A progress update on the biological effects of biodegradable microplastics on soil and ocean environment: A perfect substitute or new threat?

Conventional plastics are inherently difficult to degrade, causing serious plastic pollution. With the development of society, biodegradable plastics (BPs) are considered as an alternative to traditional plastics. However, current research indicated that BPs do not undergo complete degradation in natural environments. Instead, they may convert into biodegradable microplastics (BMPs) at an accelerated rate, thereby posing a significant threat to environment. In this paper, the definition, application, distribution, degradation behaviors, bioaccumulation and biomagnification of BPs were reviewed. And the impacts of BMPs on soil and marine ecosystems, in terms of physicochemical property, nutrient cycling, microorganisms, plants and animals were comprehensively summarized. The effects of combined exposure of BMPs with other pollutants, and the mechanism of ecotoxicity induced by BMPs were also addressed. It was found that BMPs reduced pH, increased DOC content, and disrupted the nitrification of nitrogen cycle in soil ecosystem. The shoot dry weight, pod number and root growth of soil plants, and reproduction and body length of soil animals were inhibited by BMPs. Furthermore, the growth of marine plants, and locomotion, body length and survival of marine animals were suppressed by BMPs. Additionally, the ecotoxicity of combined exposure of BMPs with other pollutants has not been uniformly concluded. Exposure to BMPs induced several types of toxicity, including neurotoxicity, gastrointestinal toxicity, reproductive toxicity, immunotoxicity and genotoxicity. The future calls for heightened attention towards the regulation of the degradation of BPs in the environment, and pursuit of interventions aimed at mitigating their ecotoxicity and potential health risks to human.

Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics.

BACKGROUND: Nanoplastics (NPs) could be released into environment through the degradation of plastic products, and their content in the air cannot be ignored. To date, no studies have focused on the cardiac injury effects and underlying mechanisms induced by respiratory exposure to NPs. RESULTS: Here, we systematically investigated the cardiotoxicity of 40 nm polystyrene nanoplastics (PS-NPs) in mice exposed via inhalation. Four exposure concentrations (0 µg/day, 16 µg/day, 40 µg/day and 100 µg/day) and three exposure durations (1 week, 4 weeks, 12 weeks) were set for more comprehensive information and RNA-seq was performed to reveal the potential mechanisms of cardiotoxicity after acute, subacute and subchronic exposure. PS-NPs induced cardiac injury in a dose-dependent and time-dependent manner. Acute, subacute and subchronic exposure increased the levels of injury biomarkers and inflammation and disturbed the equilibrium between oxidase and antioxidase activity. Subacute and subchronic exposure dampened the cardiac systolic function and contributed to structural and ultrastructural damage in heart. Mechanistically, violent inflammatory and immune responses were evoked after acute exposure. Moreover, disturbed energy metabolism, especially the TCA cycle, in the myocardium caused by mitochondria damage may be the latent mechanism of PS-NPs-induced cardiac injury after subacute and subchronic exposure. CONCLUSION: The present study evaluated the cardiotoxicity induced by respiratory exposure to PS-NPs from multiple dimensions, including the accumulation of PS-NPs, cardiac functional assessment, histology observation, biomarkers detection and transcriptomic study. PS-NPs resulted in cardiac injury structurally and functionally in a dose-dependent and time-dependent manner, and mitochondria damage of myocardium induced by PS-NPs may be the potential mechanism for its cardiotoxicity.

Recent consequences of micro-nanaoplastics (MNPLs) in subcellular/molecular environmental pollution toxicity on human and animals.

Microplastics and Nanoplastics (MNPLs) pollution has been recognized as the important environmental pollution caused by human activities in addition to global warming, ozone layer depletion and ocean acidification. Most of the current studies have focused on the toxic effects caused by plastics and have not actively investigated the mechanisms causing cell death, especially at the subcellular level. The main content of this paper focuses on two aspects, one is a review of the current status of MNPLs contamination and recent advances in toxicological studies, which highlights the possible concentration levels of MNPLs in the environment and the internal exposure of humans. It is also proposed to pay attention to the compound toxicity of MNPLs as carriers of other environmental pollutants and pathogenic factors. Secondly, subcellular toxicity is discussed and the modes of entry and intracellular distribution of smaller-size MNPLs are analyzed, with particular emphasis on the importance of organelle damage to elucidate the mechanism of toxicity. Importantly, MNPLs are a new type of environmental pollutant and researchers need to focus not only on their toxicity, but also work with governments to develop measures to reduce plastic emissions, optimize degradation and control plastic aggression against organisms, especially humans, from multiple perspectives.

Research advances of microplastics and potential health risks of microplastics on terrestrial higher mammals: a bibliometric analysis and literature review.

Microplastics (MPs) have become increasingly serious global problems due to their wide distribution and complicated impacts on living organisms. To obtain a comprehensive overview of the latest research progress on MPs, we conducted a bibliometric analysis combined with a literature review. The results showed that the number of studies on MPs has grown exponentially since 2010. Recently, the hotspot on MPs has shifted to terrestrial ecosystems and biological health risks, including human health risks. In addition, the toxic effects, identification and quantification of MPs are relatively new research hotspots. We subsequently provide a review of MPs studies related to health risks to terrestrial higher mammals and, in particular, to humans, including detection methods and potential toxicities based on current studies. Currently, MPs have been found existing in human feces, blood, colon, placenta and lung, but it is still unclear whether this is associated with related systemic diseases. In vivo and in vitro studies have demonstrated that MPs cause intestinal toxicity, metabolic disruption, reproductive toxicity, neurotoxicity, immunotoxicity through oxidative stress, apoptosis and specific pathways, etc. Notably, in terms of combined effects with pollutants and neurotoxicity, the effects of MPs are still controversial. Future attention should be paid to the detection and quantification of MPs in human tissues, exploring the combined effects and related mechanisms of MPs with other pollutants and clarifying the association between MPs and the development of pre-existing diseases. Our work enhances further understanding of the potential health risks of MPs to terrestrial higher mammals.

In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model.

Nanoplastics, including polystyrene nanoplastics (PS-NPs), are widely existed in the atmosphere, which can be directly and continuously inhaled into the human body, posing a serious threat to the respiratory system. Therefore, it is urgent to estimate the potential pulmonary toxicity of airborne NPs and understand its underlying mechanism. In this research, we used two types of human lung epithelial cells (bronchial epithelium transformed with Ad12-SV40 2B, BEAS-2B) and (human pulmonary alveolar epithelial cells, HPAEpiC) to investigate the association between lung injury and PS-NPs. We found PS-NPs could significantly reduce cell viability in a dose-dependent manner and selected 7.5, 15 and 30 µg/cm2 PS-NPs as the exposure dosage levels. Microarray detection revealed that 770 genes in the 7.5 µg/cm2 group and 1951 genes in the 30 µg/cm2 group were distinctly altered compared to the control group. Function analysis suggested that redox imbalance might play central roles in PS-NPs induced lung injury. Further experiments verified that PS-NPs could break redox equilibrium, induce inflammatory effects, and triggered apoptotic pathways to cause cell death. Importantly, we found that PS-NPs could decrease transepithelial electrical resistance by depleting tight junctional proteins. Result also demonstrated that PS-NPs-treated cells increased matrix metallopeptidase 9 and Surfactant protein A levels, suggesting the exposure of PS-NPs might reduce the repair ability of the lung and cause tissue damage. In conclusion, nanoplastics could induce oxidative stress and inflammatory responses, followed by cell death and epithelial barrier destruction, which might result in tissue damage and lung disease after prolonged exposure.

Bioinspired in Vitro Lung Airway Model for Inflammatory Analysis via Hydrophobic Nanochannel Membrane with Joint Three-Phase Interface.

Because of the extremely low solubility of gas pollution, elucidating the pathogenetic mechanism between air pollution and the lung inflammatory response has remained a significant challenge. Here, we develop a bioinspired nanoporous membrane (BNM) with a three-phase interface as a gas exposure model that mimicks the airway mechanism, gas molecules contacting with alveolar cells directly, enabling high cell viability and sensitive inflammatory response analysis. Specifically, the top side of the porous anodic alumina (PAA) membrane was in contact with the medium for cell culture, and the bottom side contacted the gas phase directly for gas exposure. Compared with the two-phase interface, the viability of cells on the BNM was enhanced up to 3-fold. Additionally, results demonstrated that the inflammatory responses of cells stimulated by gas pollution (formaldehyde and benzene as models) from the gas phase were more obvious than those induced by gas pollution from solution, especially the increment of interleukin-2 (IL-2), IL-6, and tumor necrosis factor α (TNF-α), which was almost 2 times greater than that induced by gas pollution from solution. Furthermore, an enzyme inhibitor was introduced to evaluate potential applications of the BNM.

Galactosylated 2-hydroxypropyl methacrylamide-s-3-guanidinopropyl methacrylamide copolymer as a small hairpin RNA carrier for inhibiting human telomerase reverse transcriptase expression.

BACKGROUND: In the present study, a well-defined glucose and guanidine based copolymer, galactosylated 2-hydroxypropyl methacrylamide-s-3-guanidinopropyl methacrylamide (HPMA-s-GPMA) abbreviated as GGH was prepared and self-assembled with small hairpin RNA (shRNA) to inhibit human telomerase reverse transcriptase (hTERT) gene expression in vitro to develop a shRNA carrier. METHODS: First, HPMA-s-APMA copolymers were synthesized by aqueous reversible addition-fragmentation chain transfer polymerization, followed by galactosylation and guanidinylation. Then, three target shRNAs containing green fluorescent protein gene as a reporter were combined with GGH to form shRNA/GGH polyplexes. RESULTS: GGH copolymers could condense shRNA to form shRNA/GGH polyplex particles with a diameter in the range 122.8-331.6 nm in phosphate-buffered saline, and zeta potential values ranging from +3.7 to +16.5 mV at various charge ratios (N/P). That the cytotoxicity of GGH copolymers was significantly lower than that of PEI in human hepatocellular liver carcinoma cells (HepG2) and human cervix epithelial carcinoma cells. The transfection efficiency of shRNA/GGH polyplexes was higher than that of PEI at a charge ratio of 12 in the HepG2 cell line. Furthermore, shRNA/GGH polyplexes could effectively silence hTERT mRNA expression in serum-free medium (p < 0.01) and decrease the aggregation of protein in the medium with the presence of 10% serum. In addition, hTERT mRNA expression in HepG2 cells demosntrate a significant difference between siRNA/GGH polyplexes and blank samples (p < 0.05). CONCLUSIONS: GGH copolymers could integrate advantages relating to galactose content for hepatocyte targeting, guanidino groups for cell penetration and HPMA component for shielding, showing great potential for effective hepatocyte targeting gene delivery.

Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment.

Nanoplastics are widely distributed in indoor and outdoor air and can be easily inhaled into human lungs. However, limited studies have investigated the impact of nanoplastics on inhalation toxicities, especially on the initiation and progression of chronic obstructive pulmonary disease (COPD). To fill the gap, the present study used oronasal aspiration to develop mice models. Mice were exposed to polystyrene nanoplastics (PS-NPs) at three concentrations, as well as the corresponding controls, for acute, subacute, and subchronic exposure. As a result, PS-NPs could accumulate in exposed mice lungs and influence lung organ coefficient. Besides, PS-NPs induced local and systemic oxidative stress, inflammation, and protease-antiprotease imbalance, resulting in decreased respiratory function and COPD-like lesions. Meanwhile, PS-NPs could trigger the subcellular mechanism to promote COPD development by causing mitochondrial dysfunctions and endoplasmic reticulum (ER) stress. Mechanistically, ferroptosis played an important role in the COPD-like lung injury induced by PS-NPs. In summary, the present study comprehensively and systematically indicates that PS-NPs can damage human respiratory health and increase the risk for COPD.

Polystyrene micro- and nanoplastics induce gastric toxicity through ROS mediated oxidative stress and P62/Keap1/Nrf2 pathway.

Microplastics (MPs) exist widely in the environment and can enter the human body indirectly through the food chain or directly through inhalation or ingestion. The primary organ that MPs contaminated food or water enters the human body through the digestive tract is the stomach. However, at present, the effects of MPs on the stomach and the related mechanism remain unclear. In this study, our results indicated that 50 nm and 250 nm polystyrene MPs (PS-MPs) at environmental related dose significantly decreased stomach organ coefficient, inhibited gastric juice secretion and mucus secretion, disrupted gastric barrier function and suppressed antioxidant ability in mice. In vitro experiments showed that PS-MPs inhibited cell viability, increased ROS generation, and induced apoptosis through mitochondria-dependent pathway. Simultaneously, PS-MPs also decreased mitochondrial membrane potential, ATP level, disrupted mitochondrial kinetic homeostasis, and activated P62 / Nrf2 / Keap1 pathway. Furthermore, blocking ROS (NAC) partially alleviated ROS and apoptosis caused by PS-MPs. Based on above findings, the potential adverse outcome pathway (AOP) of PS-MPs-caused gastric toxicity was proposed which provides a new insight into the risk assessment of MP related gastric damage. Our study unveils the gastric injury induced by PS MPs is dependent on ROS - mediated P62 / Nrf2 / Keap1 signaling pathway, and provides scientific basis for further exploration the mechanism of gastric toxicity of PS MPs.

Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis.

The emerging contaminant nanoplastics (NPs) have received considerable attention. Due to their tiny size and unique colloidal properties, NPs could more easily enter the body and cross biological barriers with inhalation exposure. While NPs-induced hepatotoxicity has been reported, the hepatic impact of inhaled NPs was still unknown. To close this gap, a 40 nm polystyrene NPs (PS-NPs) inhalation exposure mice model was developed to explore the hepatotoxicity during acute (1 week), subacute (4 weeks), and subchronic period (12 weeks), with four exposure doses (0, 16, 40, and 100 µg/day). Results showed that inhaled PS-NPs caused a remarkable increase of ALT, AST, and ALP with a decrease of CHE, indicating liver dysfunction. Various histological abnormalities and significantly higher levels of inflammation in a dose- and time-dependent manner were observed. Moreover, after 4 weeks and 12 weeks of exposure, Masson staining and upregulated expression of TGF-ß, α-SMA, and Col1a1 identified that inhaled PS-NPs exposure triggered the progression of liver fibrosis with the exposure time prolonged. From the mechanistic perspective, transcriptome analysis revealed that ferroptosis was involved in PS-NPs-induced liver hepatotoxicity, and key features of ferroptosis were detected, including persistent oxidative stress, iron overload, increased LPO, mitochondria damage, and the expression changes of GPX4, TFRC, and Ferritin. And in vitro and in vivo recovery tests showed that ferroptosis inhibitor Fer-1 treatment alleviated liver injury and fibrosis. The above results confirmed the critical role of ferroptosis in PS-NPs-induced hepatotoxicity. Furthermore, to better conclude our findings and understand the mechanistic causality within it, an adverse outcome pathway (AOP) framework was established. In total, this present study conducted the first experimental assessment of inhalation exposure to PS-NPs on the liver, identified that continuous inhaled PS-NPs could cause liver injury and fibrosis, and PS-NPs- ferroptosis provided a novel mechanistic explanation.

Flow injection chemiluminescence immunoassay of microcystin-LR by using PEI-modified magnetic beads as capturer and HRP-functionalized silica nanoparticles as signal amplifier.

A rapid sandwiched immunoassay of microcystin-LR (MC-LR) in water is proposed with flow injection chemiluminescence detection. The magnetic beads (MBs) were first modified with polyethyleneimine (PEI) by acylamide bond between the carboxyl group on the surface of MBs and the primary amine group in PEI, followed by immobilizing of anti-MC-LR (Ab1) onto PEI with glutaraldehyde as linkage. The resulting Ab1 modified MBs captured the target MC-LR in water, reacted with the horseradish peroxidase and anti-MC-LR co-immobilized silica nanoparticles, and were detected with flow injection chemiluminescence. When using PEI/MBs as the carrier of anti-MC-LR, the CL signal was greatly enhanced up to 9-fold compared to that using MBs without PEI modification. The CL signal was further amplified 13-fold when Si/Ab2 was used as the signal probe. Under the optimal conditions, the present immunoassay exhibited a wide quantitative range from 0.02 to 200 µg L(-1) with a detection limit of 0.006 µg L(-1), which was much lower than the WHO provisional guideline limit of 1.0 µg L(-1) for MC-LR in drinking water. The relative standard deviation was 4.8% and the recoveries for the spiked samples ranged from 84% to 115%, which indicated acceptable precision and accuracy for MC-LR. The present method is easier to perform and less time-consuming (the entire analysis process lasted about 40 minutes) and has been applied to the detection of MC-LR in different water samples successfully.

Ferritinophagy Mediated by Oxidative Stress-Driven Mitochondrial Damage Is Involved in the Polystyrene Nanoparticles-Induced Ferroptosis of Lung Injury.

Nanoplastics are a common type of contaminant in the air. However, no investigations have focused on the toxic mechanism of lung injury induced by nanoplastic exposure. In the present study, polystyrene nanoplastics (PS-NPs) caused ferroptosis in lung epithelial cells, which could be alleviated by ferrostatin-1, deferoxamine, and N-acetylcysteine. Further investigation found that PS-NPs disturbed mitochondrial structure and function and triggered autophagy. Mechanistically, oxidative stress-derived mitochondrial damage contributed to ferroptosis, and autophagy-dependent ferritinophagy was a pivotal intermediate link, resulting in ferritin degradation and iron ion release. Furthermore, inhibition of ferroptosis using ferrostatin-1 alleviated pulmonary and systemic toxicity to reverse the mouse lung injury induced by PS-NPs inhalation. Most importantly, the lung-on-a-chip was further used to clarify the role of ferroptosis in the PS-NPs-induced lung injury by visualizing the ferroptosis, oxidative stress, and alveolar-capillary barrier dysfunction at the organ level. In summary, our study indicated that ferroptosis was an important mechanism for nanoplastics-induced lung injury through different lung cells, mouse inhalation models, and three-dimensional-based lung-on-a-chip, providing an insightful reference for pulmonary toxicity assessment of nanoplastics.

Sentinel supervised lung-on-a-chip: A new environmental toxicology platform for nanoplastic-induced lung injury.

Nanoplastics are prevalent in the air and can be easily inhaled, posing a threat to respiratory health. However, there have been few studies investigating the impact of nanoplastics on lung injury, especially chronic obstructive pulmonary disease (COPD). Furthermore, cell and animal models cannot deeply understand the pollutant-induced COPD. Existing lung-on-a-chip models also lack interactions among immune cells, which are crucial in monitoring complex responses. In the study, we built the lung-on-a-chip to accurately recapitulate the structural features and key functions of the alveolar-blood barrier while integrating multiple immune cells. The stability and reliability of the lung-on-a-chip model were demonstrated by toxicological application of various environmental pollutants. We Further focused on exploring the association between COPD and polystyrene nanoplastics (PS-NPs). As a result, the cell viability significantly decreased as the concentration of PS-NPs increased, while TEER levels decreased and permeability increased. Additionally, PS-NPs could induce oxidative stress and inflammatory responses at the organ level, and crossed the alveolar-blood barrier to enter the bloodstream. The expression of α1-antitrypsin (AAT) was significantly reduced, which could be served as early COPD checkpoint on the lung-chips. Overall, the lung-on-a-chip provides a new platform for investigating the pulmonary toxicity of nanoplastics, demonstrating that PS-NPs can harm the alveolar-blood barrier, cause oxidative damage and inflammation, and increase the risk of COPD.

Microplastics induce neurotoxicity in aquatic animals at environmentally realistic concentrations: A meta-analysis.

Microplastics (MPs) draw international attention owing to their widespread distribution in water ecosystems, but whether MPs cause neurotoxic effects in aquatic animals at environmentally realistic concentrations is still controversial. This meta-analysis recompiled 35 studies to determine whether MPs could change the levels of brain (in vivo) neurotransmitters in aquatic animals at environmentally realistic concentrations (≤1 mg/L, median = 0.100 mg/L). Then, a group comparison was conducted to compare the effects of different factors on the effect size and to explore the significant factors affecting the neurotoxicity of MPs. The results demonstrated that MP exposure could considerably decrease the levels of acetylcholinesterase (AchE) in the brain of aquatic animals by 16.2%. However, the effects of MPs on cholinesterase (CHE), acetylcholine (ACh), dopamine (DA) and γ-aminobutyric acid (GABA) were not statistically significant due to the small number of studies and samples. The neurotoxicity of MPs was closely linked with particle size and exposure time but independent of animal species, MP compositions, MP morphology and MP concentrations. Further literatures review indicated that MP-induced neurotoxicity and behavioral changes are related with multiple biological processes, including nerve damage, oxidative stress, intestinal flora disturbance and metabolic disorder. Furthermore, some factors influencing MP neurotoxicity in the real environment (e.g. the aging of MPs, the release of MP additives, and the co-exposure of MPs and pollutants) were discussed. Overall, this study preliminarily explored whether MPs induced changes in neurotoxicity-related indicators in aquatic animals through meta-analysis and provided scientific evidence for evaluating the health risks and neurotoxicity of MPs at the environmental level.

The hepatotoxicity assessment of micro/nanoplastics: A preliminary study to apply the adverse outcome pathways.

Plastic pollution has become a significant global problem over the years, leading to the continuous decomposition and accumulation of micro/nanoplastics (MNPLs) in the environment. As a result, human exposure to these MNPLs is inevitable. The liver, in particular, is highly susceptible to potential MNPL toxicity. In this study, we systematically reviewed the current literature on MNPLs-induced hepatotoxicity and collected data on toxic events occurring at different biological levels. Then, to better understand the cause-mechanism causality, we developed an Adverse Outcome Pathway (AOP) framework for MNPLs-induced hepatotoxicity. The AOP framework provided insights into the mechanism of MNPL-induced hepatotoxicity and highlighted potential health risks such as liver dysfunction and inflammation, metabolism disorders and liver fibrosis. Moreover, we discussed the potential application of emerging toxicological models in the hepatotoxicity study. Liver organoids and liver-on-chips, which can simulate the structure and function of the liver in vitro, offer a promising alternative platform for toxicity testing and risk assessment. We proposed combining the AOP framework with these emerging toxicological models to improve our understanding of the hepatotoxic effects of MNPLs. Overall, this study performed a preliminary exploration of novel toxicological methodologies to assess the hepatotoxicity of MNPLs, providing a deeper understanding of environmental toxicology.

Optimized method for preparation of TiO2 nanoparticles dispersion for biological study.

The objective of the present study was to develop a practical method to prepare a stable dispersion of TiO2 nanoparticles for biological studies. To address this matter a variety of different approaches for suspension of nanoparticles were conducted. TiO2 (rutile/anatase) dispersions were prepared in distilled water following by treated with different ultrasound energies and various dispersion stabilizers (1.0% carboxymethyl cellulose, 0.5% hydroxypropyl methyl cellulose K4M, 100% fetal bovine serum, and 2.5% bovine serum albumin). The average size of dispersed TiO2 (rutile/anatase) nanoparticles was measured by dynamic light scattering device. Agglomerate sizes of TiO2 in distilled water and 100% FBS were estimated using TEM analysis. Sedimentation rate of TiO2 (rutile/anatase) nanoparticles in dispersion was monitored by optical absorbance detection. In vitro cytotoxicity of various stabilizers in 16-HBE cells was measured using MTT assay. The optimized process for preparation of TiO2 (rutile/anatase) nanoparticles dispersion was first to vibrate the nanoparticles by vortex and disperse particles by ultrasonic vibration in distilled water, then to add dispersion stabilizers to the dispersion, and finally to sonicate the nanoparticles in dispersion. TiO2 (rutile/anatase) nanoparticles were disaggregated sufficiently with an ultrasound energy of 33 W for 10 min. The formation of TiO2 (rutile/anatase) agglomerates in distilled water was decreased obviously by addition of 1.0% CMC, 0.5% HPMC K4M, 100% FBS and 2.5% BSA. For the benefit of cell growth, FBS is the most suitable stabilizer for preparation of TiO2 (rutile/anatase) particle dispersions and subsequent investigation of the in vivo and in vitro behavior of TiO2 (rutile/anatase) nanoparticles. This method is practicable to prepare a stable dispersion of TiO2 (rutile/anatase) nanoparticles for at least 120 h.

[In vivo degradation and tissue compatibility of poly-L-lactide/beta-tricalcium phosphate composite rods for internal fixation of bone fractures].

Abstract Poly-l-lactide/beta-tricalcium phosphate (PLLA/betaTCP) composite was obtained by combining ground beta-TCP with PLLA, and absorbable rods were prepared by injection moulding. Degradations of the rods were investigated by scanning electron microscope (SEM), mass loss, molecular weight and bending strength changes. At the beginning of in vivo degradation of the rods, the molecular weight of PLLA decreases sharply with the less mass losses of the rods. As in vivo degradation progress, the surfaces of the rods changed roughly, while micropores and fine groove were observed in the inner part of the rods. The bending strength of composite rods decreased from 151 MPa to 106 MPa after in vivo degradation of 12 weeks. Tissue test reveal that PLLA/beta-TCP composite has good tissue compatibility compared with PLLA.

Systemic and immunotoxicity of pristine and PEGylated multi-walled carbon nanotubes in an intravenous 28 days repeated dose toxicity study.

The numerous increasing use of carbon nanotubes (CNTs) derived from nanotechnology has raised concerns about their biosafety and potential toxicity. CNTs cause immunologic dysfunction and limit the application of CNTs in biomedicine. The immunological responses induced by pristine multi-walled carbon nanotubes (p-MWCNTs) and PEGylated multi-walled carbon nanotubes (MWCNTs-PEG) on BALB/c mice via an intravenous administration were investigated. The results reflect that the p-MWCNTs induced significant increases in spleen, thymus, and lung weight. Mice treated with p-MWCNTs showed altered lymphocyte populations (CD3+, CD4+, CD8+, and CD19+) in peripheral blood and increased serum IgM and IgG levels, and splenic macrophage ultrastructure indicated mitochondria swelling. p-MWCNTs inhibited humoral and cellular immunity function and were associated with decreased immune responses against sheep erythrocytes and serum hemolysis level. Natural killer (NK) activity was not modified by two types of MWCNTs. In comparison with two types of MWCNTs, for a same dose, p-MWCNTs caused higher levels of inflammation and immunosuppression than MWCNTs-PEG. The results of immunological function suggested that after intravenous administration with p-MWCNTs caused more damage to systemic immunity than MWCNTs-PEG. Here, we demonstrated that a surface functional modification on MWCNTs reduces their immune perturbations in vivo. The chemistry-modified MWCNTs change their preferred immune response in vivo and reduce the immunotoxicity of p-MWCNTs.

[A study on the repair of bone defects with deproteinized bone surrounded by titanium mesh and osteoblasts].

To investigate the ability of composite graft of osteobalsts and deproteinized bone-titanium mesh (DPB-TM) scaffold to repair cranial bone defect. 30 rabbits were randomly divided into 3 groups. The passage 3 fetal rabbit osteoblasts were seeded into porous DPB-TM scaffolds at the density of 5 x 10(6) ml(-1) as the experimental group. The same defects were respectively reconstructed by DPB-TM or osteoblasts as the control groups. After 12 weeks, the result was evaluated by three-dimensional computed tomographic scanning, gross inspection, scanning electron microscopy, histological examination and mechanics test, respectively. In the experimental group, bone trabecula was observed to pass the defect and interface was mixed. No demarcation between the region of the bone defect and the normal bone was observed. There was plenty of new bone on the scaffold. Part of the scaffold was absorbed. In view of mechanics, the intensity of artificial bone (18.93+/-1.12 MPa) was higher than that of normal bone (16.96+/-1.60 MPa) (P<0.05). In the control groups, only fibrous tissue was observed in the defect region, there was no new bone formation. The tissue engineering bone constructed by osteoblasts and DPB-TM scaffold can be applied to the repair of bone defect.

[Study on hydroxyapatite porous scaffold bonded by phosphates and its biocompatibility].

The porous scaffolds for bone tissue engineering were prepared by foam impregnation. The magnesium and aluminum acid phosphates were used as bonder and the hydroxyapatite ((Ca10 (PO4)6(OH)2, HA) powder as raw materials. Scanning electron microscopy (SEM) examination indicated that the 3D interconnected porous structure of the organic foam was replicated well by the scaffolds calcined at high temperature and the structural requirement of tissue engineering was satisfied. XRD analysis showed that the scaffold was composed of HA and Ca7Mg2P6O24 while calcined at 1150 degrees C for shorter time and of (Ca, Mg)3(PO4)2 when the time prolonged to 2 h. There was no peak of CaO found in the scaffolds by XRD. According to the culture in vitro, the scaffold possesses good biocompatibility and certain degree of degradability.