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1.
Manganese (Mn) is an essential metal for biological systems; however, occupational or clinical exposure to high levels of Mn can produce a neurological disorder called manganism. Oxidative stress and neuroinflammation play major roles in the Mn-induced neurodegeneration leading to dysfunction of the basal ganglia. We investigated the toxic effects of MnCl 2 in an immortalized rat brain endothelial cell line (RBE4) and the protective effects of the radical scavenging aminosalicylic acids, 5-aminosalicylic acid (5-ASA) and 4-aminosalicylic acid (4-PAS). Mn cytotoxicity was determined with 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) reduction and lactate dehydrogenase (LDH) activity. A significant decrease in MTT reduction concomitant with increased LDH release was noted in RBE4 cells exposed for 24 h to MnCl 2 (600 and 800 μM; p?<?0.0001). Our results establish that compared to 4-PAS, 5-ASA has greater efficacy in protecting RBE4 cells from Mn-induced neurotoxicity after preexposure to MnCl 2 800 μM ( p?<?0.0001). 相似文献
2.
Manganese (Mn) is a potent neurotoxin involved in the initiation and progression of various cognitive disorders. Oxidative
stress is reported as one of accepted mechanisms of Mn toxicity. The present study was designed to explore the effects of
silymarin, a natural antioxidant, in attenuating the toxicity induced by Mn in rat cerebellum. In this investigation, rats
were treated orally with MnCl 2 (20 mg/ml) for 30 days, subsets of these animals were treated intraperitoneally daily with silymarin (100 mg/kg) along with
respective controls. Mn exposure caused a marked oxidative stress in cerebellum as indicated by a significant decrease in
the activities of enzymatic antioxidants like superoxide dismutase, catalase and glutathione peroxidase and in the levels
of non-enzymatic antioxidants like reduced glutathione (GSH), total thiols and vitamin C. Conversely an increase was obtained
in lipid and protein markers such as thiobarbituric reactive acid substances, lipid hydroperoxide and protein carbonyl products
contents. A Significant increase in acetylcholinesterase and a decrease in Na +/K +-ATPase activities were also shown, with a substantial rise in the expression of acetylcholinesterase and inducible nitric
oxide synthase (iNOS), and nitric oxide levels. The potential effect of SIL to prevent Mn induced neurotoxicity was also reflected
by histopathological observations. Rats exposed to Mn showed a reduced number and morphological alterations of cerebellar
Purkinje cells. These phenomenons were completely reversed by SIL co-treatment. We concluded that silymarin may protect against
Mn-induced oxidative stress in cerebellum by inhibiting both lipid and protein oxidation and by activating acetylcholinesterase
and inducible nitric oxide synthase (iNOS) gene expression. 相似文献
3.
Manganese (Mn) is neurotoxic: the underlying mechanisms have not been fully elucidated. l-Buthionine-( S, R)-sulfoximine (BSO) is an irreversible inhibitor of γ-glutamylcysteine synthetase, an important enzyme in glutathione (GSH) synthesis. To test the hypothesis that BSO modulates Mn toxicity, we investigated the effects of treatment of U-87 or SK-N-SH cells with MnCl 2, BSO, or MnCl 2 plus BSO. We monitored cell viability using MTT assay, staining with HO-33342 to assess live and/or apoptotic cells, and staining with propidium iodide (PI) to assess necrotic cells; we also measured cellular glutathione. Our results indicate decreased viability in both cell types when treated with MnCl 2 or BSO: Mn was more toxic to SK-N-SH cells, whereas BSO was more toxic to U-87 cells. Because BSO treatment accentuated Mn toxicity in both cell lines, GSH may act to combat Mn toxicity. Thus, further investigation in oxidative stress mediated by glutathione depletion will unravel new Mn toxicity mechanism(s). 相似文献
4.
Manganese (Mn) is an essential element for biological systems, nevertheless occupational exposure to high levels of Mn can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects with similarities to Parkinson’s disease. The aim of this study was to investigate the potential effects of silymarin (SIL), an antioxidant flavonoid, against manganese chloride induced neurotoxicity both in vivo (cerebral cortex of rats) and in vitro (Neuro2a cells). Twenty-eight male Wistar rats were randomly divided into four groups: the first group (C) received vehicle solution (i.p.) served as controls. The second group (Mn) received orally manganese chloride (20 mg/ml). The third group (Mn + SIL) received both Mn and SIL. The fourth group (SIL) received only SIL (100 mg/kg/day, i.p.). Animals exposed to Manganese chloride showed a significant increase in TBARS, NO, AOPP and PCO levels in cerebral cortex. These changes were accompanied by a decrease of enzymatic (SOD, CAT, GPx) and non-enzymatic (GSH, NpSH, Vit C) antioxidants. Co-administration of silymarin to Mn-treated rats significantly improved antioxidant enzyme activities and attenuated oxidative damages observed in brain tissue. The potential effect of SIL to prevent Mn induced neurotoxicity was also reflected by the microscopic study, indicative of its neuroprotective effects. We concluded that silymarin possesses neuroprotective potential, thus validating its use in alleviating manganese-induced neurodegenerative effects. 相似文献
5.
Manganese (Mn) is an essential trace element for humans. However, manganism would be caused by excessive Mn. The mechanisms
underlying excitotoxicity induced by manganism are poorly understood. As it is known to us, glutamate (Glu) is the most prevalent
excitatory neurotransmitter. To determine the possible role of dysfunction of Glu transportation and metabolism in Mn-induced
excitotoxicity, the rats were ip injected with different dose of MnCl 2 (0, 50, 100, and 200 μmol/kg), the levels of Mn and activities of GS, PAG, Na +-K +-ATPase, and Ca 2+-ATPase in striatum were investigated. In addition, effect of 20.38 μmol/kg pinacidil (K + channel opener) or 2.4 μmol/kg nimodipine (Ca 2+ channel blocker) were studied at 200 μmol/kg MnCl 2. With dose-dependent inhibition of GS, Na +-K +-ATPase, and Ca 2+-ATPase activities, increase of Mn levels and PAG activity were observed. Further investigation indicated that pre-treatment
of pinacidil or nimodipine reversed toxic effect of MnCl 2 significantly. These results suggested that MnCl 2 could induce dysfunction of Glu transportation and metabolism by augmenting the excitotoxicity dose-dependently; pinacidil
and nimodipine might antagonize manganese neurotoxicity. 相似文献
6.
Previous studies have shown that the in ovo injection of equol can markedly improve the water-holding capacity of muscles
of broilers chickens at 7 wk of age through promotion of the antioxidant status. We aimed to investigate directly the antioxidant
effects of equol on muscle cells in broilers. Muscle cells were separated from leg muscle of embryos on the 11th day of incubation
and treated with equol and H 2O 2, either alone or together. Cells were pretreated with medium containing 1, 10, or 100 μM equol for 1 h prior to the addition
of 1 mM H 2O 2 for a further 1 h. Photomicrographs of cells were obtained. Cell viability, malondialdehyde (MDA) content, and L-lactate
dehydrogenase (LDH) activity in the cell supernatant, as well as intracellular total superoxide dismutase (T-SOD) and glutathione
peroxidase (GSH-Px) activities were determined. Treatment with 1 mM H 2O 2 caused serious damage to cells, indicated by comets with no clear head region but a very apparent tail of DNA fragments.
Pretreatment with low (1 μM) but not high concentrations of equol (10 μM) inhibited cell damage, while 100 μM equol caused
more serious damage than H 2O 2 alone. Pretreatment with 1 μM equol had no effect on cell viability, while pretreatment with 10 and 100 μM equol significantly
decreased cell viability in a dose-dependent manner. Compared with H 2O 2 alone, pretreatment with low-dosage equol markedly decreased LDH activity and MDA production in the supernatant, significantly
increased intracellular T-SOD activity ( P < 0.05) and tended to increase intracellular GSH-Px activity (0.05 < P < 0.1). Pretreatment with high-dosage equol (10 and 100 μM) significantly enhanced LDH activity, but had no effect on MDA
content, T-SOD or GSH-Px activity induced by H 2O 2, except for an obvious increase in GSH-Px activity caused by 10 μM equol. These results indicate that equol at low dosage
can prevent skeletal muscle cell damage induced by H 2O 2, while pretreatment with high-dosage equol shows a synergistic effect with H 2O 2 in inducing cell damage. 相似文献
7.
Metal homeostasis is increasingly being evaluated as a therapeutic target in stroke and neurodegenerative diseases. Metal
dysregulation has been shown to lead to protein aggregation, plaque formation and neuronal death. In 2007, we first reported
that voltage-gated calcium channels act as a facile conduit for the entry of free ferrous (Fe 2+) ions into neurons. Herein, we evaluate differential iron toxicity to central nervous system cells and assess the ability
of the typical L-type voltage-gated calcium channel blocker nimodipine to attenuate iron-induced toxicity. The data demonstrate
that iron sulfate induces a dose-dependent decrease in cell viability in rat brain endothelial cells (RBE4; LC 50 = 150 μM), neuronal cells (Neuro-2α neuroblastoma; LC 50 = 400 μM), and in astrocytes (DI TNC1; LC 50 = 1.1 mM). Pre-treatment with nimodipine prior to iron sulfate exposure provided a significant ( P < 0.05) increase in viable cell numbers for RBE4 (2.5-fold), Neuro2-α (~2-fold), and nearly abolished toxicity in primary
neurons. Astrocytes were highly resistant to iron toxicity compared to the other cell types tested and nimodipine had no ( P > 0.05) protective effect in these cells. The data demonstrate variable susceptibility to iron overload conditions in different
cell types of the brain and suggest that typical L-type voltage-gated calcium channel blockers (here represented by nimodipine),
may serve as protective agents in conditions involving iron overload, particularly in cell types highly susceptible to iron
toxicity. 相似文献
8.
To evaluate the protective potential of lycopene (Lyc) and proanthocyanidins (PCs) against mercuric chloride (HgCl 2)-induced hepatotoxicity, the study focused on the mechanism of oxidative stress. Firstly, the rats were subcutaneously (s.c.)
injected with 0, 2.2, 4.4, and 8.8 μmol/kg HgCl 2. Additionally, 40 mg/kg Lyc and 450 mg/kg PCs were given to the rats intragastrically (i.g.) before exposure to 8.8 μmol/kg
HgCl 2. Then, body weight, liver weight coefficient, mercury (Hg) contents, histological feature, ultrastructure, apoptosis, reactive
oxygen species (ROS), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and malondialdehyde
(MDA) in the liver were measured. Lactate dehydrogenase (LDH) and alanine transaminase (ALT) in serum were determined. After
exposure to different concentrations of HgCl 2,it was found that Hg contents, pathological and ultrastructure injury, activities of LDH and ALT, apoptosis, and levels of
ROS, GSH, and MDA increased and the activities of SOD and GSH-Px decreased in a concentration-dependent manner. Further investigation
found that pretreatment with Lyc and PCs inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity.
We concluded that Lyc and PCs had hepatoprotective effects on HgCl 2-induced toxicity by antagonizing oxidative stress in rat liver. 相似文献
9.
Present study showed the responses of pea seedlings to exogenous indole acetic acid (IAA; 10 and 100 μM) application under
manganese (Mn; 50, 100 and 250 μM) toxicity. Manganese and 100 μM IAA alone as well as in combination decreased growth of
pea seedlings compared to control. Moreover, some parameters of oxidative stress—hydrogen peroxide (H 2O 2) and malondialdehyde (MDA) were also increased by single and combined treatments of Mn and 100 μM IAA compared to control.
In contrast, addition of 10 μM IAA together with Mn, alleviated Mn toxicity symptoms and promoted growth led to the decrease
in H 2O 2 and MDA levels compared to Mn treatments alone. Under single and combined treatments of Mn and 100 μM IAA, catalase activity
decreased while superoxide dismutase and ascorbate peroxidase activities increased and glutathione reductase and dehydroascorbate
reductase exhibited differential responses. However, addition of 10 μM IAA together with Mn, increased activities of studied
enzymatic antioxidants. Root and shoot reduced ascorbate (AA) and reduced glutathione (GSH) and, their reduced/oxidized ratios
decreased while dehydroascorbate (DHA) and oxidized glutathione (GSSG) contents increased compared to control following single
and combined treatments of Mn and 100 μM IAA. However, supply of 10 μM IAA together with Mn, increased AA and GSH, and their
reduced/oxidized ratios in root and shoot compared to Mn treatments alone. This study thus suggests that 10 μM of IAA was
able to increase Mn tolerance in pea seedlings under Mn toxicity while opposite was noticed for 100 μM IAA. 相似文献
10.
The present work was conducted to investigate the antioxidant activity and neuroprotective effects of Tripterygium regelii extract (TRE) on H 2O 2-induced apoptosis in human dopaminergic cells, SH-SY5Y. TRE possessed considerable amounts of phenolics (282.73 mg tannic
acid equivalents/g of extract) and flavonoids (101.43 mg naringin equivalents/g of extract). IC 50 values for reducing power and DPPH radical scavenging activity were 52.51 and 47.83 μg, respectively. The H 2O 2 scavenging capacity of TRE was found to be 57.68 μM × μg −1 min −1. By examining the effects of TRE on SH-SY5Y cells injured by H 2O 2, we found that after incubation of cells with TRE prior to H 2O 2 exposure, the H 2O 2 induced cytotoxicity was significantly reversed and the apoptotic features such as change in cellular morphology, nuclear
condensation and DNA fragmentation was inhibited. Moreover, TRE was very effective attenuating the disruption of mitochondrial
membrane potential and apoptotic cell death induced by H 2O 2. TRE extract effectively suppressed the up-regulation of Bax, Caspase-3 and -9, and down-regulation of Bcl-2. Moreover, TRE
pretreatment evidently increased the tyrosine hydroxylase (TH) and brain-derived neurotrophic factor (BDNF) in SH-SY5Y cells.
These findings demonstrate that TRE protects SH-SY5Y cells against H 2O 2-induced injury and antioxidant properties may account for its neuroprotective actions and suggest that TRE might potentially
serve as an agent for prevention of neurodegenerative disease associated with oxidative stress. 相似文献
11.
Background Very little is known about the effects of manganese (Mn)-excess on citrus photosynthesis and antioxidant systems. Seedlings
of sour pummelo ( Citrus grandis) were irrigated for 17 weeks with nutrient solution containing 2 μM (control) or 500 μM (excess) MnSO 4. The objective of this study were to understand the mechanisms by which Mn-excess leads to a decrease in CO 2 assimilation and to test the hypothesis that Mn-induced changes in antioxidant systems differ between roots and leaves. 相似文献
12.
Prior chemical and physical analysis of lunar soil suggests a composition of dust particles that may contribute to the development
of acute and chronic respiratory disorders. In this study, fine Al 2O 3 (0.7 μm) and fine SiO 2 (mean 1.6 μm) were used to assess the cellular uptake and cellular toxicity of lunar dust particle analogs. Respiratory cells,
murine alveolar macrophages (RAW 264.7) and human type II epithelial (A549), were cultured as the in vitro model system. The
phagocytic activity of both cell types using ultrafine (0.1 μm) and fine (0.5 μm) fluorescent polystyrene beads was determined.
Following a 6-h exposure, RAW 264.7 cells had extended pseudopods with beads localized in the cytoplasmic region of cells.
After 24 h, the macrophage cells were rounded and clumped and lacked pseudopods, which suggest impairment of phagocytosis.
A549 cells did not contain beads, and after 24 h, the majority of the beads appeared to primarily coat the surface of the
cells. Next, we investigated the cellular response to fine SiO 2 and Al 2O 3 (up to 5 mg/ml). RAW 264.7 cells exposed to 1.0 mg/ml of fine SiO 2 for 6 h demonstrated pseudopods, cellular damage, apoptosis, and necrosis. A549 cells showed slight toxicity when exposed
to fine SiO 2 for the same time and dose. A549 cells had particles clustered on the surface of the cells. Only a higher dose (5.0 mg/ml)
of fine SiO 2 resulted in a significant cytotoxicity to A549 cells. Most importantly, both cell types showed minimal cytotoxicity following
exposure to fine Al 2O 3. Overall, this study suggests differential cellular toxicity associated with exposure to fine mineral dust particles. 相似文献
13.
Although manganese (Mn) is an essential element, exposure to excessive levels of Mn and its accumulation in the brain can
cause neurotoxicity and extrapyramidal syndrome. We have investigated the differences in the accumulated levels of Mn, the
degree of lipid peroxidation, and its effects on the levels of trace elements (Fe, Cu, and Zn) in various regions in the brain
of rats having undergone acute Mn exposure. The rats in the dose—effect group were injected intraperitoneally (ip) with MnCl 2 (25, 50, or 100 mg MnCl 2/kg) once a day for 24 h. The Mn significantly accumulated ( p<0.05) in the frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus medulla, cerebellum, and spinal cord in
each case. The rats in the timecourse group were ip injected with MnCl 2 (50 mg MnCl 2/kg) and then monitored 12, 24, 48, and 72 h after exposure. The Mn accumulated in the frontal cortex, corpus callosum, hippocampus,
striatum hypothalamus, medulla, cerebellum, and spinal cord after these periods of time, In both the dose—effect and time-course
studies, we observed that the concentration of malondialdehyde, an end product of lipid peroxidation, increased significantly
in the frontal cortex, hippocampus, striatum, hypothalamus, medulla, and cerebellum. However, no relationship between the
concentrations of Mn in the brain and the extent of lipid peroxidation was observed. In addition, we found that there was
a significant increase ( p<0.05) in the level of Fe in the hippocampus, striatum, hypothalamus, medulla, and cerebellum, but the Cu and Zn levels had
not changed significantly. These findings indicated that Mn induces an increase in the iron level, which provides direct evidence
for Fe-mediated lipid peroxidation in the rats' brains; these phenomena might play important roles in the mechanisms of Mn-induced
neurotoxicology. 相似文献
14.
Manganese (Mn) is an essential metal for the development and function of the mammalian brain; however, excess Mn accumulation may cause neurological abnormalities resembling Parkinson’s disease due to reductions in brain dopamine levels. Because dopamine also regulates many functions in crustaceans, this study examined the effects of Mn accumulation in Dilocarcinus pagei, a Neotropical freshwater crab. Following a 72-h exposure to graded concentrations of MnCl 2, Mn accumulation was assessed in several tissues. Glycaemia and the tyrosine hydroxylase (TH) immunostaining response were also examined as indicators of catecholaminergic function and catecholaminergic cell integrity, respectively. Tissue Mn accumulation was variable and occurred in the following order: gills > hepatopancreas > claw muscle > haemolymph. Exposure to 2 mM Mn reduced the gill levels of calcium, copper and iron, whereas Mn at all concentrations decreased zinc levels. All Mn-exposed animals showed lower copper levels in the hepatopancreas and haemolymph. Exposure to 2.0 mM Mn increased the haemolymph calcium. Mn exposure had no effect on glycaemia, whereas exposure to low Mn concentrations reduced the TH immunostaining response. Analysis of the central nervous system revealed the greatest Mn effect in the cerebral ganglion and the least effect in the abdominal ganglia. These results suggest the operation of an adaptive mechanism for tissue accumulation that could be responsible for the lack of an association between Mn concentrations and metal accumulation. The findings also suggest that Mn, calcium, iron and zinc share a transporter in gill cells and that Mn resistance is greater in the TH-positive cells of this crustacean than in mammalian cells. 相似文献
15.
In the present study, we have investigated the effects of nitric oxide (NO) on alleviating manganese (Mn)-induced oxidative
stress in rice leaves. Exogenous MnCl 2 treatment to excised rice leaves for 24 and 48 h resulted in increased production of H 2O 2 and lipid peroxides, decline in the levels of antioxidants, glutathione and ascorbic acid, and increased activities of antioxidative
enzymes, superoxide dismutase, guaiacol peroxidase, catalase, ascorbate peroxidase, dehydroascorbate reductase, and glutathione
reductase. Treatment of rice leaves with 100 μM sodium nitroprusside (SNP), a NO donor, was effective in reducing Mn-induced
increased levels of H 2O 2, lipid peroxides and increased activities of antioxidative enzymes. The levels of reduced ascorbate and glutathione were
considerably recovered due to SNP treatment. The effect of SNP was reversed by the addition of NO scavenger, 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide
(c-PTIO) suggesting that ameliorating effect of SNP is due to release of NO. The results indicate that MnCl 2 induces oxidative stress in excised rice leaves, lowers the levels of reduced ascorbate and glutathione, and elevates activities
of the key antioxidative enzymes. NO appears to provide a protection to the rice leaves against Mn-induced oxidative stress
and that exogenous NO application could be advantageous in combating the deleterious effects of Mn-toxicity in rice plants. 相似文献
16.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder with a prevalence of 1–2% in people over the age of 50.
Mitochondrial dysfunction occurred in PD patients showing a 15–30% loss of activity in complex I. Asiatic acid (AA), a triterpenoid,
is an antioxidant and used for depression treatment, but the effect of AA against PD-like damage has never been reported.
In the present study, we investigated the protective effects of AA against H 2O 2 or rotenone-induced cellular injury and mitochondrial dysfunction in SH-SY5Y cells. Mitochondrial membrane potential (MMP)
and the expression of voltage-dependent anion channel (VDAC) were detected with or without AA pretreatment following cellular
injury to address the possible mechanisms of AA neuroprotection. The results showed that pre-treatment of AA (0.01–100 nM)
protected cells against the toxicity induced by rotenone or H 2O 2. In addition, MMP dissipation occurred following the exposure of rotenone, which could be prevented by AA treatment. More
interestingly, pre-administration of AA inhibited the elevation of VDAC mRNA and protein levels induced by rotenone(100 nM)
or H 2O 2 (300 μM).These data indicate that AA could protect neuronal cells against mitochondrial dysfunctional injury and suggest
that AA might be developed as an agent for PD prevention or therapy.
Special issue article in honor of Dr. Akitane Mori. 相似文献
18.
It is known that oxidative stress may cause neuronal injury and several experimental models showed that As2O3 exposure causes oxidative stress. Lycopene, a carotenoid, has been shown to have protective effect in neurological disease models due to antioxidant activity, but its effect on As2O3-induced neurotoxicity is not identified yet. The aim of this study is to investigate the effects of lycopene on As2O3-induced neuronal damage and the related mechanisms. Cell viability was determined by the MTT assay. Lycopene was administrated with different concentrations (2, 4, 6 and 8 µM) one hour before 2 µM As2O3 exposure in SH-SY5Y human neuroblastoma cells. The anti-oxidant effect of lycopene was determined by measuring superoxide dismutase (SOD), catalase (CAT) hydrogen peroxide (H2O2), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS). MTT results and LDH cytotoxicity analyses showed that pretreatment with 8 µM lycopene significantly improved the toxicity due to As2O3 exposure in SH?SY5Y neuroblastoma cells. Pretreatment with lycopene significantly increased the activities of anti?oxidative enzymes as well as total antioxidant status and decreased total oxidative status in As2O3 exposed cells. The results of this study indicate that lycopene may be a potent neuroprotective against oxidative stress and could be used to prevent neuronal injury or death in several neurological diseases. 相似文献
19.
Aging is a natural process in living organisms that is defined by some molecular and cellular changes with time. Various causes such as mitochondrial DNA aberrations, aggregation of proteins, telomere shortening, and oxidative stress have an influential role in aging of the cells. Natural antioxidants are compounds that are potent to protect the body from detrimental effects of molecules such as free radicals. The aim of this study was to evaluate the anti-aging properties of ellagic acid (EA) and silybin (SIL), as natural antioxidant compounds on rat embryonic fibroblast (REF) cells. These cells were pre-incubated with EA and SIL, thereafter were exposed to hydrogen peroxide (H 2O 2). Then, the cell viability, SA-β-GAL activity, distribution of cell cycle, NF-κB, and mitochondrial complex I, II/IV enzyme activity were measured. The results of this study revealed the protective effects of EA and SIL in H 2O 2-treated REF cells, which confirm the previous achieved data on antioxidant and anti-inflammatory characteristics of EA and SIL against H 2O 2 in the treated REF cells. However, more new in vivo experiments are required to discover the anti-aging effects and mechanism of action of such compounds. 相似文献
20.
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 μM 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 μM 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 × 10 8 L mol −1 and 2.15 × 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. 相似文献
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