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Nano TiO 2 has been widely used in food industry as a coloring agent, whether the application has adverse effects on stomach for humans and animals is rarely concerned. This study determined whether intragastric administration with nano TiO 2 every day for nine months cause gastric damages and dysfunction, and is associated with changes of stomach damage-related protein expression in mice. Our results suggested that nano TiO 2 exposure resulted in significant titanium accumulation in the stomach, reductions in daily food intake and water intake, stomach weight, and stomach indices. Importantly, mice exhibited severe gastric damages such as gastric mucosa atrophy, erosion, inflammatory cell infiltration and cell morphologic damages including apoptosis, and coupled with reductions of serum pepsin activity, stomach total acidity and H + concentration, and increases of serum gastrin concentration and gastric pH. Furthermore, these are associated with decreased expression of IκB, TFF 1, 2, and increased expression of NF-κB, TNF-α, IL-lβ, -6, -8, COX-2, and PGE2 in the stomach. The findings showed that gastric toxicity of mice induced by chronic exposure to nano TiO 2 may be associated with alterations of gastritis-related protein expression in mice. It implies that the potential adverse effects to digestive system health should be concerned. [ABSTRACT FROM AUTHOR]

The evaluation of toxicological effects of nanoparticles (NPs) is increasingly important due to their growing occupational use and presence as compounds in consumer products. Recent researches have demonstrated that long-term exposure to air particulate matter can induce cardiovascular events, but whether cardiovascular disease, such as cardiac damage, is induced by NP exposure and its toxic mechanisms is rarely evaluated. In the present study, when mice were continuously exposed to TiO 2 NPs at 2.5, 5 or 10 mg/kg BW by intragastric administration for 90 days, obvious histopathological changes, and great alterations of NF-κB and its inhibitor I-κB, as well as TNF-α, IL-1β, IL-6 and IFN-α expression were induced. The NPs significantly decreased Ca 2+ -ATPase, Ca 2+ /Mg 2+ -ATPase and Na + /K + -ATPase activities and enhanced NCX-1 content. The NPs also considerably increased CAMK II and α1/β1-AR expression and up-regulated p-PKCε and p-ERK 1/2 in a dose-dependent manner in the mouse heart. These data suggest that low-dose and long-term exposure to TiO 2 NPs may cause cardiac damage such as cardiac fragmentation or disordered myocardial fibre arrangement, tissue necrosis, myocardial haemorrhage, swelling or cardiomyocyte hypertrophy, and the inflammatory response was potentially mediated by NF-κB activation via the PKCε or ERK 1/2 signalling cascades in mice. [ABSTRACT FROM AUTHOR]

Although TiO 2 nanoparticles (NPs) exposure has been demonstrated to cross blood–testis barrier and accumulate in the testis resulting in the reduction of sperm numbers, limited data with respect to the molecular mechanism of decreased spermatogenesis caused by TiO 2 NP exposure. In this research, testicular damage, sperm number and alterations in testis-specific gene expressions in male mice induced by intragastric administration with TiO 2 NPs for six months were investigated. It was found out that TiO 2 NPs could migrate to cells, deposit in the testis and epididymis and thus cause damages to relevant organs, which are, to be more specific, the reductions of total sperm concentrations and sperm motility and an enhancement in the number of abnormal sperms in the cauda epididymis. Furthermore, the individual expression regarding to the mRNAs and proteins of testis-specific genes, including Cdc2, Cyclin B1, Dmcl, TERT, Tesmin, TESP-1, XPD and XRCCI, were significantly declined, whereas Gsk3-β and PGAM4 expressions were greatly elevated in mouse testis due to the exposures, which in fact implied that the reduced spermatogenesis may be involved in the alternated testis-specific gene expressions in those exposed male mice. [ABSTRACT FROM AUTHOR]

Numerous studies have indicated that nano-titanium dioxide (TiO 2 ) can induce neurotoxicity in vitro and in vivo , however, it is unclear whether nano-TiO 2 affects neurite outgrowth of hippocampal neurons. In order to investigate the mechanism of neurotoxicity, rat primary cultured hippocampal neurons on the fourth day of culture were exposed to 5, 15, and 30 μg/mL nano-TiO 2 for 24 h, and nano-TiO 2 internalization, dendritic growth, glutamate metabolism, expression of N-methyl- d -aspartate (NMDA) receptor subunits (NR1, NR2A and NR2B), calcium homeostasis, sodium current (I Na ) and potassium current (I K ) were examined. Our findings demonstrated that nano-TiO 2 crossed the membrane into the cytoplasm or nucleus, and significantly suppressed dendritic growth of primary cultured hippocampal neurons in a concentration-dependent manner. Furthermore, nano-TiO 2 induced a marked release of glutamate to the extracellular region, decreased glutamine synthetase activity and increased phosphate-activated glutaminase activity, elevated intracellular calcium ([Ca 2+ ]i), down-regulated protein expression of NR1, NR2A and NR2B, and increased the amplitudes of the I Na and I K . In addition, nano-TiO 2 increased nitric oxide and nitrice synthase, attenuated the activities of Ca 2+ -ATPase and Na + /K + -ATPase, and increased the ADP/ATP ratio in the primary neurons. Taken together, these findings indicate that nano-TiO 2 inhibits neurite outgrowth of hippocampal neurons by interfering with glutamate metabolism and impairing NMDA receptor function. [ABSTRACT FROM AUTHOR]

Abstract: In this study, Eu3+-doped nanocrystalline Ca10(PO4)6(OH)2 (Ca10− x Eu x (PO4)6(OH)2) with different particle sizes have been prepared by the thermal decomposition of precursors. Size-dependent microstructure could be observed in nanocrystalline Ca10− x Eu x (PO4)6(OH)2. The lattices of Ca10− x Eu x (PO4)6(OH)2 nanocrystals were more distorted in comparison with the bulk, and the smaller the particle size, the more distorted the lattices. Room temperature photoluminescence showed europium site preference was also size-dependent, with the majority of Eu3+ ions occupying Ca(II) sites in the bulk, but more and more Eu3+ ions occupying Ca(I) sites in Ca10− x Eu x (PO4)6(OH)2 with decreasing particle size. Fluorescent properties of Ca10− x Eu x (PO4)6(OH)2 were considered to be influenced by both microstructure and site preference of Eu3+ ions. An abnormal strong intensity of 5D0–7F0 transition was observed in bulk and larger Ca10− x Eu x (PO4)6(OH)2 nanocrystals, but the relative intensities of 5D0–7F0 transition to 5D0–7F1,2,3,4 transition of Eu3+ became weaker as the particle sizes decreased. As the particle sizes became smaller, the ratios of the red emission transition (5D0–7F2) to the orange emission transition (5D0–7F1) (R/O values) first increased by comparing the bulk sample with 96nm sample, and then decreased by comparing 96nm sample to 57nm sample. The quenching concentrations of Ca10− x Eu x (PO4)6(OH)2 samples increased with decreasing particle size. Possible mechanisms responsible for these phenomena were proposed. Since nanosized Ca10− x Eu x (PO4)6(OH)2 showed higher fluorescent intensities, higher R/O values and higher quenching concentrations, this material is considered to be a promising phosphor. [Copyright &y& Elsevier]

Abstract: Lead (Pb2+) is a well-known highly toxic element. The mechanisms of the Pb2+ toxicity are not well understood for photosynthesis. In this paper, we reported the effect of Pb2+ on light absorption, distribution and conversion of spinach chloroplast by spectroscopy, and photochemical reaction activities. Several effects of Pb2+ were observed: (1) the absorption peak intensity of chloroplast obviously decreased in red and blue region and produced optical flattering; (2) fluorescence quantum yield nearby 680nm of chloroplast greatly declined; (3) the excitation band nearby 440nm of chloroplast significantly descended; (4) Pb2+ treatments reduced of the rate of whole chain electron transport, photochemical activities of PSII DCPIP photoreduction and oxygen evolution, but the photoreduction activities of PSI were little changed. Together, the studies of the experiments showed that Pb2+ decreased absorption of light on spinach chloroplast and inhibited excitation energy to be absorbed by LHCII and transferred to PSII, then reduced the conversion from light energy to electron energy, and decelerated electron transport, water photolysis and oxygen evolution. [Copyright &y& Elsevier]

Abstract: A direct interaction of lead (Pb) with kidney DNA from silver crucian carp (Carassius auratus gibelio) has been systematically studied in vitro using multi-techniques, including UV–vis absorption, extended X-ray absorption fine structure, vacuum ultraviolet circular dichroism spectral methods and gel electrophoresis. We find that Pb is bound with four oxygen or nitrogen atoms of DNA in its fresh shell at the distances of 2.64Å. Additionally, Pb may bind to the oxygen atom of nucleic acid or nitrogen atom of base pairs of DNA in that obvious changes in the secondary structure of DNA are found after Pb treatment. However, this direct interaction of Pb with DNA do not cause DNA cleavage in vitro. [Copyright &y& Elsevier]

Abstract: A rare earth element (REE) hyperaccumulator, Dicranopteris dichotoma, sampled from an REE mining area in South-Jiangxi region, was chosen for analysis of 15 REEs at subcellular and molecular levels by inductively coupled plasma-mass spectrometry (ICP-MS). The sum of the concentrations of 15 REEs (∑REEs) of D. dichotoma leaf was about 0.1% dry mass. Results indicated that the ∑REEs of different subcellular fractions of D. dichotoma leaf were cell walls>organelles>the ‘soluble’ fraction (i.e., cytosol and vacuoles)>cell membranes. ICP-MS results also showed that REEs existed in chlorophylls and lutein, though REE concentrations in carotene and pheophytin were both lower than the procedural blank levels. The ∑REEs of crude lipopolysaccharide and Ribulose 1,5-bisphosphate carboxylase/oxygenase (Rubisco) obtained from D. dichotoma leaf were 1200 and 343 mg/kg, respectively. The extended X-ray absorption fine structure (EXAFS) study of D. dichotoma chlorophyll a indicated that yttrium was bound to the porphyrin ring of chlorophyll a, and one yttrium atom was surrounded by four nitrogen atoms with the average yttrium–nitrogen bond length being 0.236 nm. These data might be useful for understanding of the physiological role of REEs in hyperaccumulator D. dichotoma. [Copyright &y& Elsevier]

Abstract: By optimizing chromatographic conditions of an ion chromatographic system, we identified and measured the major inorganic and organic anions (chloride, nitrate, malate, sulfate, phosphate and citrate) in the xylem saps of two contrasting tolerant oilseed rape (Brassica juncea L.) varieties (the high Cd-accumulating genotype Xikou Huazi and the low Cd-accumulating genotype Liangting Huazi). Cadmium concentrations in xylem saps were determined by graphite furnace atomic absorption spectrometry. By analyzing the relationship between anion and cadmium concentrations, we considered that the relatively low phosphate concentrations in Xikou Huazi xylem saps might relate to the relatively high xylem transport of Cd for this genotype, and malate in oilseed rape xylem saps seemed to participate in the long-distance Cd translocation process. Our work might not only be very useful for understanding the mechanisms of Cd hyperaccumulation for Xikou Huazi, but also very beneficial for future application of Xikou Huazi in phytoremediation. [Copyright &y& Elsevier]

Prevention of obesity-induced cognitive decline is an important public health goal. Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has beneficial potentials including antioxidant and neuroprotective activity. Evidence shows that anthocyanins can activate AMP-activated protein kinase (AMPK), a critical mediator of autophagy induction. This study investigated whether PSPC could improve cognitive function through regulating AMPK/autophagy signaling in HFD-fed obese mice. Our results showed that PSPC significantly ameliorated obesity, peripheral insulin resistance and memory impairment in HFD-fed mice. Moreover, enhanced autophagy was observed, along with the decreased levels of protein carbonyls, malondialdehyde and reactive oxygen species (ROS) in the hippocampus of HFD-fed mice due to PSPC administration. PSPC also promoted hippocampal brain-derived neurotrophic factor (BDNF) expression and neuron survival in HFD-fed mouse. These improvements were mediated, at least in part, by the activation of AMPK, which was confirmed by metformin treatment. It is concluded that PSPC has great potential to improve cognitive function in HFD-fed mice via AMPK activation that restores autophagy and protects against hippocampal apoptosis. [ABSTRACT FROM AUTHOR]

The evaluation of toxicological effects of nanoparticulate matter is increasingly important due to their growing occupational use and presence as compounds in consumer products. Numerous studies have shown that exposure to nanosized particles lead to systemic inflammation in experimental animals, but whether long-term exposure to nanosized particles induces atherogenesis is rarely evaluated. In the current study, mice were continuously exposed to TiO 2 nanoparticles (NPs) at 1.25, 2.5, or 5 mg/kg body weight, administered by nasal instillation for nine consecutive months, and the association between serum parameter changes and atherosclerosis in mice were investigated. The present findings suggested that chronic exposure to TiO 2 NPs resulted in atherogenesis coupling with pulmonary inflammation, increased levels of serum triglycerides, glucose, total cholesterol, low-density lipoprotein cholesterol, advanced glycation end products, reactive oxygen species, NAD(P)H oxidases 4, C-reaction protein, E-selectin, endothelin-1, tissue factor, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, and reduced levels of serum high-density lipoprotein cholesterol, nitric oxide and tissue plasminogen activator. Our study suggests an association of long-term exposure to TiO 2 NPs with atherosclerosis and pulmonary inflammation. This finding demonstrates the hypothesized role of TiO 2 NPs as a risk factor for atherogenesis. [ABSTRACT FROM AUTHOR]

Highlights: [•] Phoxim exposure resulted in decrease of the cocooning rate of B. mori. [•] TiO2 NPs could increase the cocooning rate of B. mori under phoxim toxicity. [•] Phoxim exposure damaged silk gland and decreased Fib-L, Ser2, Ser3, and P25 expressions. [•] TiO2 NPs could relieve silk gland damage and increase Fib-L, Ser2, Ser3, and P25 expressions. [Copyright &y& Elsevier]

Highlights: [•] We performed a DGE analysis of the midgut in the B. mori at 24h exposed to phoxim. [•] The impact on detoxification, apoptosis and immune defense were addressed. [•] Phoxim exposure leads to increased apoptosis. [Copyright &y& Elsevier]

Highlights: [•] TiO2 NPs exposure resulted in hippocampus injury and decreased spatial recognition of mice. [•] TiO2 NPs exposure resulted in decreased long-term potentiation. [•] TiO2 NPs exposure caused down-regulation of NR2A and NR2B expression in hippocampus. [•] TiO2 NPs decreased expression of CaMKIV, CREB-1 and FosB/DFosB. [Copyright &y& Elsevier]

Highlights: [•] Exposure to lanthanides impaired renal function in mice. [•] Exposure to lanthanides induced cell necrosis in kidney. [•] Exposure to lanthanides promoted ROS accumulation in kidney. [•] Exposure to lanthanides caused the reduction of antioxidant capacity in kidney. [•] The order of kidney damages was Ce exposure>Nd exposure>La exposure. [Copyright &y& Elsevier]

Abstract: Numerous studies have demonstrated that the brain is one of the target organs in acute or chronic titanium dioxide (TiO2) nanoparticles (NPs) toxicity, and oxidative stress plays an important role in this process. However, whether brain oxidative injury responds to TiO2 NPs by activating the P38-nuclear factor-E2-related factor-2 (Nrf-2) pathway is not fully understood. The present study aimed to examine activation of the P38-Nrf-2 signaling pathway associated with oxidative stress in the mouse brain induced by intranasal administration of TiO2 NPs for 90 consecutive days. Our findings indicate that TiO2 NPs caused overproliferation of spongiocytes and hemorrhage in the mouse brain. Furthermore, TiO2 NPs significantly activated p38, c-Jun N-terminal kinase, nuclear factor kappa B, Nrf-2 and heme oxygenase-1 expression in the brain, which in turn, led to increased production of reactive oxygen species, as well as lipid, protein and DNA peroxidation. These findings suggest that TiO2 NPs-induced oxidative damage in the mouse brain may occur via the p38-Nrf-2 signaling pathway. Therefore, application of TiO2 NPs in the environment should be performed with caution. [Copyright &y& Elsevier]

Highlights: [•] Exposure to TiO2 NPs could cross blood–testis barrier and be accumulated in testis. [•] Exposure to TiO2 NPs caused testis and sperm lesions in male mice. [•] Exposure to TiO2 NP decreased sperm numbers and sperm motility in male mice. [•] Exposure to TiO2 NP resulted in imbalance of sex hormones in male mice. [•] Exposure to TiO2 NP caused alteration of 142 genes expression of known function in testis. [ABSTRACT FROM AUTHOR]

Abstract: Although numerous studies have described the accumulation of titanium dioxide nanoparticles (TiO2 NPs) in the liver, kidneys, lung, spleen, and brain, and the corresponding damage, it is unclear whether or not TiO2 NPs can be translocated to the ovary and cause ovarian injury, thus impairing fertility. In the current study, ovarian injury and gene-expressed characteristics in female mice induced by intragastric administration of TiO2 NPs (10mg/kg) for 90 consecutive days were investigated. Our findings indicated that TiO2 NPs can accumulate in the ovary and result in ovarian damage, cause an imbalance of mineral element distribution and sex hormones, decrease fertility or the pregnancy rate and oxidative stress in mice. Microarray analysis showed that in ovaries from mice treated with TiO2 NPs compared to controls, 223 genes of known function were up-regulated, while 65 ovarian genes were down-regulated. The increased expression of Cyp17a1 following TiO2 NPs treatment suggested that the increase in estradiol biosynthesis may be a consequence of increased TiO2 NPs. In addition, the elevated expression of Akr1c18 implied that progesterone metabolism was accelerated, thus causing a decrease in the progesterone concentration. Taken together, the apparent regulation of key ovarian genes supports the hypothesis that TiO2 NPs directly affects ovarian function. [Copyright &y& Elsevier]

Abstract: Exposure to titanium dioxide nanoparticles (TiO2 NPs) has been demonstrated to result in pulmonary inflammation in animals; however, very little is known about the molecular mechanisms of pulmonary injury due to TiO2 NPs exposure. The aim of this study was to evaluate the oxidative stress and molecular mechanism associated with pulmonary inflammation in chronic lung toxicity caused by the intratracheal instillation of TiO2 NPs for 90 consecutive days in mice. Our findings suggest that TiO2 NPs are significantly accumulated in the lung, leading to an obvious increase in lung indices, inflammation and bleeding in the lung. Exposure to TiO2 NPs significantly increased the accumulation of reactive oxygen species and the level of lipid peroxidation, and decreased antioxidant capacity in the lung. Furthermore, TiO2 NPs exposure activated nuclear factor-κB, increased the levels of tumor necrosis factor-α, cyclooxygenase-2, heme oxygenase-1, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-18, interleukin-1β, and CYP1A1 expression. However, TiO2 NPs exposure decreased NF-κB-inhibiting factor and heat shock protein 70 expression. Our results suggest that the generation of pulmonary inflammation caused by TiO2 NPs in mice is closely related to oxidative stress and the expression of inflammatory cytokines. [Copyright &y& Elsevier]

Abstract: Phoxim insecticide is widely used in agriculture, which is toxic to insect pests and nontarget organisms. The phoxim poisoning is hard to prevent for silkworms. TiO2 NPs have been widely applied in whitening, brightening foods, toothpaste or sunscreens, and orally-administered drugs. However, whether TiO2 NPs can increase resistance of silkworm to phoxim poisoning has not been reported. The results demonstrated that added TiO2 NPs significantly decreased reduction of protein, glucose and pyruvate contents, lactate dehydrogenase, succinate dehydrogenase and malate dehydrogenase activities, and attenuated increases of free amino acids, urea, uric acid and lactate levels, activities of protease, alanine aminotransferase and aspartate aminotransferase in the hemolymph of silkworms caused by phoxim exposure. From the present study, it is clearly evident that added TiO2 NPs may relieve toxic impacts of phoxim insecticide on silkworm metabolism, which in turn may result in an increase in silk yield. [Copyright &y& Elsevier]

Abstract: The accumulation of intracellular sodium ions changes the ratio of K+:Na+ under salt stress, which seems to affect the bioenergetic processes of photosynthesis. However, very little work has been done to evaluate the photosynthetic damage to maize resulting from a combination of salt stress and K+ deficiency. Thus, our study investigated the effects of a combination of salt stress and K+ deficiency on chlorophyll (Chl) fluorescence in maize seedlings by a dual-wavelength pulse-amplitude modulated fluorescence monitoring system. The results showed that the reductions in plant growth, Chl, carotenoids, K+, Mg2+, maximum quantum efficiency (Fv/Fm), quantum yield (Y(II)), non-photochemical quenching (such as NPQ and qN) and photochemical quenching (such as qP and qL) of photosystem II (PSII), photochemical efficiency (Y(I)) of photosystem I (PSI) and non-photochemical quantum yield of PSI accepted side (Y(NA)), and electron transport rates of two photosystems of maize seedlings caused by a combination of salt stress and K+ deficiency were greater than those of each individual stress. Moreover, significant increases in Na+, Cl− and the parameters of quantum yield of energy dissipation of two photosystems, including Y(NPQ), Y(NO), and Y(ND), of maize leaves subjected to the combined stresses were observed. This implied that a combination of salt stress and K+ deficiency impaired the light reaction pathways of PSI and II in maize seedlings. [Copyright &y& Elsevier]

Abstract: Numerous studies have demonstrated that damage of kidney of mice can be caused by exposure to titanium dioxide nanoparticles (TiO2 NPs). However, the molecular mechanism of TiO2 NPs-induced nephric injury remains unclear. In this study, the mechanism of nephric injury in mice induced by an intragastric administration of TiO2 NPs was investigated. The results showed that TiO2 NPs were accumulated in the kidney, resulting in nephric inflammation, cell necrosis and dysfunction. Nucleic factor-κB was activated by TiO2 NPs exposure, promoting the expression levels of tumor necrosis factor-α, macrophage migration inhibitory factor, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-18, interleukin-1β, cross-reaction protein, transforming growth factor-β, interferon-γ and CYP1A1, while heat shock protein 70 expression was inhibited. These findings implied that TiO2 NPs-induced nephric injury of mice might be associated with alteration of inflammatory cytokine expression and reduction of detoxification of TiO2 NPs. [Copyright &y& Elsevier]

Abstract: Previous studies demonstrate that the exposure to titanium dioxide nanoparticles (TiO2 NPs) damages the central nervous system of mice; however, very little is known about the effects of TiO2 NPs on hippocampal apoptosis or its molecular mechanism. The present study investigated the molecular mechanism associated with hippocampal apoptosis in mice induced by intragastric administration of TiO2 NPs for consecutive 60 days. Our findings indicate that TiO2 NPs accumulate in the mouse hippocampus, and this accumulation, in turn, led to hippocampal apoptosis and impairment in spatial recognition memory in mice. In addition, TiO2 NPs significantly activated caspase-3 and -9, inhibited Bcl-2, and promoted the levels of Bax and cytochrome c. Furthermore, TiO2 NPs induced accumulation of reactive oxygen species in the mouse hippocampus. These findings suggest that TiO2 NP-induced apoptosis in the mouse hippocampus may result from an intrinsic pathway, and workers and consumers should take great caution when handling nanomaterials. [Copyright &y& Elsevier]

Abstract: With their widespread application in agriculture, industry, culture, medicine, and daily life, lanthanide compounds are being brought into the ecological environment and human body through food chains. It is important to know the acute and chronic effects of lanthanides on the environment, nature balance, and the human body after their entry into bodies and the environment. Lanthanides have been demonstrated to cause spleen apoptosis and decreased immunity of mice, but very little is known about the molecular aspects of these mechanism. In order to understand the spleen apoptotic mechanism induced by intragastric administration of 2, 10 and 20mgkg−1 body weight CeCl3 for consecutive 60d, we investigated the cerium accumulation, apoptosis, the expression levels of the apoptosis-related cytokines into apoptosis-related genes and proteins. The results demonstrated that cerium had obvious accumulation in the mouse spleen, leading to the significant increase of the spleen indices and splenocyte apoptosis. Furthermore, CeCl3 could effectively activate caspase-3 and -9, decrease the Bcl-2 the levels of gene and protein, and increase the levels of Bax, and cytochrome c genes and their protein expressions, and promote reactive oxygen species production. It implied CeCl3-induced apoptosis in the mouse spleen via intrinsic pathway. Our findings suggest the need for great caution to handle the lanthanides for workers and consumers. [Copyright &y& Elsevier]

Abstract: While the hepatocyte apoptosis induced by TiO2 nanoparticules (NPs) has been demonstrated, very little is known about the molecular mechanisms underlying this mouse liver apoptosis. In order to understand the hepatocyte apoptosis induced by intragastric administration of TiO2 NPs for consecutive 60 days, the hepatocyte apoptosis, various oxidative stress parameters and the stress-related gene expression levels were assayed for the mouse liver. 60 days of TiO2 NPs exposure, hepatocyte apoptosis in the liver could be observed, which was followed by increased reactive oxygen species accumulation, and decreased the stress-related gene expression levels of superoxide dismutase, catalase, glutathione peroxidase, metallothionein, heat shock protein 70, glutathione S transferase, P53, and transferrin; and the significant enhancement of the cytochrome p450 1A expression level. It implied that hepatocyte apoptosis, oxidative stresses, and alteration of expression levels of the genes related with TiO2 NPs detoxification/metabolism regulation and radical scavenging action. Therefore, the application of TiO2 NPs and exposure effects especially on human liver for long-term and low-dose treatment should be cautious. [Copyright &y& Elsevier]

Abstract: Titanium dioxide nanoparticles (TiO2 NPs) are now in daily use including popular sunscreens, toothpastes, and cosmetics. However, the effects of TiO2 NPs on human body, especially on the central nervous system, are still unclear. The aim of this study was to determine whether TiO2 NPs exposure results in persistent alternations in nervous system function. ICR mice were exposed to TiO2 NPs through intragastric administration at 0, 5, 10 and 50 mg/kg body weight every day for 60 days. The Y-maze test showed that TiO2 NPs exposure could significantly impair the behaviors of spatial recognition memory. To fully investigate the neurotoxicological consequence of TiO2 NPs exposure, brain elements and neurochemicals were also investigated. The contents of Ca, Mg, Na, K, Fe and Zn in brain were significantly altered after TiO2 NPs exposure. Moreover, TiO2 NPs significantly inhibited the activities of Na+/K+-ATPase, Ca2+-ATPase, Ca2+/Mg2+-ATPase, acetylcholine esterase, and nitric oxide synthase; the function of the central cholinergic system was also noticeably disturbed and the contents of some monoamines neurotransmitters such as norepinephrine, dopamine and its metabolite 3, 4-dihydroxyphenylacetic acid, 5-hydroxytryptamine and its metabolite 5-hydroxyindoleacetic acid were significantly decreased, while the contents of acetylcholine, glutamate, and nitric oxide were significantly increased. These first findings indicated that exposure to TiO2 NPs could possibly impair the spatial recognition memory ability, and this deficit may be possibly attributed to the disturbance of the homeostasis of trace elements, enzymes and neurotransmitter systems in the mouse brain. Therefore, the application of TiO2 NPs and exposure effects especially on human brain for long-term and low-dose treatment should be cautious. [Copyright &y& Elsevier]

Abstract: Nanoparticulate titanium dioxide (TiO2) has been demonstrated to decrease immunity of mice, but very little is known about the injury of spleen involved immunomodulation and its molecular mechanism. In order to understand the spleen injury induced by intraperitoneal injection of TiO2 nanoparticules (NPs) for consecutive 45 days, the spleen pathological changes, apoptosis, the expression levels of the apoptotic genes and their proteins, and oxidative stress in the mouse spleen were investigated. The results demonstrated that TiO2 NPs had obvious accumulation in the mouse spleen, leading to congestion and lymph nodule proliferation of spleen tissue, and splenocyte apoptosis. TiO2 NPs effectively activated caspase-3 and -9, decreased the Bcl-2 the levels of gene and protein, and increase the levels of Bax, and cytochrome c genes and their protein expression, promoted ROS accumulation. Taken together, this study indicated that TiO2 NPs-induced apoptosis in the mouse splenocyte via mitochondrial-mediated pathway. These findings provide strong evidence that the TiO2 NPs can induce the spleen pathological changes, apoptosis, leading to the reduction of immunity of mice. [Copyright &y& Elsevier]

Abstract: In an effort to examine liver injury, immune response, and other physiological effects in mice caused by intragastric administration of nanoparticulate anatase titanium dioxide (5nm), we assessed T lymphocytes, B lymphocyte and NK lymphocyte counts, hematological indices, biochemical parameters of liver functions, and histopathological changes in nanoparticulate titanium dioxide -treated mice. Indeed, mice treated with higher dose nanoparticulate titanium dioxide displayed a reduction in body weight, an increase in coefficients of the liver and histopathological changes in the liver. Specifically, in these nanoparticulate titanium dioxide -treated mice, interleukin-2 activity, white blood cells, red blood cells, haemoglobin, mean corpuscular haemoglobin concentration, thrombocytes, reticulocytes, T lymphocytes (CD3+, CD4+, CD8+), NK lymphocytes, B lymphocytes, and the ratio of CD4 to CD8 of mice were decreased, whereas NO level, mean corpuscular volume, mean corpuscular haemoglobin, red (cell) distribution width, platelets, hematocrit, mean platelet volume of mice were increased. Furthermore, liver functions were also disrupted, as evidenced by the enhanced activities of alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, lactate dehydrogenase and cholinesterase, an increase of the total protein, and the reduction of ratio of albumin to globulin, the total bilirubin, triglycerides, and the total cholesterol levels. These results suggested that the liver function damage observed in mice treated with higher dose nanoparticulate titanium dioxide is likely associated with the damage of haemostasis blood system and immune response. However, low dose nanoparticulate anatase TiO2 has little influences on haemostasis blood system and immune response in mice. [Copyright &y& Elsevier]

Abstract: The organ-toxicity of high-dose lanthanides on organisms had been recognized, but very little is known about the injury of immune organ such as spleen induced by Ln. In order to understand the splenic toxicity of Ln, various biochemical and chemical parameters were assayed in the mouse spleen. Abdominal exposure to LaCl3, CeCl3, and NdCl3 at dose of 20mg/kg body weight caused splenomegaly and oxidative stress to the spleen. Evident Ln deposition, congestion, mitochondria swelling, and apoptosis in the spleen could be observed, followed by increased generation of reactive oxygen species, lipid peroxidation and SOD activity, and decreased GSH-Px activity as well as nonenzymatic antioxidants such as glutathione and ascorbic acid content. In addition, the high amount of NO and increased NOS activities caused by Ln were measured. Furthermore, both Ce3+ and Nd3+ exhibited higher oxidative stress and toxicity on spleen than La3+, and Ce3+ caused more serve splenocyte injuries and oxidative stress than Nd3+, implying that the difference in the splenic injuries caused by Ln was related to the number of 4f electrons of Ln. [Copyright &y& Elsevier]

Abstract: In order to study the mechanisms underlying the effects of TiO2 nanoparticles on the brain, ICR mice were injected with nanoparticulate anatase TiO2 (5nm) of various doses into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of nanoparticulate anatase TiO2 and levels of neurochemicals in the brain. The results showed that high-dose nanoparticulate anatase TiO2 could induce some neurons to turn into filamentous shapes and others into inflammatory cells. The concentration of nanoparticulate anatase TiO2 in the brain was increased as increases in nanoparticulate anatase TiO2 dosages used. The oxidative stress and injury of the brain occurred as nanoparticulate anatase TiO2 appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total anti-oxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the reduction of glutamic acid, and the downregulated level of acetylcholinesterase activities. We concluded that TiO2 nanoparticles injected at the abdominal cavity could be translocated into the brain and in turn caused the brain injury. [Copyright &y& Elsevier]

Abstract: Nano-TiO2 and superoxide dismutase (SOD, EC 1.15.1.1) have been added to cosmetics and used to prevent injury of skin from UV-radiation, which might be related to the decrease of oxidative damage of skin. In previous studies we had proven that nano-anatase could increase the activity of SOD and decrease the oxidative damage in vivo. The mechanisms by which nano-anatase promoted SOD activity, however, are still not clearly understood. In the present work, nano-anatase in various concentrations was added to SOD from rat erythrocytes in vitro to gain insight into the mechanism of molecular interactions between nano-anatase and SOD by various spectral methods, suggesting that the reaction between SOD and nano-anatase was two-order, which meant that the SOD activity was greatly increased by low concentration of nano-anatase and inhibited by high concentration of nano-anatase. The spectroscopic assays suggested that the nano-anatase was determined to directly bind to SOD; the binding site of nano-anatase to SOD was 0.256 and the binding constants were 6.54×105 and 3.6×105 Lmol−1; Ti was bound with three oxygen or nitrogen atoms and a sulfur atoms of amino acid residues at the Ti–O(N) and Ti–S bond lengths of 1.86 and 2.37Å, respectively, the binding nano-anatase entirely altered the secondary structure of SOD. It implied that the nano-anatase coordination created a new metal ion-active site form in SOD, thus leading to an enhancement in SOD activity. [Copyright &y& Elsevier]

Abstract: Previous researches approved that photocatalysis activity of nano-TiO2 could obviously increase photosynthetic effects of spinach, but the mechanism of improving light energy transfer and conversion is still unclear. In the present we investigated effects of nano-anatase TiO2 on the spectral responses and photochemical activities of D1/D2/Cyt b559 complex of spinach. Several effects of nano-anatase TiO2 were observed: (1) UV–vis spectrum was blue shifted in both Soret and Q bands, and the absorption intensity was obviously increased; (2) resonance Raman spectrum showed four main peaks, which are ascribed to carotene, and the Raman peak intensity was as 6.98 times as that of the control; (3) the fluorescence emission peak was blue shifted and the intensity was decreased by 23.59%; (4) the DCPIP photoreduction activity showed 129.24% enhancement; (5) the oxygen-evolving rate of PS II was elevated by 51.89%. Taken together, the studies of the experiments showed that nano-anatase TiO2 had bound to D1/D2/Cyt b559 complex, promoted the spectral responses, leading to the improvement of primary electron separation, electron transfer and light energy conversion of D1/D2/Cyt b559 complex. [Copyright &y& Elsevier]