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The widespread application of lanthanoids (Lns) in manufacturing industries has raised occupational and environmental health concerns about the possible increased health risks to humans exposed to Lns in their working and living environments. Numerous studies have shown that exposures to Ln cause pulmonary injury in animals, but very little is known about the molecular mechanisms of the pulmonary inflammation caused by cerium chloride (CeCl3) exposure. In this study, we evaluated the oxidative stress and molecular mechanism underlying with the pulmonary inflammation associated with chronic lung toxicity in mice treated with nasally instilled CeCl3 for 90 consecutive days. Our findings suggest that significant cerium accumulated in the lung, leading the obvious increase of the lung indices, significant increases in inflammatory cells and levels of lactate dehydrogenase, alkaline phosphate, and total protein, overproduction of reactive oxygen species and peroxidation of lipids, reduced antioxidant capacity, and pulmonary inflammation. CeCl3 exposure also activated nuclear factor κB, increased the expression 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. However, CeCl3 reduced the expression of nuclear factor κB (NF-κB)-inhibiting factor and heat shock protein 70. These findings suggest that the pulmonary inflammation caused by CeCl3 in mice is closely associated with oxidative stress and inflammatory cytokine expression.

This study aimed to investigate the effects of titanium dioxide nanoparticles (TiO2 NPs) on feed efficiency of silkworm (Bombyx mori) (B. mori). The results showed that the amount of ingested food was increased by 3.31%, the percentage of ingested food was increased by 16.36%, the instar was prolonged by 6.77 h, the body mass of mature silkworm was increased by 11.41%, the cocoon mass was increased by 5.47%, the cocoon shell mass was increased by 9.80%, and the ratio of cocoon shell was increased by 3.54%. Average cocoon filament length, reelability, and neatness were increased by 3.15, 17.57, and 1.72%, respectively, whereas the cocoon filament size was decreased by 0.19%. The gene expression profiles were also examined with digital gene expression (DGE). The results showed that among 4,011 genes detected, 127 genes were differentially expressed including 57 genes whose expression was upregulated and 70 genes whose expression was downregulated. The expression levels of five genes related to metabolism were verified with quantitative real-time PCR, and the results were consistent with the DGE data. The activities of three major digestive enzymes in the midgut were also assayed; the results showed that the activities of trehalase, protease, and lipase in TiO2 NP-fed group were increased by 42.55, 78.13, and 33.33%, respectively. These results indicate that feeding B. mori with TiO2 NPs can stimulate the transcriptional level of genes related to digestion and absorption of nutrients in the midgut and increase the activities of trehalase, protease, and lipase and, thus, increase the feed efficiency of B. mori.

Added Ce(3+) can partly substitute for Ca(2+) or Mg(2+) and improve photosynthesis under the deficiency of these elements, but very few studies focused on photosynthetic improvement in maize seedlings caused by K(+) deficiency, salt stress, especially a combination of K(+) deficiency and salt stress. In the present study, the effects of Ce(3+) on the photosynthesis of maize seedlings under the three different stresses were investigated. The results showed that added Ce(3+) under various stresses increased the ratios of free water/bound water and of K(+)/Na(+), the pigment contents, the values of Fv/Fm, Y(II), ETR(II), Y(NPQ), Qp, qL, NPQ, and qN of photosystem II (PSII), the values of Y(I) and ETR(I) of photosystem I (PSI) and the expression levels of LhcII cab1 and rbcL, and decreased the values of Y(NO) and Y(NA). This implied that added Ce(3+) depressed ion toxicity, photodamage of PSII, and acceptor side constraints of PSI, and enhanced adjustable energy dissipation, the responses of photochemistry, and carbon assimilation caused by K(+) deficiency, salt stress, and the combination of K(+) deficiency and salt stress. However, Ce(3+) mitigation of photosynthetic inhibition in maize seedlings caused by the combined stresses was greater than that of salt stress, and Ce(3+) mitigation under salt stress was greater than that under K(+) deficiency. In addition, the results also showed that Ce(3+) cannot improve photosynthesis and growth of maize seedlings under K(+) deficiency by substituting for K(+).

Bombyx mori nucleopolyhedrovirus (BmNPV) causes infection in the silkworm that is often lethal. The infection is hard to prevent, partly because of the nature of the virus particles and partly because of the different strains of B. mori. Titanium dioxide nanoparticles (TiO₂ NPs) have been demonstrated to have antimicrobial properties. The present study investigated whether TiO₂ NPs added to an artificial diet can increase the resistance of B. mori larvae to BmNPV and examined the molecular mechanism behind any resistance shown. The results indicated that ingested TiO₂ NPs decreased reactive oxygen species and NO accumulation in B. mori larvae under BmNPV infection, which in turn led to a decrease in their growth inhibition and mortality. In addition, the TiO₂ NPs significantly promoted the expression of resistance-related genes, including those encoding superoxide dismutase, catalase, glutathione peroxidase, acetylcholine esterase, carboxylesterase, heat shock protein 21, glutathione S transferase o1, P53, and transferring and of genes encoding cytochrome p302 and nitric oxide synthase. These findings are a useful addition to the understanding of the mechanism of BmNPV resistance of B. mori larvae in response to TiO₂ NPs addition. Such information also provides a theoretical basis for the use of TiO₂ NPs in sericulture.

The organophosphorus pesticide poisoning of the silkworm Bombyx mori is one of the major events causing serious damage to sericulture. Added low-dose rare earths are demonstrated to increase resistance in animals. However, very little is known about whether or not added CeCl₃ can increase resistance of silkworm to phoxim poisoning. The present findings suggested that added CeCl₃ to mulberry leaves markedly increased contents of protein, glucose and pyruvate, and carbohydrate metabolism-related enzyme activities, including lactate dehydrogenase, succinate dehydrogenase and malate dehydrogenase, and attenuated free amino acids, urea, uric acid and lactate levels and inhibited the protein metabolism-related enzymes activities, such as protease, alanine aminotransferase and aspartate aminotransferase in the haemolymph of B. mori, under phoxim toxicity. These findings suggest that added CeCl₃ may improve protein and carbohydrate metabolisms, thus leading to increases of growth and survival rate of B. mori under phoxim stress.

Magnesium (Mg) deficiency has been reported to affect plant photosynthesis and growth, and cerium (Ce) was considered to be able to improve plant growth. However, the mechanisms of Mg deficiency and Ce on plant growth remain poorly understood. The main aim of this work is to identify whether or not Mg deprivation affects the interdependent nitrogen and carbon assimilations in the maize leaves and whether or not Ce modulates the assimilations in the maize leaves under Mg deficiency. Maize plants were cultivated in Hoagland’s solution. They were subjected to Mg deficiency and to cerium chloride administration in the Mg-present Hoagland’s media and Mg-deficient Hoagland’s media.After 2 weeks,we measured chlorophyll (Chl) a fluorescence and the activities of nitrate reductase (NR), sucrose-phosphate synthase(SPS), and phosphoenolpyruvate carboxylase (PEPCase)in metabolic checkpoints coordinating primary nitrogen and carbon assimilations in the maize leaves. The results showed that Mg deficiency significantly inhibited plant growth and decreased the activities of NR, SPS, and PEPCase and the synthesis of Chl and protein. Mg deprivation in maize also significantly decreased the oxygen evolution, electron transport,and efficiency of photochemical energy conversion by photosystem II (PSII). However, Ce addition may promote nitrogen and carbon assimilations, increase PSII activities,and improve maize growth under Mg deficiency. Moreover,our findings would help promote usage of Mg or Ce fertilizers in maize production.

One of the most important agents causing lethal disease in the silkworm is the Bombyx mori nucleopolyhedrovirus (BmNPV), while low-dose rare earths are demonstrated to increase immune capacity in animals. However, very little is known about the effects of added CeCl(3) on decreasing BmNPV infection of silkworm. The present study investigated the effects of added CeCl(3) to an artificial diet on resistance of fifth-instar larvae of silkworm to BmNPV infection. Our findings indicated that added CeCl(3) significantly decreased inhibition of growth and mortality of fifth-instar larvae caused by BmNPV infection. Furthermore, the added CeCl(3) obviously decreased lipid peroxidation level and accumulation of reactive oxygen species such as O(2)(-), H(2)O(2), (·)OH, and NO and increased activities of the antioxidant enzymes including superoxide dismutase, catalase, ascorbate peroxidase, glutathione peroxidase, ascorbate, and glutathione contents in the BmNPV-infected fifth-instar larvae. In addition, the added CeCl(3) could significantly promote acetylcholine esterase activity and attenuate the activity of inducible nitric oxide synthase in the BmNPV-infected fifth-instar larvae. These findings suggested that added CeCl(3) may relieve oxidative damage and neurotoxicity of silkworm caused by BmNPV infection via increasing antioxidant capacity and acetylcholine esterase activity.

The mechanism of the fact that manganese deprivation and cerium addition affect the photochemical efficiency of plants is unclear. In this study, we investigated the improvement by cerium of the damage of the photochemical function of maize chloroplasts under manganese-deprived stress. Chlorophyll fluorescence induction measurements showed that the ratio of variable to maximum fluorescence (Fv/Fm) underwent great decreases under manganese deficiency, which was attributed to the reduction of intrinsic quantum efficiency of the photosystem II units. The electron flow between the two photosystems, activities of Mg(2+)-ATPase and Ca(2+)-ATPase, and rate of photophosphorylation on the thylakoid membrane of maize chloroplasts were reduced significantly by exposure to manganese deprivation. Furthermore, the inhibition of cyclic photophosphorylation was more severe than non-cyclic photophosphorylation under manganese deficiency. However, added cerium could relieve the inhibition of the photochemical reaction caused by manganese deprivation in maize chloroplasts. It implied that manganese deprivation could disturb photochemical reaction of chloroplasts strongly, which could be improved by cerium addition.

Due to increasing applications of lanthanides (Ln) in industry and daily life, numerous studies confirmed that Ln exposure may result in organ damages in mice and rats, while very few studies focused on several organs damages simultaneously. In order to compare the toxicity of Ln on organs, mice were exposed to LaCl(3), CeCl(3), and NdCl(3) of a dose of 20 mg/kg body weight for consecutive 60 days, respectively, then histopathological changes of liver, kidney, and heart, and their function were investigated. The results showed that long-term exposure to Ln caused cell necrosis and basophilia of liver, ambiguity of renal tubule architecture, congestion of blood vessel and capillary of kidney, and heart hemorrhage. The histopathological changes of liver, kidney, and heart in mice caused by Ce(3+) was most severe; the effect by Nd(3+) was slighter than Ce(3+) but more severe than La(3+). The assay of serum biochemical parameters suggested that Ln exposure severely impaired the functions of liver, kidney, and myocardium in mice. These findings suggested that long-term exposure to Ln resulted in histopathological changes of liver, kidney, and heart, and their function damages. Therefore, we thought that long-term application of the products containing Ln on human should be cautious.

Manganese is one of the essential microelements for plant growth, and cerium is a beneficial element for plant growth. However, whether manganese deficiency affects nitrogen metabolism of plants and cerium improves the nitrogen metabolism of plants by exposure to manganese-deficient media are still unclear. The main aim of the study was to determine the effects of manganese deficiency in nitrogen metabolism and the roles of cerium in the improvement of manganese-deficient effects in maize seedlings. Maize seedlings were cultivated in manganese present Meider's nutrient solution. They were subjected to manganese deficiency and to cerium chloride administered in the manganese-present and manganese-deficient media. Maize seedlings grown in the various media were measured for key enzyme activities involved in nitrogen metabolism, such as nitrate reductase, glutamate dehydrogenase, glutamine synthetase, and glutamic-oxaloace transaminase. We found that manganese deficiency restricted uptake and transport of NO(3)(-), inhibited activities of nitrogen-metabolism-related enzymes, such as nitrate reductase, glutamine synthetase, and glutamic-oxaloace transaminase, thus decreasing the synthesis of chlorophyll and soluble protein, and inhibited the growth of maize seedlings. Manganese deficiency promoted the activity of glutamate dehydrogenase and reduced the toxicity of excess ammonia to the plant, while added cerium relieved the damage to nitrogen metabolism caused by manganese deficiency in maize seedlings. However, cerium addition exerted positively to relieve the damage of nitrogen metabolism process in maize seedlings caused by exposure to manganese-deficient media.

Cerium (Ce) compounds are now widely applied in medicine, agriculture, animal breeding, and daily life; however, the effects of Ce on human body, especially on the central nervous system, are still unclear. In order to investigate whether Ce exposure cause neurotoxicological effects, ICR mice were exposed to CeCl(3) through intragastric administration at 0, 2, 10, and 20 mg/kg body weight doses everyday for 60 days. The behaviors of spatial recognition memory, brain histopathology, the brain elements and neurochemicals, as well as enzymes activities in mice were determined. The Y-maze test showed that CeCl(3) exposure could significantly impair the behaviors of spatial recognition memory. Specifically, in these Ln(3+)-treated mice, the contents of Ca, Mg, Na, K, Fe, and Zn in brain were significantly altered, the activities of Na(+)/K(+)-ATPase, Ca(2+)-ATPase, Ca(2+)/Mg(2+)-ATPase, acetylcholine esterase, and nitric oxide synthase were significantly inhibited; monoamines neurotransmitters such as norepinephrine, dopamine, and 5-hydroxytryptamine were significantly decreased, while the contents of acetylcholine, glutamate, and nitric oxide were significantly increased. These results indicated that CeCl(3) exposure could impair the learning ability, which is attributed to the disturbance of the homeostasis of trace elements, enzymes, and neurotransmitter systems in the mouse brain. Therefore, our study aroused the attention of Ln application and long-term exposure effects.

The main aim of this work is to identify how the combined stresses affect the interdependent nitrogen and photosynthetic carbon assimilations in maize. Maize plants were cultivated in Meider's solution. They were subjected to salt stress and potassium deficiency in the K-present Meider's media and K-deficient Meider's media. After 5 weeks, we measured chlorophyll a fluorescence and the activities of several enzymes in metabolic checkpoints coordinating primary nitrogen and carbon assimilation in the leaves of maize. The study showed that the combination of salt stress and potassium-deficient stress more significantly decreased nitrate uptake, plant growth, the activities of nitrate reductase, glutamate dehydrogenase, glutamate synthase, urease, glutamic-pyruvic transaminase, glutamic-oxaloace transaminase, sucrose-phosphate synthase, phosphoenolpyruvate carboxylase, and the synthesis of free amino acids, chlorophyll, and protein than those of each individual stress, respectively. However, the combined stresses significantly increased the accumulation of ammonium and carbohydrate products. The combined stresses also significantly decreased the oxygen evolution, the electron transport, and the efficiency of photochemical energy conversion by photosystem II in maize seedlings. Taken together, a combination of salt stress and potassium-deficient stress impaired the assimilations of both nitrogen and carbon and decreased the photosystem II activity in maize.

Recent studies demonstrated that titanium dioxide nanoparticles (TiO2 NPs) could significantly promote photosynthesis and plant growth, but its mechanism is still unclear. In this article, we studied the mechanism of light absorption and transfer of chloroplasts of Arabidopsis thaliana caused by TiO2 NPs treated. The results showed that TiO2 NPs could induce significant increases of light-harvesting complex II (LHCII) b gene expression and LHCII II content on the thylakoid membrane in A. thaliana, and the increases in LHCII were higher than the non-nano TiO2 (bulk-TiO2) treatment. Meanwhile, spectroscopy assays indicated that TiO2 NPs obviously increased the absorption peak intensity of the chloroplast in red and blue region, the fluorescence quantum yield near 680 nm, the excitation peak intensity near 440 and 480 nm and/or near 650 and 680 nm of the chloroplast. TiO2 NPs treatment could reduce F480/F440 ratio and increase F650/F680 ratio and accelerate the rate of whole chain electron transport and oxygen evolution of the chloroplast. However, the photosynthesis improvement of the non-nanoTiO2 treatment was far less effective than TiO2 NPs treatment. Taken together, TiO2 NPs could promote the light absorption of chloroplast, regulate the distribution of light energy from PS I to PS II by increasing LHCII and accelerate the transformation from light energy to electronic energy, water photolysis, and oxygen evolution.

Cerium (Ce) was shown to cause various toxic effects both in rats and mice; however, the molecular mechanism by which Ce exert theirs toxicity is still understood. In this report, the impairment of liver DNA conformation and liver apoptosis of mice caused by CeCl(3) was studied in vivo using inductively coupled plasma-mass spectrometry, various spectral methods, gel electrophoresis, and transmission electron micrograph. We found that the coefficients of liver to body weight of the mice treated with CeCl(3) were significantly increased. Ce(3+) could be significantly accumulated in the liver, and it insert itself into DNA base pairs and/or bind to DNA nucleotide, and alter the conformation of DNA. Furthermore, the evaluation by gel electrophoresis and transmission electron micrograph showed that higher dose of Ce(3+) could cause DNA cleavage and hepatocyte apoptosis in mice. Therefore, our study aroused the attention of Ce application and exposure effects especially on human liver for long-term and low-dose treatment.

The influence of LaCl(3), CeCl(3), and NdCl(3) on the antioxidative defense system in maize seedlings under cold stress was investigated. It was found that maize seedlings cultivated in cold stress developed distinct cold symptoms, and the plant growth was significantly inhibited as expected, while Ln-treated seedling growth was improved. Cold stress in maize seedlings also increased the permeability of plasma membrane, malondialdehyde as a degradation product of lipid peroxidation, and reactive oxygen species such as superoxide radicals and hydrogen peroxide, and decreased activities of the antioxidant enzymes such as superoxide dismutase, catalase, ascorbate peroxidase, and glutathione content; however, Ln treatments cultivated in cold stress decreased the permeability of plasma membrane, malondialdehyde, and reactive oxygen species, and increased activities of the antioxidative defense system. It implied that Ln could increase oxidative-stress resistance under cold stress. On the other hand, the assay of physiological and biochemical parameters demonstrated that Ce relieving chilling injury of maize seedlings caused by cold stress was most significant, medium in the Nd treatment, and last in the La treatment. These results suggested that the increase of cold resistance of maize seedlings caused by Ln might be closely related to its properties of 4f electron shell and variable valence.

Rare earth elements can promote photosynthesis, but their mechanisms are still poorly understood under magnesium deficiency. The present study was designed to determine the role of cerium in magnesium-deficient maize plants. Maize was cultivated in Hoagland's solution added with cerium with and without adequate quantities of magnesium. Under magnesium-deficient conditions, cerium can prevents inhibition of synthesis of photosynthetic pigment, improves light energy absorption and conversion, oxygen evolution, and the activity of photo-phosphorelation and its coupling factor Ca(2+)-ATPase. These results suggest that cerium could partly substitute magnesium, improving photosynthesis and plant growth.

The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl(3), CeCl(3), and NdCl(3) 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 Ln and levels of neurochemicals in the brain. The results showed that CeCl(3) and NdCl(3) could induce some neurons to turn inflammatory cells and slight edema but did not observe the brain pathological changes from LaCl(3)-treated group. The concentrations of La, Ce, and Nd in the brain were significantly different and ranked in the order of Ce, Nd, and La. The injury of the brain and oxidative stress occurred as Ln appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total antioxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the increase of glutamic acid, and the downregulated level of acetylcholinesterase activities. Furthermore, both Ce(3+) and Nd(3+) exhibited higher oxidative stress and toxicity on brain than La(3+), and Ce(3+) caused more severe brain injuries and oxidative stress than Nd(3+), implying that the differences in the brain injuries caused by Ln might be related to the number of 4f electrons of Ln.

It had been proved that manganese (Mn) deficiency could damage the photosynthesis of plants, and lanthanides could improve photosynthesis and greatly promote plant growth. However, the mechanisms on how Mn deficiency and cerium (Ce) addition affects the photosynthetic carbon reaction of plants under manganese deficiency are still poorly understood. In this study, the main aim was to determine Mn deficiency and cerium addition effects in key enzymes of CO(2) assimilation of maize. Maize plants were cultivated in Hoagland's solution. They were subjected to Mn deficiency and to Ce administered in the Mn-present Hoagland's media and Mn-deficient Hoagland's media. The growth condition, chlorophyll synthesis, and oxygen evolution were significantly destroyed by manganese deficiency, the activities of ribulose-1, 5-bisphosphate caroxylase/oxygenase (Rubisco), and Rubisco activase, and their genes expressions were inhibited by Mn deficiency. However, Ce treatment promoted the chlorophyll synthesis, oxygen evolution, and the activities of two key enzymes in CO(2) assimilation. Reverse transcription polymerase chain reaction was carried out, and the results showed that the mRNA expressions of Rubisco small subunit (rbcS), Rubisco large subunit (rbcL), and Rubisco activase subunit (rca) in the cerium-treated maize were obviously increased. One of the possible mechanisms of carbon reaction promoted by Ce is that the Ce treatment resulted in the enhancements of Rubisco and Rubisco activase mRNA amounts, the protein levels, and activities of Rubisco and Rubisco activase, thereby leading to the high rate of photosynthetic carbon reaction and enhancement of maize growth under Mn-deficient conditions. Together, the experimental study implied that Ce could partly substitute for magnesium and increase the oxidative stress-resistance of spinach chloroplast grown in Mn-deficiency conditions, but the mechanisms need further study.

It has been proven that higher dose of lanthanoid (Ln) can induce liver toxicities, but the mechanisms and the molecular pathogenesis are still unclear. In this study, LaCl₃, CeCl₃, and NdCl₃ at a higher dose of 20 mg/kg body weight was injected into the abdominal cavity of ICR mice for 14 consecutive days, and the inflammatory responses of liver of mice were investigated by histopathological test, real-time quantitative reverse transcription polymerase chain reaction (RT-PCR), and enzyme-linked immunosorbent assay (ELISA) methods. The results showed the significant accumulation of Ln in the liver results in liver histopathological changes and, therefore, liver malfunctions. The real-time quantitative RT-PCR and ELISA analyses showed that Ln could significantly alter the mRNA and protein expressions of several inflammatory cytokines, including nucleic factor-κB, macrophage migration inhibitory factor, tumor necrosis factor-α, interleukin-1β, interleukin-6, cross-reaction protein, interleukin-4, and interleukin-10. Our results also implied that the inflammatory responses and liver injury likely are caused by 4f shell and alterable valence properties of Ln-induced liver toxicity.

Some recent studies have been previously suggested that nanoparticulate titanium dioxide (TiO(2)) damaged liver function and decreased immunity of mice, but the spleen injury and its oxidative stress mechanism are still unclear. To understand the spleen injury induced by intragastric administration of nanoparticulate anatase TiO(2) for consecutive 30 days, the spleen pathological changes, the oxidative stress, and p38 and c-Jun N-terminal kinase signaling pathways, along with nuclear factor-κB and nuclear factor-E2-related factor-2 (Nrf-2), were investigated as the upstream events of oxidative stress in the mouse spleen from exposure to nanoparticulate TiO(2). The results suggested that nanoparticulate TiO(2) caused congestion and lymph nodule proliferation of spleen tissue, which might exert its toxicity through oxidative stress, as it caused significant increases in the mouse spleen reactive oxygen species accumulations, subsequently leading to the strong lipid peroxidation and the significant expression of heme oxygenase-1 via the p38-Nrf-2 signaling pathway. The studies on the mechanism by which nanoparticulate TiO(2) induced the p38-Nrf-2 signaling pathway are helpful to a better understanding of the nanoparticulate TiO(2)-induced oxidative stress and reduction of immune capacity.

In order to study the mechanisms underlying the effects of lanthanoid (Ln) on the liver, ICR mice were injected with LaCl₃, CeCl₃, and NdCl₃ at a dose of 20 mg/kg BW into the abdominal cavity daily for 14 days. We then examined oxidative stress-mediated responses in the liver. The increase of lipid peroxide in the liver produced by Ln suggested an oxidative attack that was activated by a reduction of antioxidative defense mechanisms as measured by analyzing the activities of superoxide dismutase, catalase, and ascorbate peroxidase, as well as antioxidant levels such as glutathione and ascorbic acid, which were greatest in Ce(3+) treatment, medium in Nd(3+), and least in La(3+). Our results also implied that the oxidative stress in the liver caused by Ln likely is Ce(3+) > Nd(3+) >La(3+), but the mechanisms need to be further studied in future.

The effects of Mn(2+) deficiency on light absorption, transmission, and oxygen evolution of maize chloroplasts were investigated by spectral methods. Several effects of Mn(2+) deficiency were observed: (1) the skeleton of pigment protein complexes and oxygen-evolving center and the combination between pigment and protein were damaged; (2) the light absorption of chloroplasts was obviously decreased; (3) the energy transfer among amino acids within PS II protein-pigment complex and decreased energy transport from tyrosine residue to chlorophyll a and from chlorophyll b and carotenoid to chlorophyll a were inhibited; (4) the oxygen-evolving of chloroplast was significantly inhibited. However, Mn(2+) addition decreased the damage of light absorption, transmission, and oxygen evolution of maize chloroplasts caused by Mn(2+) deficiency.

In order to study the mechanisms underlying the effects of TiO(2) nanoparticles on lactate dehydrogenase (LDH, EC1.1.1.27), Institute of Cancer Research region mice were injected with nanoparticulate anatase TiO(2) (5 nm) of various doses into the abdominal cavity daily for 14 days. We then examined LDH activity in vivo and in vitro and direct evident for interaction between nanoparticulate anatase TiO(2) and LDH using spectral methods. The results showed that nanoparticulate anatase TiO(2) could significantly activate LDH in vivo and in vitro; the kinetics constant (Km) and Vmax were 0.006 microM and 1,149 unit mg(-1) protein min(-1), respectively, at a low concentration of nanoparticulate anatase TiO(2), and 3.45 and 0.031 microM and 221 unit mg(-1) protein min(-1), respectively, at a high concentration of nanoparticulate anatase TiO(2). By fluorescence spectral assays, the nanoparticulate anatase TiO(2) was determined to be directly bound to LDH, and the binding constants of the binding site were 1.77 x 10(8) L mol(-1) and 2.15 x 10(7) L mol(-1), respectively, and the binding distance between nanoparticulate anatase TiO(2) and the Trp residue of LDH was 4.18 nm, and nanoparticulate anatase TiO(2) induced the protein unfolding. It was concluded that the binding of nanoparticulate anatase TiO(2) altered LDH structure and function.

The activity of alanine aminotransferase (ALT; E.C. 2.6.1.2) is often changed upon inflammatory responses in animals. Rare earths was shown to provoke various inflammatory responses both in rats and mice; however, the molecular mechanism by which rare earths exert its toxicity has not been completely understood, especially, we know little about the mechanism of the interaction between CeCl(3) and ALT. In this report, we investigated the mechanisms of CeCl(3) on ALT activity in vivo and in vitro. Our results showed that Ce(3+) could significantly activate ALT in vivo and in vitro; the kinetics constant (Km) and Vmax were 0.018 microM and 1,380 unit mg(-1) protein min(-1), respectively, at a low concentration of Ce(3+), and 0.027 microM and 624 unit mg(-1) protein min(-1), respectively, at a high concentration of Ce(3+). By UV absorption and fluorescence spectroscopy assays, the Ce(3+) was determined to be directly bound to ALT; the binding site of Ce(3+) to ALT was 1.72, and the binding constants of the binding site were 4.82 x 10(8) and 9.05 x 10(7) L mol(-1). Based on the analysis of the circular dichroism spectra, it was concluded that the binding of Ce(3+) altered the secondary structure of ALT, suggesting that the observed enhancement of ALT activity was caused by a subtle structural change in the active site through the formation of the complex with Ce(3+).

This study was performed with the objective of assessing the antioxidant response of the lung of mice to different rare earths. LaCl(3), CeCl(3), and NdCl(3) at a higher dose of 20 mg/kg body weight were injected into the nasal cavity of ICR mice for consecutive 14 days, respectively. The increase of pulmonary lipids peroxide produced by Ln suggested an oxidative attack that was activated by a reduction of antioxidative defense mechanisms as measured by analyzing the activities of superoxide dismutase, catalase, ascorbate peroxidase, and total antioxidant capacity, as well as antioxidant levels such as glutathione and ascorbic acid, which were greatest in Ce(3+) treatment, medium in Nd(3+), and least in La(3+). It implied that the antioxidative responses of lung may be involved in 4f shell and alternable valence properties of Ln-induced lung toxicity.

The activity of lactate dehydrogenase (LDH, EC1.1.1.27) is often changed upon inflammatory responses in animals. Lanthanoid (Ln) was shown to provoke various inflammatory responses both in rats and mice; however, the molecular mechanism by which Ln3+ exert its toxicity has not been completely understood, especially that we know little about the mechanism of the interaction between Ln with 4f electron shell and alternation valence and LDH. In this report, we investigated the mechanisms of LaCl3, CeCl3, and NdCl3 on LDH activity in vivo and in vitro. Our results showed that La3+, Ce3+, and Nd3+ could significantly activate LDH in vivo and in vitro; the order of activation was Ce3+>Nd3+> La3+>control. The affinity of LDH for Ce3+ was higher than Nd3+ and La3+; the saturated binding sites for Ce3+ on the LDH protein were 1.2 and for La3+ and Nd3+ 1.55. Ln3+ caused the reduction of exposure degree of cysteine or tryptophan/tyrosine of LDH, the increase of space resistance, and the enhancement of α-helix in secondary structure of LDH, which was greatest in Ce3+ treatment, medium in Nd3+ treatment, and least in La3+ treatment. It implied that the changes of structure-function on LDH caused by Ln3+ were closely related to the characteristics of 4f electron shell and alternation valence in Ln.

Magnesium is one of the essential elements for plant growth and cerium is a beneficial element for plant growth. However, the effects of the fact that cerium improves the nitrogen metabolism of plants under magnesium deficiency is poorly understood. The main aim of the study was to determine the role of cerium in the amelioration of magnesium-deficiency effects in spinach plants. Spinach plants were cultivated in Hoagland's solution. They were subjected to magnesium deficiency and to cerium chloride administered in the magnesium-present media and magnesium-deficient media. Spinach plants grown in the magnesium-present media and magnesium-deficient media were measured for key enzyme activities involved in nitrogen metabolism such as nitrate reductase, nitrite reductase, glutamate dehydrogenase, glutamate synthase, urease, glutamic–pyruvic transaminase, and glutamic–oxaloace protease transaminase. As the nitrogen metabolism in spinach was significantly inhibited by magnesium deficiency, it caused a significant reduction of spinach plant weight, leaf turning chlorosis. However, cerium treatment grown in magnesium-deficiency media significantly promoted the activities of the key enzymes as well as the contents of the free amino acids, chlorophyll, soluble protein, and spinach growth. It implied that Ce3+ could partly substitute for magnesium to facilitate the transformation from inorganic nitrogen to organic nitrogen, leading to the improvement of spinach growth, although the metabolism needs to be investigated further.

Lactate dehydrogenase (LDH, EC1.1.1.27), widely expressed in the heart, liver, and other tissues, plays an important role in glycolysis and glyconeogenesis. The activity of LDH is often altered upon inflammatory responses in animals. Nano-TiO(2) was shown to provoke various inflammatory responses both in rats and mice; however, the molecular mechanism by which TiO(2) exerts its toxicity has not been completely understood. In this report, we investigated the mechanisms of nano-anatase TiO(2) (5 nm) on LDH activity in vitro. Our results showed that LDH activity was greatly increased by low concentration of nano-anatase TiO(2), while it was decreased by high concentration of nano-anatase TiO(2). The spectroscopic assays revealed that the nano-anatase TiO(2) particles were directly bound to LDH with mole ratio of [nano-anatase TiO(2)] to [LDH] was 0.12, indicating that each Ti atom was coordinated with five oxygen/nitrogen atoms and a sulfur atoms of amino acid residues with the Ti-O(N) and Ti-S bond lengths of 1.79 and 2.41 A. We postulated that the bound nano-anatase TiO(2) altered the secondary structure of LDH, created a new metal ion-active site for LDH, and thereby enhanced LDH activity.

Previous research on the biological and toxic effects of nano-TiO(2) particles on animals only limit to a single dose. However, the toxicity caused by single dose nano-TiO(2) does not truly represent ecological and health effects of nano-TiO(2) retained in the environment. In order to further evaluate the toxicity of nano-TiO(2) particles, nano-anatase TiO(2) (5 nm) was injected into the abdominal cavity of ICR mice everyday for 14 days and the coefficients of organs and serum biochemical parameters were investigated. The results showed that, with increasing doses of nano-anatase TiO(2), the coefficients of liver, kidney, and spleen increased gradually, while the coefficients of lung and brain decreased gradually, and the coefficient of heart had little change. The order of the titanium accumulation in the organs was liver > kidneys > spleen > lung > brain > heart. The serum biochemical parameters with lower dose of nano-anatase TiO(2) showed little difference compared with the control mice, while with higher dose of nano-anatase TiO(2), the indicators of liver function, such as alkaline phosphatase, alanine aminotransferase, leucine acid peptide, pseudocholinesterase, total protein, and albumin level, were enhanced significantly; the indicators of kidney function, such as uric acid and blood urea nitrogen, were decreased; the activities of aspartate aminotransferase, creatine kinase, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase, indicator of the myocardium function, were increased. The contents of triglycerides, glucose, and high-density lipoprotein cholesterol were significantly elevated. Taken together, nano-anatase TiO(2) in higher dose caused serious damage to the liver, kidney, and myocardium of mice and disturbed the balance of blood sugar and lipid in mice. The accumulation of titanium in the organs might be closely related to the coefficients of organs and the inflammatory responses of mice.

Seedlings of spinach were grown in Hoagland's medium containing 0, 20, 40, 60, 80, 100 microM PbCl2, respectively, for 4 weeks. Chloroplasts were assayed for overproduction of reactive oxygen species (ROS) such as superoxide radicals (O2(*-)) and hydrogen peoxide (H2O2) and of lipid peroxide (malonyldialdehyde) and for activities of the antioxidant enzymes such as superoxide dismutase, catalase, ascorbate peroxidase, and guaiacol peroxidase and glutathione content, oxygen-evolving rate, and chlorophyll content. Increase in both ROS and lipid peroxide content and reduction in photosynthesis and activities of the antioxidant defense system indicated that spinach chloroplast underwent a stress condition due to an oxidative attack. Seedling growth cultivated in containing Pb2+ media was significantly inhibited. The results imply that spinach chloroplast was not able to tolerate the oxidative stress induced by Pb2+ due to having no effective antioxidant defense mechanism.

Ce3+ in various concentrations was added to superoxide dismutase (SOD) from rat eryhrocyte in vitro to gain insight into the mechanism of molecular interactions between Ce3+ and SOD. The results showed that the reaction between SOD and Ce3 was two order, which meant that the SOD activity was markedly accelerated by a low concentration of Ce3+ and inhibited by a high concentration of Ce3+. The spectroscopic assays suggested that the Ce3+ was determined to directly bind to SOD; the binding site of Ce3+ to SOD was 0.96, and the binding constants (K(A)) were 6.78 x 10(5) and 1.68 x 10(5)L.mol(-1); the binding Ce3+ entirely altered the secondary structure of SOD. It implied that the Ce(3+) coordination created a new metal ion-active site form in SOD, thus leading to an enhancement in SOD activity.

To further evaluate the photosynthetic effects of nanoanatase, the improvement of spinach chloroplast photosynthesis damaged by linolenic acid was investigated in the present paper. Several results showed that after the addition of nanoanatase to the linolenic acid-treated chloroplast, the light absorption increased by linolenic acid could be decreased, but the excitation energy distribution from photosystem (PS) I to PS II was promoted, and the decrease of PS II fluorescence yield caused by linolenic acid was reduced and the inhibition of oxygen evolution caused by linolenic acid of several concentrations was decreased. It was considered that nanoanatase could combine with linolenic acid and decrease the damage of linolenic acid on the structure and function of chloroplast.

Linolenic acid is an inhibitor of electron transport in chloroplasts of higher plants. It has obvious effects on the structure and function of chloroplasts. In the present paper, we investigated the nano-anatase relieving the inhibition of photoreduction activity and oxygen evolution caused by linolenic acid in spinach chloroplasts. The results showed that linolenic acid in various concentrations could obviously reduce the whole chain electron transport and the photoreduction activity of two photosystems, especially on the oxidative reside and reduce reside of photosystem II (PS II). After adding nano-anatase to chloroplasts treated by linolenic acid, the whole chain electron transport rate, the photoreduction activity of two photosystems, and the oxygen evolution rate were increased significantly, indicating that nano-anatase could obviously decrease the inhibition of linolenic acid on the electron transport, photoreduction activity, and oxygen evolution of spinach chloroplasts.

Lead (Pb(2+)) is a well-known highly toxic element. The mechanisms of the Pb(2+) toxicity are not well understood for nitrogen metabolism of higher plants. In this paper, we studied the effects of various concentrations of PbCl(2) on the nitrogen metabolism of growing spinach. The experimental results showed that Pb(2+) treatments significantly decreased the nitrate nitrogen (NO(-)(3)-N) absorption and inhibited the activities of nitrate reductase, glutamate dehydrogenase, glutamine synthase, and glutamic-pyruvic transaminase of spinach, and inhibited the synthesis of organic nitrogen compounds such as protein and chlorophyll. However, Pb(2+) treatments increased the accumulation of ammonium nitrogen NH(+)(4)-N)in spinach cell. It implied that Pb(2+) could inhibit inorganic nitrogen to be translated into organic nitrogen in spinach, thus led to the reduction in spinach growth.

In the article, we report that effects of nano-anatase on the spectral characteristics and content of light-harvesting complex II (LHCII) on the thylakoid membranes of spinach were investigated. The results showed that nano-anatase treatment could increase LHCII content on the thylakoid membranes of spinach and the trimer of LHCII; nano-anatase could enter the spinach chloroplasts and bind to PSII. Meanwhile, spectroscopy assays indicated that the absorption intensity of LHCII from nano-anatase-treated spinach was obviously increased in the red and the blue region, fluorescence quantum yield near 685 nm of LHCII was enhanced, the fluorescence excitation intensity near 440 and 480 nm of LHCII significantly rose and F 480/F 440 ratio was reduced. Oxygen evolution rate of PSII was greatly improved. Together, nano-anatase promoted energy transferring from chlorophyll (chl) b and carotenoid to chl a, and nano-anatase TiO2 was photosensitized by chl of LHCII, which led to enhance the efficiency of absorbing, transferring, and converting light energy.

Being a proven photocatalyst, nano-anatase is capable of undergoing electron transfer reactions under light. In previous studies we had proven that nano-anatase improved photosynthesis and greatly promoted spinach growth. The mechanisms by which nano-anatase promotes energy transfer and the conversion efficiency of the process are still not clearly understood. In the present paper, we report the results obtained with the photosystem II (PSII) isolated from spinach and treated by nano-anatase TiO2 and studied the effect of nano-anatase TiO2 on energy transfer in PSII by spectroscopy and on oxygen evolution. The results showed that nano-anatase TiO2 treatment at a suitable concentration could significantly change PSII microenvironment and increase absorbance for visible light, improve energy transfer among amino acids within PSII protein complex, and accelerate energy transport from tyrosine residue to chlorophyll a. The photochemical activity of PSII (fluorescence quantum yield) and its oxygen-evolving rate were enhanced by nano-anatase TiO2. This is viewed as evidence that nano-anatase TiO2 can promote energy transfer and oxygen evolution in PSII of spinach.

The improvement of spinach growth is proved to relate to N2 fixation by nano-anatase TiO2 in this study. The results show that all spinach leaves kept green by nano-anatase TiO2 treatment and all old leaves of control turned yellow white under culture with N-deficient solution. And the fresh weight, dry weight, and contents of total nitrogen, NH4(+), chlorophyll, and protein of spinach by nano-anatase TiO2 treatment presented obvious enhancement compared with control. Whereas the improvements of yield of spinach were not as good as nano-anatase TiO2 treatment under N-deficient condition, confirming that nano-anatase TiO2 on exposure to sunlight could chemisorb N2 directly or reduce N2 to NH3 in the spinach leaves, transforming into organic nitrogen and improving the growth of spinach. Bulk TiO2 effect, however, was not as significant as nano-anatase TiO2. A possible metabolism of the function of nano-anatase TiO2 reducing N2 to NH3 was discussed.

The effects of nano-anatase TiO2 on light absorption, distribution, and conversion, and photoreduction activities of spinach chloroplast were studied by spectroscopy. Several effects of nano-anatase TiO2 were observed: (1) the absorption peak intensity of the chloroplast was obviously increased in red and blue region, the ratio of the Soret band and Q band was higher than that of the control; (2) the great enhancement of fluorescence quantum yield near 680 nm of the chloroplast was observed, the quantum yield under excitation wavelength of 480 nm was higher than the excitation wavelength of 440 nm; (3) the excitation peak intensity near 440 and 480 nm of the chloroplast significantly rose under emission wavelength of 680 nm, and F 480 / F 440 ratio was reduced; (4) when emission wavelength was at 720 nm, the excitation peaks near 650 and 680 nm were obviously raised, and F 650 / F 680 ratio rose; (5) the rate of whole chain electron transport, photochemical activities of PSII DCPIP photoreduction and oxygen evolution were greatly improved, but the photoreduction activities of PSI were a little changed. Together, the studies of the experiments showed that nano-anatase TiO2 could increase absorption of light on spinach chloroplast and promote excitation energy to be absorbed by LHCII and transferred to PSII and improve excitation energy from PSI to be transferred to PSII, thus, promote the conversion from light energy to electron energy and accelerate electron transport, water photolysis, and oxygen evolution.