Nanoparticles are currently used in a wide range of applications including industrially processes, consumer products, and as drug delivery vehicles. The potential toxicity of these nanoparticles in living organisms is concerning due to their ever-expanding applications and accumulation in the environment. The effects of properties of the human body on the potential harmful nature of these nanoparticles must be understood in order to ensure safety in workplaces and at-home products. In this thesis, the interactions between nanoparticles and the most abundant blood protein, serum albumin, were investigated. The effects of changing the aqueous environment was investigated over a range of different pH values and with different ionic salts dissolved in water. The effects of changing the nanoparticle substrate were investigated to determine if different nanoparticles affect proteins differently. Finally, the effects of changing the concentration of nanoparticles and the presence of protein were investigated in a model lung cell line in vitro. The studies over different pH values revealed that serum albumin was able to adsorb to the silica nanoparticle surface, and retained its secondary structure both as a function of pH and adsorption in a 2-hour time frame. However, adsorption was greater on the titanium dioxide nanoparticle surface and the protein lost secondary structure at acidic pH (pH 2.0). Studies with different ionic salts revealed a possible correlation between BSA adsorption and nanoparticle aggregation in that the attractive interactions between nanoparticles were least when the least amount of protein was adsorbed. To the nanoparticle surface. In vitro studies with A549 human adenocarcinoma lung cells were inconclusive in determining the potential toxicity of these nanoparticles, but preliminary results suggested that the addition of protein to the system decreased toxicity compared with nanoparticles alone. This research aims to inform the field of nanotechnology to investigate the safety and efficacy of nanoparticles before they reach the consumer.

Objective: We proposed that women who develop preeclampsia have a low ratio of 'protective' toxicity preventing activity (TxPA) to 'toxic' very low density lipoproteins (VLDL) late in pregnancy. Having confirmed this hypothesis, we then tested whether this low ratio would manifest itself early in the pregnancy of women who develop preeclampsia. Methods: Serially collected plasma from women who developed preeclampsia and from matched controls was assayed blind for TxPA, triglycerides, cholesterol, high-density lipoproteins, albumin, and nonesterified fatty acids (NEFA). Main Outcome Measures: Plasma concentrations of lipids, NEFA, and proteins which bind NEFA (TxPA and albumin) were measured in normal and preeclamptic women. These parameters were formulated prior to data collection because of the low albumin/triglyceride' ratios and the elevated NEFA levels reported to occur in preeclampsia. Results: In late pregnancy, TxPA was lower (1.82 ± 0.63 vs. 2.30 ± 0.40 g/dL, P = 0.008) and VLDL higher (292 ± 130 vs. 206 ± 60 mg/dL, P = 0.013) in preeclamptics than in controls. Discrimination analysis (TxPA and triglyceride), correctly classified 95% of the preeclamptics and 79% of the controls in late pregnancy. The ratio of TxPA to non-TxPA and triglyceride correctly classified 92% of the preeclamptics and 85% of the controls in early pregnancy. Conclusions: The ratio of TxPA to VLDL accurately distinguishes preeclamptic from normal pregnant women, suggesting that both these factors are involved in the development of preeclampsia.

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The supine posture has been shown to limit exercise-induced plasma volume expansion. Differences in hydrostatic pressure gradients between the standing and seated position indicate that treadmill exercise might promote a greater plasma volume expansion than cycle ergometer exercise. To test this hypothesis ten subjects performed intermittent high intensity exercise (4 min at 85% VO2max, 5 min at 40% VO2max repeated 8 times) on separate days on the treadmill and cycle ergometer. Changes in plasma volume expansion were calculated from changes in hematocrit and hemoglobin. Stroke volume (SV), trans-thoracic impedance (Z0), HR, and arterial blood pressure (non-invasive arm cuff, SBP & DBP) were assessed in the seated position before and postexercise. Zo increased (p<0.05) as subjects started exercise (both treadmill and cycling), indicating a reduction in central blood volume (CBV), which returned to baseline towards the end of exercise. Postexercise Zo returned to control levels within 30 min regardless of the previous exercise mode. A significant post-exercise hypotension was observed following cycle ergometer exercise (p<0.05) but not following treadmill exercise. Plasma volume increased 6.1±1.0% and 7.0 ± 1.1% (p<0.05) following treadmill and cycle ergometer exercise, respectively. The increase in PV was similar for both exercise modes. Initial differences in central blood volume disappeared over the course of the exercise protocol and during recovery, possibly indicating that there is a postural threshold and moving beyond it yields no further effect. The lack of differences between modes of exercise on plasma albumin content and Z0 indicate that the upright postures were not different from each other. As such, PV expansion following high intensity intermittent exercise appears to be independent of upright exercise mode.

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