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PurposeThis study developed two presentation modes of scientific articles and evaluated their usability with user experiments.Design/methodology/approachTwo presentation modes of scientific articles, simply referred to as “genre presentation mode” and “argument presentation mode”, were constructed based on their genre structure and argument structure respectively. Their usability was evaluated by being compared against the existing RichHTML presentation mode in the experiments using eye-tracking and questionnaire methods.FindingsThe participants who were going to find the specific information of scientific articles rated the genre presentation mode higher than they did with either the argument or the RichHTML presentation mode for effectiveness. In contrast, those who were going to understand the general idea of scientific articles rated both the genre and argument presentation mode higher than they did with the RichHTML mode. In terms of efficiency, the participants took less reading time when the articles of non-native language were presented with the genre mode than they did when the articles were presented with the argument mode. When reading the articles in native language to understand the general idea, the participants took less reading time for the articles presented with the argument mode than they did for the articles presented with the genre mode. In comparison, they took less reading time when the articles were presented with the argument mode if they were going to find specific information. For satisfaction, the genre presentation mode was more popular than the argument mode and the RichHTML mode. However, the participants were less satisfied with the argument presentation mode than the other two when reading in native language and intending to find specific information.Originality/valueThe two presentation modes of scientific articles are found to improve the accuracy of information acquisition, shorten the total reading time and be more acceptable by readers.

Lead exposure is one of the most concerning public health problems worldwide, particularly among children. Yet the impact of chronic lead exposure on the thyroid status and related intelligence quotient performance among school-age children remained elusive.The aim of this study was to evaluate the influence of lead exposure on the thyroid hormones, amino acid neurotransmitters balances, and intelligence quotient (IQ) among school-age children living nearby a lead-zinc mining site. Other factors such as rice lead levels, mothers' smoking behavior, and diet intake were also investigated.A total of 255 children aged 7-12 years old were recruited in this study. Blood lead level (BLL), thyroid hormones including free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH), and amino acid neurotransmitters such as glutamate (Glu), glutamine (Gln), and γ-aminobutyric acid (GABA) were measured using graphite furnace atomic absorption spectroscopy (GFAAS), chemiluminescence immunoassay, high performance liquid chromatography (HPLC). Raven's standard progressive matrices (SPM) and the questionnaire were used to determine IQ and collect related influence factors.The average BLL of children was 84.8 μg/L. The occurrence of lead intoxication (defined as the BLL ≥ 100 μg/L) was 31.8%. Serum TSH levels and IQ of lead-intoxicated children were significantly lower than those without lead toxicity. The GABA level of girls with the lead intoxication was higher than those with no lead-exposed group. Correlation analyses revealed that BLL were inversely associated with the serum TSH levels (R= -0.186, p0.05), but positively related with IQ grades (R = 0.147, p0.05). Moreover, BLL and Glu were inversely correlated with IQ. In addition, this study revealed four factors that may contribute to the incidence of lead intoxication among children, including the frequency of mother smoking (OR = 3.587, p0.05) and drinking un-boiled stagnant tap water (OR = 3.716, p0.05); eating fresh fruits and vegetables (OR = 0.323, p0.05) and soy products regularly (OR = 0.181, p0.05) may protect against lead intoxication.Lead exposure affects the serum TSH, GABA levels and IQ of school-aged children. Developing good living habits, improving environment, increasing the intake of high-quality protein and fresh vegetable and fruit may improve the condition of lead intoxication.

Lead (Pb), a corrosion-resistant heavy non-ferrous metal, is one of the most common environmental neurotoxic metals. The effects of Pb on other essential metal elements are contradictory. Therefore, this in vivo study addressed the effects of sub-chronic Pb exposure on the distribution of other divalent metals, exploring the relationships between Pb levels in blood, teeth, bones, hair, and brain tissues. Thirty-two healthy male C57BL/6 mice received intragastric administration (i.g.) with 0, 12.5, 25, and 50 mg/kg Pb acetate, once a day for 8 weeks. Levels of Pb and other metal elements [including iron(Fe), zinc (Zn), magnesium (Mg), copper (Cu), and calcium(Ca)] in the whole blood, teeth, the right thighbone, hair, and brain tissues (including cortex, hippocampus, striatum, and hypothalamus) were detected with inductively coupled plasma-mass spectrometry (ICP-MS). Pb levels in all detected organs were increased after Pb-exposed for 8 weeks. The results of relationship analysis between Pb levels in the tissues and lifetime cumulative Pb exposure (LCPE) showed that Pb levels in the blood, bone, and hair could indirectly reflect the Pb accumulation in the murine brain. These measures might serve as valuable biomarkers for chronic Pb exposure reflective of the accumulation of Pb in the central nervous system (CNS). Sub-chronic Pb exposure for 8 weeks altered Ca, Cu, Fe, and Zn levels, but no effects were noted on Mg levels in any of the analyzed tissues. Pb decreased Ca in teeth, Cu in thighbone and teeth, Zn in whole blood and hair, and Fe in hair. In contrast, Pb increased Ca levels in corpus striatum and hypothalamus, Cu levels in striatum, Zn levels in teeth, and Fe levels in hippocampus, thighbone, and teeth. The Pb-induced changes in metal ratios in various tissues may serve as valuable biomarkers for chronic Pb exposure as they are closely related to the accumulations of Pb in the murine CNS. The results suggest that altered distribution of several essential metal elements may be involved in Pb-induced neurotoxicity. Additional studies should address the interaction between Pb and essential metal elements in the CNS and other organs.

Background Sodium para-aminosalicylic acid (PAS-Na), an anti-tuberculosis drug, has been demonstrated its function in facilitating the Mn elimination in manganism patients and Mn-exposed models in vivo and improving the symptoms of Mn poisoning. But whether it can improve the growth retardation and inflammatory responses induced by Mn have not been reported. Objectives This study was designed to investigate the preventive effects of PAS-Na on the development of retardation and inflammatory responses in Mn-exposed rats. Methods Male Sprague Dawley (SD) rats (8 weeks old, weighing 180 ± 20 g) were randomly divided into normal control group and Mn-exposed group in the 4 weeks experiment observation and normal control group, Mn-exposed group, PAS-Na preventive group and PAS-Na control group in the 8 weeks experiment observation. The Mn-exposed group received an intraperitoneal injection (i.p.) of 15 mg/kg MnCl2 and the normal control group i.p. physiological Saline in the same volume once a day for 4 or 8 weeks, 5 days per week. The PAS-Na preventive group i.p. 15 mg/kg MnCl2 along with back subcutaneous (s.c.) injection of 240 mg/kg PAS-Na once a day for 8 weeks, 5 days per week. PAS-Na control group received s.c. injection of 240 mg/kg PAS-Na along with i.p. injection of saline once daily. The body weight was determined once a week until the end of the experiment. The manganese contents in the blood were detected by graphite furnace atomic absorption spectrometry. The inflammatory factor levels (TNF-α, IL-1β, IL-6, and PGE2) in the blood were detected by using enzyme-linked immunosorbent assay (Elisa) and each organ taking from rats were weighed and recorded. Results Mn exposure significantly suppressed the growth in rats and increased heart, liver, spleen and kidney coefficients as compared with the control group. The whole blood Mn level and serum levels of IL-1β, IL-6, PGE2, and TNF-α in sub-chronic Mn-exposure group were markedly higher than those in the control group. However, preventive treatment with PAS-Na obviously reduced the whole blood Mn level, the spleen and liver coefficients of the Mn-exposed rats. And serum levels of IL-1β and TNF-α were significantly reduced by 33.9% and 14.7% respectively in PAS-Na prevention group. Conclusions PAS-Na could improve the growth retardation and alleviate inflammatory responses in Mn-exposed rats.

Sodium p-aminosalicylic acid (PAS-Na) has been previously shown to protect the brain from manganese (Mn)-induced toxicity. However, the efficacy of PAS-Na in protecting other organs from Mn toxicity and the mechanisms associated with this protection have yet to be addressed. Therefore, here, we assessed pancreatic damage in response to Mn treatment and the efficacy of PAS-Na in limiting this effect, along with specific mechanisms that mediate PAS-Na's protection. Mn exposure led to increased blood Mn content in dose- and time-dependent manner. Furthermore, subchronic Mn exposure (20 mg/kg for 8 weeks) led to pancreatic damage in a dose-dependent manner. In addition, the elevated Mn levels increased iron and decreased zinc and magnesium content in the pancreas. These effects were noted even 8 weeks after Mn exposure cessation. Mn exposure also affected the levels of amylase, lipase, and inflammatory factors such as tumor necrosis factor (TNF-α) and interleukin-1 β (IL-1β). PAS-Na significantly inhibited the increase in Mn concentration in both blood and pancreas, restored Mn-induced pancreatic damage, reversed the Mn-induced alterations in metal levels, and restored amylase and lipase concentrations. Taken together, we conclude that in rats, PAS-Na shows pharmacological efficacy in protecting the pancreas from Mn-induced damage.

Sodium p-aminosalicylic acid (PAS-Na) has been previously shown to protect the brain from manganese (Mn)-induced toxicity. However, the efficacy of PAS-Na in protecting other organs from Mn toxicity and the mechanisms associated with this protection have yet to be addressed. Therefore, here, we assessed pancreatic damage in response to Mn treatment and the efficacy of PAS-Na in limiting this effect, along with specific mechanisms that mediate PAS-Na's protection. Mn exposure led to increased blood Mn content in dose- and time-dependent manner. Furthermore, subchronic Mn exposure (20 mg/kg for 8 weeks) led to pancreatic damage in a dose-dependent manner. In addition, the elevated Mn levels increased iron and decreased zinc and magnesium content in the pancreas. These effects were noted even 8 weeks after Mn exposure cessation. Mn exposure also affected the levels of amylase, lipase, and inflammatory factors such as tumor necrosis factor (TNF-α) and interleukin-1 β (IL-1β). PAS-Na significantly inhibited the increase in Mn concentration in both blood and pancreas, restored Mn-induced pancreatic damage, reversed the Mn-induced alterations in metal levels, and restored amylase and lipase concentrations. Taken together, we conclude that in rats, PAS-Na shows pharmacological efficacy in protecting the pancreas from Mn-induced damage.

Exposure to high levels of manganese (Mn) leads to brain Mn accumulation, and a disease referred to as manganism. Activation of microglia plays an important role in Mn-induced neuroinflammation. Sodium p-aminosalicylic acid (PAS-Na) is a non-steroidal anti-inflammatory drug that inhibits Mn-induced neuroinflammation. The aim of the current study was to explore the role of NF-κB in the protective mechanism of PAS-Na on Mn-induced neuroinflammation in BV2 microglial experimental model. We treated BV2 microglia with 200 μM Mn for 24 h followed by 48 h treatment with graded concentrations of PAS-Na, using an NF-kB inhibitor, JSH-23, as a positive control. MTT results established that 200 and 400 μM PAS-Na treatment increased the Mn-induced cell viability reduction. NF-κB (P65) mRNA expression and the phosphorylation of p65 were increased in Mn-treated BV2 cell, and suppressed by PAS-Na, analogous to the effect of JSH-23 pretreatment. Furthermore, PAS-Na significantly reduced the contents of the inflammatory cytokine TNF-α and IL-1β, both of which were increased by Mn treatment. The current results show that PAS-Na attenuated Mn-induced inflammation by abrogating the activation of the NF-κB signaling pathways and reduced the release of pro-inflammatory cytokines.

Background The activation of NOD-like receptor protein 3 (NLRP3) inflammasome-dependent pyroptosis has been shown to play a vital role in the pathology of manganese (Mn)-induced neurotoxicity. Sodium para-aminosalicylic acid (PAS-Na) has a positive effect on the treatment of manganism. However, the mechanism is still unclear. We hypothesized that PAS-Na might act through NLRP3. Methods The microglial cell line BV2 and male Sprague-Dawley rats were used to investigate the impacts of PAS-Na on Mn-induced NLRP3 inflammasome-dependent pyroptosis. The related protein of the NF-κB pathway and NLRP3-inflammasome-dependent pyroptosis was detected by western blot. The reactive oxygen species and mitochondrial membrane potential were detected by immunofluorescence staining and flow cytometry. The activation of microglia and the gasdermin D (GSDMD) were detected by immunofluorescence staining. Results Our results showed that Mn treatment induced oxidative stress and activated the NF-κB pathway by increasing the phosphorylation of p65 and IkB-α in BV2 cells and in the basal ganglia of rats. PAS-Na could alleviate Mn-induced oxidative stress damage by inhibiting ROS generation, increasing mitochondrial membrane potential and ATP levels, thereby reducing the phosphorylation of p65 and IkB-α. Besides, Mn treatment could activate the NLRP3 pathway and promote the secretion of IL-18 and IL-1β, mediating pyroptosis in BV2 cells and in the basal ganglia and hippocampus of rats. But an inhibitor of NF-κb (JSH-23) treatment could significantly reduce LDH release, the expression of NLRP3 and Cleaved CASP1 protein and IL-1β and IL-18 mRNA level in BV2 cells. Interestingly, the effect of PAS-Na treatment in Mn-treated BV2 cells is similar to those of JSH-23. Besides, immunofluorescence results showed that PAS-Na reduced the increase number of activated microglia, which stained positively for GSDMD. Conclusion PAS-Na antagonized Mn-induced NLRP3 inflammasome dependent pyroptosis through inhibiting NF-κB pathway activation and oxidative stress.

Sodium p-aminosalicylic acid (PAS-Na) was reported to exhibit anti-inflammatory effect in the nervous system. However, the mechanism by which PAS-Na exhibits anti-inflammatory effects on manganese (Mn)-stimulated BV2 microglia cells remains unclear. Thus, this study investigated the role of PAS-Na in Mn-stimulated BV2 microglial cells. Microglia-like BV2 were treated with MnCl2 with or without the non-steroidal anti-inflammatory drug PAS-Na for 12 or 24 h to examine cell viability using MTT; for 24 or 48 h to examine levels of NLRP3, CASP1, IL-1β, and IL-18 mRNA using Real-Time quantitative PCR; for 48 h to examine levels of NLRP3 and CASP1 inflammasomes, measured by western blot analysis; and for 48 h to examine levels of inflammatory cytokines, measured by enzyme-linked immunosorbent assay. The MTT assay showed that PAS-Na produced significant neuroprotective effect by preventing Mn-induced inflammation in BV2 microglial cells. PAS-Na significantly concentration and time dependently inhibited Mn-induced production of NLRP3, CASP1, IL-1β, and IL-18. Taken together, our results suggest that PAS-Na exerts anti-inflammatory effects in Mn-stimulated BV2 microglial cells via downregulation of NLRP3, CASP1, IL-1β, and I L-18. Furthermore, a high concentration and prolonged PAS-Na treatment appear necessary for its therapeutic efficacy. Taken together, we conclude that PAS-Na affords therapeutic efficacy in mitigating neurological conditions associated with neuroinflammation.

Human lifespan is determined by genetic and environmental factors. Potential longevity genes are neither specific nor reproducible, and longevity-related genes are constantly confused with age-related genes. To distinguish specific age- and longevity-related genes, we analyzed a Gene Expression Omnibus (GEO) dataset established by the Leiden Longevity Study. The individuals were classified into longevity (mean age, 93.4 ± 3.0 years), longevity offspring (60.8 ± 6.1) and control (61.9 ± 6.9) groups. The series matrix files were downloaded, and average expression values were calculated. Differentially expressed genes (DEGs) between longevity and control groups and those between longevity and their offspring were identified by GEO2R online. A total of 507 longevity- and 755 age-related DEGs were visualized using a Venn diagram. Weighted gene co-expression network analysis (WGCNA) was performed on the longevity- and age-related DEGs. Age-related color modules and genes were identified. However, no longevity-related modules or genes were found. The green module, with 46 age-related DEGs, was the most biologically significant to age and aging. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and protein-protein interaction pathway analyses were conducted on these 46 DEGs, which are mainly enriched in B cell activation and receptor signaling pathways. CR2, VPREB3, MS4A1 and CCR6 were considered the most crucial candidate genes for aging.

Sodium para-aminosalicylate (PAS-Na) was first applied successfully in clinical treatment of two manganism patients with good prognosis. However, the mechanism of how PAS-Na protects against Mn-induced neurotoxicity is still elusive. The current study was conducted to explore the effects of PAS-Na on Mn-induced basal ganglia astrocyte injury, and the involvement of amino acid neurotransmitter in vitro. Basal ganglia astrocytes were exposed to 500 μM manganese chloride (MnCl2) for 24 hr, following by 50, 150, or 450 μM PAS-Na treatment for another 24 hr. MnCl2 significantly decreased viability of astrocytes and induced DNA damages via increasing the percentage of tail DNA and Olive tail moment of DNA. Moreover, Mn interrupted amino acid neurotransmitters by decreasing Gln levels and increasing Glu, Gly levels. In contrast, PAS-Na treatment reversed the aforementioned Mn-induced toxic effects on basal ganglia astrocytes. Taken together, our results demonstrated that excessive Mn exposure may induce toxic effects on basal ganglia astrocytes, while PAS-Na could protect basal ganglia astrocytes from Mn-induced neurotoxicity.

Automated discovery and analysis of customer opinions on the web holds a lot of promise for present-day practices of market research and customer relationship management. Opinion mining attempts to come up with ways to automatically analyse subjectivity expressed in natural language text. Previous research on the topic has shown that the overall subjectivity expressed in a document, such as a customer review, can be assessed with accuracy that is feasible in real-world applications. In this paper, we address the challenge of identification of customer opinions expressed towards specific features of a product, such as service quality and location of a hotel. The paper proposes and investigates a method to recognize the relationships between subjective expressions and references to features of a product. While the method has been evaluated on customer hotel reviews, it can potentially find application also in many tasks where concrete statements need to be extracted from documents on heterogeneous topics such as posts in forums, comments on blogs, or utterances in a chat room.

Web2.0 has motivated the development of mHealth. This paper intends to summarise the application status of mHealth in the environment of web2.0. By reviewing recent 10 years' studies and analysing the existing market of mHealth, we discussed the issues generated from the application, prospected its development in the future, put forward the challenge it may meet and raised the possible suggestions.

Manganese (Mn), an essential trace metal for protein synthesis and particularly neurotransmitter metabolism, preferentially accumulates in basal ganglia. However, excessive Mn accumulation may cause neurotoxicity referred to as manganism. Sodium para-aminosalicylic acid (PAS-Na) has been used to treat manganism with unclear molecular mechanisms. Thus, we aim to explore whether PAS-Na can inhibit Mn-induced neuronal injury in basal ganglia in vitro. We exposed basal ganglia neurons with 50 μM manganese chloride (MnCl2) for 24 h and then replaced with 50, 150, and 450 μM PAS-Na treatment for another 24 h. MnCl2 significantly decreased cell viability but increased leakage rate of lactate dehydrogenase and DNA damage (as shown by increasing percentage of DNA tail and Olive tail moment). Mechanically, Mn reduced glutathione peroxidase and catalase activity and interrupted amino acid neurotransmitter balance. However, PAS-Na treatment reversed the aforementioned Mn-induced toxic effects. Taken together, these results showed that PAS-Na could protect basal ganglia neurons from Mn-induced neurotoxicity.

The aim of this study was to investigate blood lead level and its relationship to essential elements (zinc, copper, iron, calcium and magnesium) in school-age children from Nanning, China.A total of 2457 children aged from 6 to 14 years were enrolled in Nanning, China. The levels of lead (Pb), zinc (Zn), copper (Cu), iron (Fe), calcium (Ca) and magnesium (Mg) were determined by an atomic absorption spectrometer.The mean blood lead level (BLL) was 57.21±35.00μg/L. 188 (7.65%) asymptomatic children had toxic lead level higher than 100μg/L. The school-age boys had similar lead level among different age groups, while the elder girls had less BLL. The blood Zn and Fe were found to be increased in the boys with elevated BLL, but similar trends were not observed in the girls. Positive correlations between Pb and Fe or Mg (r=0.112, 0.062, respectively, p0.01) and a negative correlation between Pb and Ca (r=-0.047, p0.05) were further established in the studied children.Lead exposure in school-age children was still prevalent in Nanning. The boys and girls differed in blood levels of lead and other metallic elements. Lead exposure may induce metabolic disorder of other metallic elements in body.

This study was conducted to investigate the protective effects of sodium p-aminosalicylic acid (PAS-Na) on learning and memory via increasing the number of basal forebrain choline acetyltransferase (ChAT) neurons in manganese (Mn)-exposed rats. Male Sprague Dawley rats were divided into following groups: the normal control I, II, and III groups, the model I, II, and III groups, low- and high-dose PAS-Na treatment (L- and H-PAS) group, PAS-Na prevention (PAS-P) group, and PAS-Na treatment (PAS-T) group. The model I, II, and III groups, L- and H-PAS, and PAS-T groups received intraperitoneal (i.p.) injection of 15 mg/kg manganese chloride tetrahydrate (MnCl2·4H2O) for 3 or 12 weeks, while the normal control I, II, and III groups received i.p. injection of an equal volume of saline; L- and H-PAS and PAS-T groups received back subcutaneous (s.c.) injection of PAS-Na (100 and 200 mg/kg) for the next 5 or 6 weeks, whereas model I and II group received back s.c. injection of an equal volume of saline. However, PAS-P group received back s.c. injection of 200 mg/kg PAS-Na + i.p. injection of 15 mg/kg MnCl2·4H2O for 12 weeks. Mn exposure significantly reduced the ability of spatial learning and memory capability, while PAS-Na prevention recovered it. Mn decreased the number of ChAT-positive neurons in vertical limb nucleus of the basal forebrain diagonal band/horizontal limb nucleus of the basal forebrain diagonal band and ChAT protein activity and treatment or prevention with PAS-Na restored those comparable with control. In brief, our results showed that PAS-Na may have protective effects on learning and memory against Mn via increasing the number of ChAT-positive neurons and activity of ChAT protein.

Our study aimed to assess the distribution of blood lead level and its relationship to essential elements in preschool children in an urban area of China.A total of 6741 children aged 0- to 6-year-old were recruited. Levels of lead, zinc, copper, iron, calcium, and magnesium in whole blood samples were determined using atomic absorption spectrometry.The mean blood lead level (BLL) and the prevalence of BLL≥10μg/dl (5.26±4.08μg/dl and 6.84%, respectively) increased with age gradually, and there was a gender-difference for blood lead, copper, zinc and iron levels. Compared with the group of children who had BLLs5μg/dl, the groups of 5≤BLLs10μg/dl and 10≤BLLs15μg/dl showed higher blood zinc, iron and magnesium levels, and a lower blood calcium level. A positive correlation of lead with zinc, iron and magnesium, and a negative correlation of lead with calcium were found in the group of children with BLL5μg/dl.Age- and gender-differences were found when assessing the BLL and intoxication prevalence in preschool children. Metabolic disorder of essential elements was found even with a low level of lead exposure.

OBJECTIVE: The current study was designed to evaluate the sensitivity, feasibility, and effectiveness of the pallidal index (PI) serving as a biomarker of brain manganese (Mn) accumulation, which would be used as an early diagnosis criteria for Mn neurotoxicity. METHODS: The weighted mean difference (WMD) of the PI between control and Mn-exposed groups was estimated by using a random-effects or fixed-effects meta-analysis with 95% confidence interval (CI) performed by STATA software version 12.1. Moreover, the R package "metacor" was used to estimate correlation coefficients between PI and blood Mn (MnB). RESULTS: A total of eight studies with 281 occupationally Mn-exposed workers met the inclusion criteria. Results were pooled and performed with the Meta-analysis. Our data indicated that the PI of the exposed group was significantly higher than that of the control (WMD: 7.76; 95% CI: 4.86, 10.65; I2 = 85.7%, p

Manganese (Mn) is an essential trace element of human. However, excessive Mn can cause manganism. Mn selectively accumulated in Mn-exposed workers' hippocampus which is crucial for higher brain functions such as learning, memory, and motivation during our postnatal life. Studies suggested sodium para-aminosalicylic acid (PAS) appeared to be therapeutic for manganism. We aimed to explore whether PAS could block Mn-induced neuronal injury in hippocampus in vitro. Hippocampal neurons were exposed to 50 μM manganese chloride (MnCl(2)) for 24 h, following by 50, 500, or 5000 μM PAS treatment for 24 h. Cell viability, apoptosis rate, mean fluorescence intensity of mitochondrial and DNA damage were respectively performed. MnCl(2) significantly decreased neurons' viability and fluorescence intensity of comet head of DNA, while increasing the apoptosis rate, mean fluorescence intensity of mitochondrial, percentage of tail DNA, and Olive tail moment of DNA. PAS reduced the percentage of tail DNA and Olive tail moment of Mn-exposed neurons. These data suggested that Mn caused hippocampal neurons' injury, and 50-5000 μM PAS could inhibit Mn-induced DNA damage.