Acute titanium dioxide nanoparticles exposure impaired spatial cognitive performance through neurotoxic and oxidative mechanisms in Wistar rats.

CONTEXT: Titanium dioxide nanoparticles (TiO2-NPs) are used in many commercial products. However, their effects on human and animal organism remained to be clarified. OBJECTIVE: The present study aimed to investigate the effects of TiO2-NPs on the behavioural performance, monoamine neurotransmitters and oxidative stress in the rat brain. MATERIAL AND METHODS: Rats were injected intravenously with a single dose of TiO2-NPs (20 mg/kg body weight) and were subjected to cognitive and emotional tests using Morris water maze and elevated plus maze. RESULTS: Cognitive capacity as well as the emotional reactivity were significantly disrupted, in TiO2-NPs-administered rats compared to control group. These behavioural effects were correlated with changes in brain neurotransmitter contents reflected by a significant increase in dopamine and a decrease in serotonin levels. TiO2-NPs also induced oxidative stress in the brain manifested by increased levels of H2O2 and malondialdehyde, associated with antioxidant enzymes activities disturbance, in particular, superoxide dismutase and catalase activities. Moreover, TiO2-NPs administration caused histological damages in the brain tissue with abundant lymphocytic clusters, capillary dilations, vascular congestion and oedema. CONCLUSIONS: Acute intravenous injection of TiO2-NPs impaired behaviour performances through brain biochemical and structural changes and precautions should be taken to their usage in food additive and medical applications.

Effect of nano-sized SiO2 particles on the cognitive function and biochemical response.

Several in vitro studies have convincingly demonstrated that SiO2NPs mediated cytotoxicity, which was dose-, time- and size-dependent. The data on in vivo toxicity of SiO2NPs are even more contradictory. In the present study, we investigated the effects of sub-acute exposure to SiO2-NPs on spatial learning and memory, the biochemical parameters and the histology of organs. Rats were injected intravenously with a single dose of SiO2-NPs (20 mg/kg) during five consecutive days. The analysis of spatial memory in the Morris water maze showed that SiO2-NPs disrupt the cognitive abilities of rats. Moreover, SiO2-NPs could changes the blood counts. However, biochemical markers remained unchanged. Histological examination showed that SiO2-NPs induced pathological changes in rat organs. In this finding NPs were shown to cause granuloma formation and inflammatory cells infiltration in the liver.

Zinc prevents hematological and biochemical alterations induced by static magnetic field in rats.

The present study was undertaken in order to investigate the effect of subchronic exposure of rats to static magnetic field (SMF) and/or zinc treatment on the selected hematological and biochemical parameters. Metallothioneins (MT) and zinc content in kidney and liver were studied. The exposure of rats to SMF for 1h/day during 30 consecutive days induced an increase in hemoglobin concentration, white blood cell count (WBC), red blood cell count (RBC) and platelet number. By contrast, hematocrit remained unchanged. The same treatment also increased the serum lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. However, the creatinine and urea concentrations were similar to those of controls. On the other hand, renal and hepatic zinc levels were not altered in SMF treated-rats. SMF exposure induced MT synthesis in the liver and kidney. Zinc administration (40 mg/l for 30 consecutive days, in drinking water) had no effect on hematological and biochemical parameters. However, hepatic and renal zinc content and MT levels were increased. Zinc prevented the increase in serum transaminase activities, and WBC and platelet counts induced by SMF. However, the elevation of the LDH, hemoglobin and RBC levels induced by SMF exposure was not suppressed. MT concentrations in both tissues were potentiated by zinc administration in SMF-exposed rats. It is suggested that zinc supplementation could prevent toxic effects of SMF probably by its anti-oxidant properties.