Sub-lethal effects of titanium dioxide nanoparticles on the physiology and reproduction of zebrafish.

There are limited data on the sub-lethal physiological effects of titanium dioxide nanoparticles (TiO(2) NPs) in adult fishes, and the consequences of TiO(2) NP exposure on reproductive success are also unclear. This study aimed to examine the sub-lethal effects of a 14-d aqueous TiO(2) (TiO(2) NP, 0.1 or 1.0 mg l(-1); TiO(2) bulk, 1.0 mg l(-1)) exposure on the physiology and reproductive health of zebrafish. After the 14-d exposure, fish were examined for haematology, whole body electrolyte and trace metal profiles, biochemistry, and histopathology. Then, during a 21-d post exposure recovery period, effects of the TiO(2) exposure on reproductive success were evaluated. Whole body Ti concentrations increased significantly in fish exposed to both the 1.0 mg l(-1) TiO(2) NP and bulk TiO(2) compared to controls, but concentrations returned to control levels by the end of the recovery period. No change in erythrocyte counts were observed, but there was a two-fold decline in leukocyte counts in all TiO(2) treatment groups relative to time-matched controls. Whole body electrolyte and trace metal profiles were not affected by exposure to TiO(2), and there were no changes in Na(+)K(+)-ATPase activity in brain, gill or liver tissues. Total glutathione (GSH) levels in brain, gill and liver tissues were higher in fish exposed to TiO(2) NP (both 0.1 and 1.0 mg l(-1)) compared to bulk TiO(2) and control fish. Histological examination of gill, liver, brain and gonad tissues showed little evidence of treatment-related morphological change. At the end of the 14-d exposure adult zebrafish were able to reproduce; however, the cumulative number of viable embryos produced was lower in fish exposed to 1.0 mg l(-1) TiO(2) (both NP and bulk) by the end of the 21-d recovery period. Overall, this study showed limited toxicity of bulk or nano scale TiO(2) during the exposure; however reproduction was affected in both bulk and NP 1.0 mg l(-1) groups.

Effects of manufactured nanomaterials on fishes: a target organ and body systems physiology approach.

Manufactured nanomaterials (NM) are already used in consumer products and exposure modelling predicts releases of ng to low µg l(-1) levels of NMs into surface waters. The exposure of aquatic ecosystems, and therefore fishes, to manufactured NMs is inevitable. This review uses a physiological approach to describe the known effects of NMs on the body systems of fishes and to identify the internal target organs, as well as outline aspects of colloid chemistry relevant to fish biology. The acute toxicity data, suggest that the lethal concentration for many NMs is in the mg l(-1) range, and a number of sublethal effects have been reported at concentrations from c. 100 µg to 1 mg l(-1). Exposure to NMs in the water column can cause respiratory toxicity involving altered ventilation, mucus secretion and gill pathology. This may not lead, however, to overt haematological disturbances in the short term. The internal target organs include the liver, spleen and haematopoietic system, kidney, gut and brain; with toxic effects involving oxidative stress, ionoregulatory disturbances and organ pathologies. Some pathology appears to be novel for NMs, such as vascular injury in the brain of rainbow trout Oncorhynchus mykiss with carbon nanotubes. A lack of analytical methods, however, has prevented the reporting of NM concentrations in fish tissues, and the precise uptake mechanisms across the gill or gut are yet to be elucidated. The few dietary exposure studies conducted show no effects on growth or food intake at 10-100 mg kg(-1) inclusions of NMs in the diet of O. mykiss, but there are biochemical disturbances. Early life stages are sensitive to NMs with reports of lethal toxicity and developmental defects. There are many data gaps, however, including how water quality alters physiological responses, effects on immunity and chronic exposure data at environmentally relevant concentrations. Overall, the data so far suggest that the manufactured NMs are not as toxic as some traditional chemicals (e.g. some dissolved metals) and the innovative, responsible, development of nanotechnology should continue, with potential benefits for aquaculture, fisheries and fish health diagnostics.

Influence of birth weight on adult bone mineral density.

Bone mineral density (BMD) increases during growth until a peak is reached at maturity. The risk of development of postmenopausal osteoporosis depends on the peak bone density and the rate of its subsequent loss. To identify whether low weight at birth could affect the peak bone density, we measured BMD at both the lumbar spine and femoral neck using dual energy X-ray absorptiometry (DXA) in a group of women who had low weight at birth and in a control group of normal birth weight. There was no significant correlation between the weight at birth and the adult BMD. It appears, therefore, that low weight at birth does not influence the peak bone density and that prematurity is not a risk factor for osteoporosis.

Lymphocyte targeted ricin as a potential therapy for lymphoid malignancy. I. Targeting efficiency.

Lymphocytes were studied as vehicles to target the plant toxin ricin, to lymphoid tissue in rats. Ricin-loaded thoracic duct lymphocyte (TDL) migrated normally into lymph nodes (LN) at 0.5 h, but this process was arrested by 3 h after injection. Ricin was successfully targeted to lymphoid tissue as evidenced by a 4-fold increase in ricin-associated radioactivity in LN, a 10-fold increase in the Peyers patches, a doubling in the spleen and a 35% reduction of radioactivity in the liver compared with free ricin. Nevertheless this represented a considerable shortfall in the expected targeting efficiency. The main problem was found to be high in vivo elution of ricin from TDL (70% within 0.5 h of i.v injection). This and other aspects relevant to maximising targeting efficiency are discussed.

The toxicity, distribution and excretion of ricin holotoxin in rats.

The distribution and excretion of the plant toxin ricin were studied in rats after intravenous injection. 125I-labelled ricin was equal in toxicity to native ricin. Following injection, the liver was the major organ of localisation - 46% of injected dose at 0.5 h. The spleen and muscle were next with 9.9% and 13%, respectively, at 0.5 h. Ricin was relatively concentrated in the spleen (33% of injected dose/g of tissue) compared with the liver (7.4%/g) and the bone marrow (5.5%/g). The concentration in the lymph nodes was very low (1.2%/g). Ricin was quickly cleared from the animal; only 11% of the initial radioactivity remained 24 h later with 70% excreted in the urine. Excretion into the intestine via the bile duct was less than 5% by 24 h, 10-12% of the radioactivity was found in the intestinal contents or intestinal wall between 3 h and 12 h, and much of this was reabsorbed since less than 2% was recovered in faeces.