The effects of intraperitoneal administration of gold nanoparticles size and exposure duration on oxidative and antioxidants levels in various rat organs.

As one of the toxic mechanism of nanoparticles (NPs), the reactive oxygen species (ROS) generation which has been widely studied. Nevertheless, the link between GNPs and antioxidant and oxidative stress markers has not been well established. The effects of gold nanoparticles (GNPs) size and exposure duration on antioxidant and oxidative stress markers including reduced glutathione (GSH), super oxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), total antioxidant capacity and malondialdehyde (MDA) were evaluated in different rat organs. Adult male Wistar-Kyoto rats were randomly divided into 6 groups of 5 animals each. One group served as control and received vehicle only. The 10 nm GNPs were used in this study. The GNPs electron density and homogeneity in shape and size was evaluated. Dose of 50 µl of 10 nm GNPs in aqueous solution were administered to animals via intraperitoneal administration daily for exposure duration of 3 or 7 days. The rats were sacrificed 24 h after the last injection of GNPs. The specimens of liver, lung, kidney and heart were collected for biochemical analyses. The GPx, total antioxidant capacity, GSH and MDA levels significantly increased after administration of 10 nm GNPs for exposure duration of 3 and 7 days in the organs of rats compared with the control while the GR and SOD levels significantly decreased. The GNPs have the potential to interact with the biological system and cause undesirable effects. One of these damaging effects could be the disturbance in the natural balance between oxidative stress and antioxidant defense indices, which in turn can lead to various pathological effects. The changes in antioxidant and oxidative stress markers might be attributed to the production of ROS.

Elucidation of the effects of a high fat diet on trace elements in rabbit tissues using atomic absorption spectroscopy.

BACKGROUND: The mechanism of atherogenesis is not yet fully understood despite intense study in this area. The effects of high fat diet (HFD) on the changes of trace elements [iron (Fe), copper (Cu) and zinc (Zn)] in several tissues of rabbits have not been documented before. Thus, the aim of this study was to elucidate the changes in trace elements in several tissues of rabbits fed on HFD for a period of feeding of 10 weeks. RESULTS: The HFD group was fed a NOR rabbit chow supplemented with 1.0% cholesterol plus 1.0% olive oil. Fe, Cu and Zn concentrations were measured in four types of tissue from control and HFD rabbits using atomic absorption spectroscopy (AAS). Comparing HFD rabbits to control rabbits, we found that the highest percentage change of increase of Fe was 95% in lung tissue, while the lowest percentage change of increase of Fe was 7% in kidney tissue; the highest percentage change of decrease of Cu was 16% in aortic tissue, while the lowest percentage change of decrease of Cu was 6% in kidney tissue; and the highest percentage change of decrease of Zn was 71% in kidney tissue, while the lowest percentage change of decrease of Zn was 8% in lung tissue. CONCLUSIONS: These results suggest that Fe plays a major role in atherogenesis; it may accelerate the process of atherosclerosis probably through the production of free radicals, deposition and absorption of intracellular and extracellular lipids in the intima, connective tissue formation, smooth muscle proliferation, lower matrix degradation capacity and increased plaque stability. Furthermore, inducing anemia in HFD rabbits may delay or inhibit the progression of atherosclerosis. Cu plays a minor role in atherogenesis and Cu supplements may inhibit the progression of atherogenesis, perhaps by reducing the migration of smooth muscle cells from the media to the intima. Zn plays a major role in atherogenesis and that it may act as an endogenous protective factor against atherosclerosis perhaps by reducing lesion Fe content, intracellular and extracellular lipids in the intima, connective tissue formation, and smooth muscle proliferation. These results suggest that it may be possible to use the measurement of changes in trace elements in different tissues of rabbits as an important risk factor during the progression of atherosclerosis.

Biochemical changes of hemoglobin and osmotic fragility of red blood cells in high fat diet rabbits.

The aim of this study was to assess the effects of hyperlipidemia on auto-oxidation rate of hemoglobin (Hb; absorbance at 630 nm versus time), Hb derivatives and osmotic fragility of Red Blood Cells (RBCs). These parameters were measured in twenty five 12-week-old male New Zealand white rabbits fed on a High Fat Diet (HFD) for a feeding period of 10 weeks. We found that Hb concentration and RBC count were significantly decreased while white blood cell and platelet counts were significantly increased in HFD rabbits compared with control rabbits. The Total Cholesterol (TC) was significantly increased (p < 0.01) in HFD rabbits compared with control rabbits with percentage normalized change of 1198% and Low Density Lipoprotein Cholesterol (LDLC) significantly increased (p < 0.01) in HFD rabbits compared with control rabbits with percentage normalized change of 1591%. In HFD rabbits, oxyhemoglobin (HbO2) percentage was significantly decreased while met-hemoglobin (Met-Hb) percentage was significantly increased compared with control rabbits. The auto-oxidation rate was significantly higher in HFD rabbits compared with controls. Hyperlipidemia induced an increase in the osmotic fragility of RBCs and a decrease in their membrane elasticity compared with controls. This study suggests that hyperlipidemia may produce reactive oxygen species and other free radicals which increase the auto-oxidation rate of Hb and promote the conversion of HbO2 and the fractions of unstable Hb molecules to Met-Hb and carboxyhemoglobin. Increased platelet activation in hyperlipidemic rabbits may be of pathophysiological importance for the progression of atherosclerosis and thromboembolic complications. The increase in osmotic fragility of RBCs may be attributed to the disturbance of ionic motion through the membrane and the change in molecular properties of the membrane macromolecules.