Nano nickel oxide promotes epithelial-mesenchymal transition through transforming growth factor ß1/smads signaling pathway in A549 cells.

Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation in A549 cells, which mechanism was related with the increasing transforming growth factor ß1 (TGF-ß1) secretion. However, it remains unclear understanding the role of TGF-ß1 in collagen excessive formation. Here, we found nano NiO could directly promote epithelial-mesenchymal transition (EMT) via the TGF-ß1/Smads pathway in A549 cells. First, cytotoxicity induced by nano NiO has a dose- and time-dependent manner according to methylthiaozol tetrazolium assay. Second, nano NiO led to the increased contents of type I collagen (Col-I), TGF-ß1, p-Smad2, p-Smad3, alpha-smooth muscle actin (α-SMA), vimentin, and fibronectin, indicating Smads pathway activation and EMT occurence. Third, to verify whether TGF-ß1 activated Smads signaling pathway and EMT occurence, A549 cells were exposed to nano NiO and TGF-ß1 inhibitors (10 µM SB431542). The results showed that TGF-ß1 inhibitors alleviated the nano NiO-induced cytotoxicity and Col-I excessive formation. Meanwhile, TGF-ß1 inhibitors reversed the proteins expression trends of Col-I, p-Smad2, p-Smad3, α-SMA, vimentin, fibronectin, and E-cadherin. These observations suggested that EMT occurrence via TGF-ß1/Smads pathway might play an important role in the collagen excessive formation induced by nano NiO in A549 cells.

TGF-ß1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells.

Nickel oxide nanoparticles (Nano NiO) could induce pulmonary fibrosis, however, the mechanisms are still unknown. The aim of the present study was to explore the roles of transforming growth factor-ß1 (TGF-ß1), mitogen-activated protein kinase (MAPK) pathway and MMPs/TIMPs balance in Nano NiO-induced pulmonary fibrosis. For that purpose, we first established Nano NiO-induced human lung adenocarcinoma epithelial cells (A549 cells) model of collagen excessive formation through detecting the levels of hydroxyproline (Hyp) and type I collagen (Col-I). Then the protein levels of TGF-ß1, MAPKs, and MMPs/TIMPs were assessed by Western blot. The results showed that Nano NiO resulted in the increased contents of Hyp, Col-I, and TGF-ß1, the MAPK pathway activation and MMPs/TIMPs imbalance with a dose-dependent manner. In addition, to investigate whether TGF-ß1 mediated MAPK signaling pathway, A549 cells were treated by 100 µg/mL Nano NiO combined with TGF-ß1, p38 MAPK, and ERK1/2 inhibitors (10 µM SB431542, 10 µM SB203580, and 10 µM U0126), respectively. We found that MAPK signal pathway was suppressed by TGF-ß1 inhibitor. Meanwhile, the increased contents of Hyp and Col-I, and MMPs/TIMPs imbalance were alleviated by the p38 MAPK and ERK1/2 inhibitors, respectively. These findings indicated that the MAPK pathway and MMPs/TIMPs imbalance were involved in collagen excessive formation induced by Nano NiO.

Nano-selenium attenuates nickel-induced testosterone synthesis disturbance through inhibition of MAPK pathways in Sprague-Dawley rats.

The aim of this study was to investigate the protective effects of Nano-Se against Ni-induced testosterone synthesis disorder in rats and determine the underlying protective mechanism. Sprague-Dawley rats were co-treated with Ni (5.0 mg/kg, i.p.) and Nano-Se (0.5, 1.0, and 2.0 mg/kg, oral gavage) for 14 days after which various endpoints were evaluated. The Ni-induced abnormal pathological changes and elevated 8-OHdG levels in the testes were attenuated by Nano-Se administration. Importantly, decreased serum testosterone levels in the Ni-treated rats were significantly restored by Nano-Se treatment, particularly at 1.0 and 2.0 mg/kg. Furthermore, the mRNA and protein levels of testosterone synthetase were increased by Nano-Se compared to the Ni group, whereas phosphorylated protein expression levels of mitogen-activated protein kinase (MAPK) pathways were suppressed by Nano-Se administration in the Ni-treated rats. Overall, the results suggest that Nano-Se may ameliorate the Ni-induced testosterone synthesis disturbance via the inhibition of ERK1/2, p38, and JNK MAPK pathways.

Ameliorative effects of nano-selenium against NiSO4-induced apoptosis in rat testes.

Nickel (Ni) is a common environmental pollutant, which has toxic effects on reproductive system. Nowadays, nano-selenium (Nano-Se) has aroused great attention due to its unique antioxidant effect, excellent biological activities and low toxicity. The aim of this study was to explore the protective effects of Nano-Se on NiSO4-induced testicular injury and apoptosis in rat testes. Nickel sulfate (NiSO4) (5 mg/kg b.w.) was administered intraperitoneally and Nano-Se (0.5, 1, and 2 mg Se/kg b.w., respectively) was given by oral gavage in male Sprague-Dawley rats. Histological changes in the testes were determined by H&E staining. The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and immunohistochemistry were performed to evaluate the apoptosis in testes. Expression levels of mitochondrial apoptosis-related genes and proteins were analyzed by RT-qPCR and Western blot. The results showed that Nano-Se improved lesions of testicular tissue induced by NiSO4. Nano-Se significantly alleviated NiSO4-induced apoptosis in rat testes, as well as significantly downregulated the Bak, cytochrome c, caspase-9 and caspase-3 and upregulated Bcl-2 expression levels, all of which were involved in mitochondria-mediated apoptosis. Altogether, we concluded that Nano-Se may potentially exert protective effects on NiSO4-induced testicular injury and attenuate apoptosis, at least partly, via regulating mitochondrial apoptosis pathways in rat testes.

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats.

Nickel oxide nanoparticles (nano NiO) could induce hepatocyte apoptosis, while its potential mechanisms are unclear. This study aimed to explore the role of endoplasmic reticulum (ER) stress pathways in hepatocyte apoptosis induced by nano NiO. Male Wistar rats were administrated with nano NiO (0.015, 0.06, and 0.24 mg/kg b.w.) and micro NiO (0.24 mg/kg b.w.) by intratracheal instillation twice a week for 6 weeks. We measured the hepatocyte apoptosis levels by TdT-mediated dUTP nick-end labeling (TUNEL) staining, ER stress related gene and protein expression levels in rat liver. The results showed that the TUNEL positive cells increased after exposure nano NiO, hinting hepatocyte apoptosis. The up-regulated gene and protein levels of 78 kD glucose regulated protein and CCAAT/enhancer binding protein homologous protein suggested that nano NiO triggered ER stress. Nano NiO exposure contributed to the increased protein contents of inositol-requiring enzyme 1 (IRE-1)α, p-IRE-1α, X box protein-1S, pancreatic ER kinase (PERK), p-PERK, eukaryotic initiation factor-2 alpha (eIF-2α), p-eIF-2α, caspase-12, -9, and -3, implicating that nano NiO can activate the pathways of ER stress-mediated apoptosis. These findings indicate that the ER stress pathways may play an important role in hepatocyte apoptosis induced by nano NiO.

An induced extrinsic tooth stain prevention model to investigate whitening potential of sugar-free chewing gums.

PURPOSE: To establish an accelerated clinical test method to evaluate the effectiveness of sugar-free gums in prevention of the formation of extrinsic stains when chewed over a 2-week period in conjunction with daily tooth brushing. A secondary objective was to compare three methods for measuring extrinsic stain. METHODS: 25 healthy adult volunteers were enrolled in a single center, examiner blind, randomized 4-way crossover clinical study. Starting with a stain-free baseline, subjects rinsed five times daily with freshly brewed black tea, followed either by chewing one of three different gums for 12 minutes or not chewing (negative control). Extrinsic stain was measured at 1 and 2 weeks by modified Lobene Stain Index (MLSI), digital imaging, and a Vita EasyShade spectrophotometer. RESULTS: At 2 weeks, MLSI scores showed a statistically significant mean reduction of 43% or greater versus no-gum control for all three gum treatments. Digital image analysis and Vita EasyShade measurement showed reductions of yellowness (measured by difference in ∆b* values between the three gums and the non-gum control treatment) ranging from 0.28 to 0.34 and 3.52 to 4.18 Δb* units, respectively, for subjects using the chewing gums versus no-gum control (P< 0.05) after 2 weeks. This clinical study demonstrated that sugar-free gum can effectively reduce new stain formation along with daily tooth brushing in as little as 2 weeks when used in conjunction with tea rinsing to help promote more rapid stain formation. All three test methods confirmed the results, albeit with different levels of statistical significance. A minor modification of gum base polymer, or change of flavors, did not significantly impact the prevention of new stain formation. CLINICAL SIGNIFICANCE: Regular consumption of sugar-free chewing gum helps prevent extrinsic dental stain accumulation and provides a simple and enjoyable means for consumers to maintain their natural tooth color.

Remineralization of early caries by chewing sugar-free gum: a clinical study using quantitative light-induced fluorescence.

PURPOSE: To determine whether sugar-free gum can provide remineralization and caries control of active enamel caries lesions compared to baseline (before gum chewing) and to a no-gum group, following daily chewing for 12 weeks by school children; to determine whether chewing frequency can affect the extent of remineralization. METHOD: A pragmatic cluster-randomized controlled clinical trial with schools as the unit of randomization was employed. Three schools in Chengdu, PR China comprised the clusters. The study was approved by the Internal Review Board of Sichuan University. 177 school children, 8-13 years old, with at least one visible white-spot lesion were enrolled in the study. Each of the three clusters was randomly assigned to one of three groups: (1) no gum; (2) chew 2 pieces of sugar-free gum for 20 minutes, 3x per day; (3) chew 2 pieces of sugar-free gum for 12 minutes, 5x per day. White-spot lesions were examined by quantitative light-induced fluorescence (QLF) at baseline and after 4, 8, and 12 weeks of treatment. RESULTS: 155 subjects completed the study. Of them, the mean values of fluorescence loss at baseline were 9.52, 9.83 and 9.17 for no-gum group, 3x per day group and 5x per day group, respectively. For the area, the mean values at baseline were 2.52, 2.61 and 2.57 mm2 for no-gum group, 3x per day group and 5x per day group, respectively. For AQ, the mean values at baseline were -27.91, -28.29 and -29.67 for no-gum group, 3x per day group and 5x per day group, respectively. To adjust for differences in groups at baseline, ANCOVA was used. After 12-weeks, for all QLF metrics, the absolute values of 5x per day group were the lowest and the no gum group was the highest; the differences among three groups were statistically significant (P < 0.05). For AQ, which was accepted as the most useful metrics of QLF system, the adjusted mean values at 12 weeks were -26.35, -19.81 and -17.58 for no-gum group, 3x per day group and 5x per day group, respectively. There were significant differences between groups.

Multiscale spatial-temporal evolution of energy carbon footprint in the Yellow River Basin of China based on DMSP/OLS and NPP/VIIRS integrated data.

Increased CO2 emissions from urban energy consumption pose a significant challenge to regional carbon mitigation policies. In this paper, we integrated two nighttime light (NTL) data: the Defense Meteorological Satellite Program (DMSP) Operational Linescan System (OLS) and the Visible Infrared Imaging Radiometer Suite (VIIRS) on the Suomi National Polar-orbiting Partnership (NPP) composite data to estimate the energy carbon emissions from 2000 to 2019. Then the spatiotemporal dynamics of carbon footprint and deficit in the Yellow River Basin were analyzed at the provincial, municipal, and county scales combined with NPP data. The study shows that (1) the total amount of energy consumption CO2 emissions in the Yellow River Basin had increased from 1332 Mt in 2000 to 6469 Mt in 2019, but the average annual growth rate slowed down after 2010 from 11.5 to 5.61%. (2) From 2000 to 2018, the provinces with the highest carbon footprint and carbon deficit were concentrated in Inner Mongolia and Shanxi. In 2018, Inner Mongolia's carbon footprint was 1366.91 × 104 km2, accounting for 22.8% of the total. Cities with high carbon footprint were mainly economic centers and energy-intensive areas of various provinces. High-carbon deficit counties were mainly distributed in the western region. In 2018, 954 counties exhibited carbon deficits. (3) The carbon footprint in the Yellow River Basin at the municipal and county scales have a significant spatial correlation. The H-H clusters of the carbon footprint on the municipal scale were distributed in the middle reaches of the Yellow River Basin. At the county scale, the L-L clusters were mainly in Sichuan and eastern Henan regions. Through the analysis of the spatial and temporal evolution of carbon footprint and carbon deficit in the Yellow River Basin, it is significant to measure the degree of comprehensive coordination of carbon sources and sinks in the basin, to grasp the differences in the level of regional carbon emissions, and to promote synergistic regional governance, assist in the formulation of more precise carbon emission reduction policies, and to promote green and high-quality development.

Chewing gum containing allyl isothiocyanate from mustard seed extract is effective in reducing volatile sulfur compounds responsible for oral malodor.

PURPOSE: To evaluate the in vivo effect of chewing gum containing allyl isothiocyanate alone, and in combination with zinc salts on reduction of the level of volatile sulfur compounds responsible for oral malodor. METHODS: 15 healthy volunteers between the ages of 20-50 chewed either an experimental gum or a placebo gum for 12 minutes. Their mouth air was analyzed for volatile sulfur compounds by a gas chromatograph at baseline, immediately after chewing, and at 60, 120 and 180 minutes after treatment. RESULTS: The study revealed that allyl isothiocyanate, a constituent of mustard seed extract, can effectively reduce the concentration of volatile sulfur compounds in mouth air. Chewing gum containing 0.1% zinc lactate and 0.01% of allyl isothiocyanate eliminated 89%, 55.5%, 48% and 24% of the total VSC concentration immediately after chewing and at 1, 2, and 3 hours after chewing, respectively.

Assessment of chewing sugar-free gums for oral debris reduction: a randomized controlled crossover clinical trial.

PURPOSE: To assess the oral debris removal efficacy of two commercial sugar-free chewing gums, based on a newly developed oral debris scoring system. METHODS: A randomized, examiner-blinded, three-arm crossover study was conducted, with a 1-week washout period between the crossover phases. 42 healthy adults were randomly assigned to sugar-free stick gum (Wrigley's Extra Freshmint), sugar-free pellet gum (Wrigley's Extra Fruit) or no-gum chewing groups. Subjects consumed a single chocolate cookie, and were examined at baseline, and at 2-, 5-, and 10-minute time points with or without gum-chewing treatment. Primary outcome measures were oral debris scores on the occlusal surface, interproximal and gingival margin areas. The entire test procedure was repeated on two subsequent visits. RESULTS: The baseline conditions in the three groups did not differ significantly. Chewing either stick gum or pellet gum resulted in significantly lower oral debris scores (P < 0.0001) compared to the control (no-gum) treatment for all intraoral sites, while no significant difference was observed between the two chewing gum groups. Intra-examiner repeatability of the new scoring criteria was high throughout the study (Kappa > 0.90).

Prevalence of Suboptimal Health Status and Its Influencing Factors among Chinese Software Programmers.

BACKGROUND: There is a lack of specific study of the suboptimal health status (SHS) in software programmers. The aims of the present study were to investigate the prevalence of SHS and analyze the influencing factors among Chinese software programmers. METHODS: A cross-sectional survey using a programmer SHS scale was conducted to evaluate the prevalence of SHS, as well chi-square test and multi-factor logistic regression were applied to analyze the relationship between suboptimal health and personal basic information, living and work habits in software programmers. RESULTS: The prevalence of SHS was 18.67% in software programmers. Single factor analysis found that there were differences in suboptimal health prevalence among different work cities (P = 0.031), hours of sleep per day (P = 0.046), overtime days per month (P = 0.010) and exercise frequency per week (P = 0.015). The factors for suboptimal health such as hours of sleep per day (OR = 0.307, 95% CI = 0.096∼0.984) and exercise frequency per week (OR = 0.190, 95% CI = 0.054∼0.671) significantly affected subjects of SHS via multi-factor logistic regression analysis, indicating that adequate sleep and exercise decreased the chance of SHS up to 30.70% and 19.00%, respectively. CONCLUSION: Suboptimal health had become a serious public health challenge in Chinese software programmers. Whilst, the health status of the programmers could be effectively elevated by improving lifestyles.

Grape seed proanthocyanidin extract ameliorates cisplatin-induced testicular apoptosis via PI3K/Akt/mTOR and endoplasmic reticulum stress pathways in rats.

Testicular toxicity is an adverse reaction of the effective chemotherapy drug cisplatin (CIS). Our previous study found that grape seed proanthocyanidin extract (GSPE) had a protective effect on CIS-induced testicular toxicity. However, the protective mechanism of GSPE against CIS-induced testicular toxicity remains unknown. In this study, we aimed to investigate whether GSPE can reduce CIS-induced testicular toxicity and its potential mechanism in rats. The results showed that GSPE ameliorated CIS-induced the apoptosis of testicular cells and inhibited the protein levels of Bad, Cyt c, caspase-9, caspase-3, caspase-12, GRP78, CHOP, IRE1α, p-IRE1α, XBP-1S, PERK, p-PERK, eIF2α, and p-eIF2α. Besides, GSPE reversed the downregulation of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR protein expression induced by CIS. These results indicated that GSPE can improve CIS-induced testicular cells apoptosis via activating PI3K/Akt/mTOR and inhibiting Bad/Cyt c/caspase-9/caspase-3 pathways. And GSPE relieved endoplasmic reticulum stress-mediated apoptosis via inhibiting PREK/eIF2α and IRE1α/XBP-1S/caspase-12 pathways. In conclusion, the evidence suggested that GSPE can act as a protective agent against testicular toxicity induced by CIS. PRACTICAL APPLICATIONS: Testicular toxicity was a well-known adverse effect of cisplatin (CIS) in cancer treatment. Grape seed proanthocyanidin extract (GSPE) has been reported to serve as one of the most therapeutic potentials agents. In present study, we explored the regulatory effects of GSPE on the apoptosis induced by CIS, which involved testicular apoptosis mechanisms in rats. Our results indicated that CIS caused testicular toxicity via PI3K/AKT/mTOR and ERS mediated apoptosis pathway in rats. This toxicity was attenuated by GSPE treatment via activated PI3K/Akt/mTOR pathway, and inhibiting Bad/CytC/caspase-9/caspase-3 as well as PREK/eIF2α, IRE1α/XBP-1S/caspase-12 pathways. Our findings suggest that GSPE may be a novel protective agent against testicular toxicity induced by CIS.

Trigeminal Receptor Study of High-Intensity Cooling Agents.

Compounds capable of providing trigeminal effects are important to the flavor industry. Cooling agents activate a class of transient receptor potential (TRP) channels. The objective of this study was to evaluate the effect of 18 cooling agents by high-throughput screening through TRPM-8 and TRPA-1 channels. These coolants were further evaluated by a sensory analysis panel in a sucrose solution testing for a perceived activity. The results reveal that WS-5 activates both TRPA-1 and TRPM-8 receptor channels; WS-3 actives primarily TRPM-8, whereas FEMA-4557 activates the TRPA-1 channel. Sensory evaluation shows that for the same concentration in aqueous solution, the cooling intensity follows the order WS-5 > WS-3 > FEMA-4557 > WS-23. Human sensory perception of cooling intensity correlates better for TRPM-8 than for TRPA-1.

ROS generation and MAPKs activation contribute to the Ni-induced testosterone synthesis disturbance in rat Leydig cells.

Nickel (Ni) can disorder testosterone synthesis in rat Leydig cells, whereas the mechanisms remain unclear. The aim of this study was to investigate the role of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) in Ni-induced disturbance of testosterone synthesis in rat Leydig cells. The testosterone production and ROS levels were detected in Leydig cells. The mRNA and protein levels of testosterone synthetase, including StAR, CYP11A1, 3ß-HSD, CYP17A1 and 17ß-HSD, were determined. Effects of Ni on the ERK1/2, p38 and JNK MAPKs were also investigated. The results showed that Ni triggered ROS generation, consequently resulted in the decrease of testosterone synthetase expression and testosterone production in Leydig cells, which were then attenuated by ROS scavengers of N-acetylcysteine (NAC) and 2,2,6,6-tetramethyl-1-piperidinyloxy (TEMPO), indicating that ROS are involved in the Ni-induced testosterone biosynthesis disturbance. Meanwhile Ni activated the ERK1/2, p38 and JNK MAPKs. Furthermore, Ni-inhibited testosterone synthetase expression levels and testosterone secretion were all alleviated by co-treatment with MAPK specific inhibitors (U0126 and SB203580, respectively), implying that Ni inhibited testosterone synthesis through activating ERK1/2 and p38 MAPK signal pathways in Leydig cells. In conclusion, these findings suggest that Ni causes testosterone synthesis disorder, partly, via ROS and MAPK signal pathways.

Grape seed procyanidins extract attenuates Cisplatin-induced oxidative stress and testosterone synthase inhibition in rat testes.

Cisplatin (CIS) is widely applied for its antihematological malignancies properties and as antisolid tumors drugs. However, it could cause testicular damage related with oxidative stress and testosterone synthesis disorder. Studies reported that grape seed procyanidins extract (GSPE) could improve CIS induced-testes lesion via scavenging free radicals in animals, although its mechanisms were unclear. Therefore, the purpose of the present study was to explore the antagonistic mechanisms of GSPE on CIS-induced testes lesion. Rats were treated with 10 mg/kg by weight CIS by intraperitoneal injection singly on the 11th day, and different doses of GSPE were administrated via intragastric gavage for 15 days consecutively. The results showed that GSPE improved the pathological changes of testicular tissue, and the decreased concentrations of testosterone in serum induced by CIS. GSPE inhibited CIS-induced oxidative/nitrative stress, as well as increased the mRNA and protein levels of testosterone synthetase in rat testes. In conclusion, the main protection exerted by GSPE on CIS-induced testicular toxicity is related to its effects including suppressing oxidative/nitrative stress and up-regulating expression of testosterone synthetase. ABBREVIATIONS: CIS: Cisplatin; GSPE: grape seed procyanidins extract; LH: luteinizing hormone; FSH: follicle-stimulating hormone; STAR: steroidogenic acute regulatory protein; CYP11A1: P450 side chain cleavage enzyme; HSD3B1: 3ß-hydroxysteroid dehydrogenase; CYP17A1: 17α-hydroxylase; HSD17B: 17ß-hydroxysteroid dehydrogenase; ROS: reactive oxygen species; O2-: superoxide anion; H2O2: hydrogen peroxide; •OH: hydroxyl radicals; SOD: superoxide dismutase; CAT: catalase; GSH-Px: glutathione peroxidase; LPO: lipid peroxidation; 8-OHdG: 8-hydroxy-2-deoxyguanosine; HO-1: heme oxygenase-1; MT-1: metallothionein-1; NO: nitric oxide; ONOO-: peroxynitrite; NOS: nitric oxide synthases; nNOS: neuronal NOS; iNOS: inducible NOS; eNOS: endothelial NOS; MDA: malondialdehyde; GSH: glutathione; T-AOC: total antioxidant capacity; TNOS: total nitric oxide synthases; Lhcgr: luteinizing hormone receptor; Scarb1: lipoprotein-receptor; Cyp19a1: 19α-hydroxylase; ELISA: enzyme linked immunosorbent assay; RT-qPCR: reverse transcription-quantitative polymerase chain reaction; PAS: periodic acid-Schiff; MTs: Metallothioneins; cAMP: cyclic adenosine monophosphate; cDNA: complementary DNA; RIPA: radioimmunoprecipitation buffer; PMSF: phenylmethanesulfonyl fluoride; PVDF: polyvinylidenedifluoride; ß-actin: beta-actin.

Compressed mints and chewing gum containing magnolia bark extract are effective against bacteria responsible for oral malodor.

Flavors and natural botanic extracts are often used in chewing gum and compressed mints for breath freshening and relief of oral malodor. The oral malodor is a result of bacterial putrification of proteinaceous materials from food or saliva. In this study, magnolia bark extract (MBE) and its two main components, magnolol and honokiol, were evaluated by the minimum inhibition concentration (MIC) test. The inhibitory effect of MBE mint was further evaluated by a kill-time assay study. In addition, an in vivo study was performed on nine healthy volunteers postlunch. Saliva samples were taken before and after subjects consumed mints and gum, with and without MBE. Listerine mouthwash was included as a positive control. The testing results indicated that MBE and its two main constituents demonstrated a strong germ-kill effect against bacteria responsible for halitosis and also Streptococcus mutans, bacteria involved in dental caries formation. The MIC of magnolol, honokiol, and MBE on Porphyromonas gingivalis, Fusobacterium nucleatum, and S. mutans ranged from 8 to 31 microg/mL. Kill-time assay results indicated that mints containing 0.2% MBE reduced more than 99.9% of three oral bacteria within 5 min of treatment. The in vivo study demonstrated that MBE containing mints reduced total salivary bacteria by 61.6% at 30 min and 33.8% at 60 min postconsumption. In comparison, the flavorless mint reduced total salivary bacteria by 3.6% at 30 min and increased total bacteria by 47.9% at 60 min. The MBE containing chewing gum reduced total salivary bacteria by 43.0% at 40 min, while placebo gum reduced total salivary bacteria by 18.0%. In conclusion, MBE demonstrated a significant antibacterial activity against organisms responsible for oral malodor and can be incorporated in compressed mints and chewing gum for improved breath-freshening benefits.

Nano NiO induced liver toxicity via activating the NF-κB signaling pathway in rats.

Studies have demonstrated that nano NiO could induce liver toxicity in rats, but its mechanism remains unclear. This study aimed to explore the role of the NF-κB signaling pathway in rat liver toxicity after nano NiO exposure. Male Wistar rats were exposed to nano NiO (0.015, 0.06 and 0.24 mg per kg b.w.) and micro NiO (0.24 mg per kg b.w.) by intratracheal instillation twice a week for 6 weeks. To investigate the liver toxicity induced by nano NiO, the indicators of liver function and inflammatory response were detected, and the histopathological changes were observed. The levels of NF-κB signaling pathway related gene and protein expression were examined using RT-qPCR and western blot techniques in the liver tissue. The results showed that the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) increased after nano NiO exposure. Cellular edema, hepatic sinus disappearance, and neutrophil and lymphocyte infiltration were observed. Nano NiO increased the concentrations of pro-inflammatory cytokines (IL-1ß and IL-6), but decreased the levels of anti-inflammatory cytokines (IL-4 and IL-10). It also induced the upregulation of TNF-α, NF-κB-inducible kinase (NIK), IκB kinase alpha (IKK-α) and NF-κB mRNA, while inducing the downregulation of the inhibitor kappa B (IκB) alpha. In addition, we found that the protein content of NIK, IKK-α, p-IKK-α, p-IκB-α and NF-κB was elevated, whereas that of IκB-α was reduced. The results indicated that the NF-κB signaling pathway played an important role in rat liver toxicity induced by nano NiO.

Allyl isothiocyanate from mustard seed is effective in reducing the levels of volatile sulfur compounds responsible for intrinsic oral malodor.

Oral malodor is a major social and psychological issue that affects general populations. Volatile sulfur compounds (VSCs), particularly hydrogen sulfide (H2S) and methyl mercaptan (CH3SH), are responsible for most oral malodor. The objectives for this study were to determine whether allyl isothiocyanate (AITC) at an organoleptically acceptable level can eliminate VSCs containing a free thiol moiety and further to elucidate the mechanism of action and reaction kinetics. The study revealed that gas chromatograph with a sulfur detector demonstrated a good linearity, high accuracy and sensitivity on analysis of VSCs. Zinc salts eliminate the headspace level of H2S but not CH3SH. AITC eliminates both H2S and CH3SH via a nucleophilic addition reaction. In addition, a chemical structure-activity relationship study revealed that the presence of unsaturated group on the side chain of the isothiocyanate accelerates the elimination of VSCs.

Naturally occurring phenolic antibacterial compounds show effectiveness against oral bacteria by a quantitative structure-activity relationship study.

Natural and synthetic phenolic compounds were evaluated against oral bacteria. A quantitative structure-active relationship approach was applied to the germ-kill activity for a range of phenolic compounds. The lipophilicity and steric effects were found to be two key factors in determining germ-kill activity. The optimum lipophilicity, measured by the logarithm of the octanol/water partition coefficient, or log P, was found to be 5.5 for Fusobacterium nucleatum , a Gram-negative type of oral bacteria that causes bad breath. The optimum log P was found to be 7.9 for Streptococcus mutans , a Gram-positive type of oral bacteria that causes tooth decay. The steric effect of substituents ortho to the phenolic group was found to be critical in reducing antibacterial activity despite having increased lipid solubility approaching the optimum lipophilicity value. The antibacterial activity of phenolic compounds is likely exerted by multiple functions, primarily comes from its ability to act as a nonionic surface-active agent therefore disrupting the lipid-protein interface.