Pearl Farming Micro-Nanoplastics Affect Oyster Physiology and Pearl Quality.

Pearl farming is crucial for the economy of French Polynesia. However, rearing structures contribute significantly to plastic waste, and the widespread contamination of pearl farming lagoons by microplastics has raised concerns about risks to the pearl industry. This study aimed to evaluate the effects of micro-nanoplastics (MNPs, 0.4-200 µm) on the pearl oyster (Pinctada margaritifera) over a 5-month pearl production cycle by closely mimicking ecological scenarios. MNPs were produced from weathered plastic pearl farming gear and tested at environmentally relevant concentrations (0.025 and 1 µg L-1) to decipher biological and functional responses through integrative approaches. The significant findings highlighted the impacts of MNPs on oyster physiology and pearl quality, even at remarkably low concentrations. Exposure to MNPs induced changes in energy metabolism, predominantly driven by reduced assimilation efficiency of microalgae, leading to an alteration in gene expression patterns. A distinct gene expression module exhibited a strong correlation with physiological parameters affected by MNP conditions, identifying key genes as potential environmental indicators of nutritional-MNP stress in cultured oysters. The alteration in pearl biomineralization, evidenced by thinner aragonite crystals and the presence of abnormal biomineral concretions, known as keshi pearls, raises concerns about the potential long-term impact on the Polynesian pearl industry.

A cascade nanosystem with "Triple-Linkage" effect for enhanced photothermal and activatable metal ion therapy for hepatocellular carcinoma.

Due to the limitations of single-model tumor therapeutic strategies, multimodal combination therapy have become a more favorable option to enhance efficacy by compensating for its deficiencies. However, in nanomaterial-based multimodal therapeutics for tumors, exploiting synergistic interactions and cascade relationships of materials to achieve more effective treatments is still a great challenge. Based on this, we constructed a nanoplatform with a "triple-linkage" effect by cleverly integrating polydopamine (PDA), silver nanoparticles (AgNPs), and glucose oxidase (GOx) to realize enhanced photothermal therapy (PTT) and activatable metal ion therapy (MIT) for hepatocellular carcinoma (HCC) treatment. First, the non-radiative conversion of PDA under light conditions was enhanced by AgNPs, which directly enhanced the photothermal conversion efficiency of PDA. In addition, GOx reduced the synthesis of cellular heat shock proteins by interfering with cellular energy metabolism, thereby enhancing cellular sensitivity to PTT. On the other hand, H2O2, a by-product of GOx-catalyzed glucose, could be used as an activation source to activate non-toxic AgNPs to release cytotoxic Ag+, achieving activatable Ag+-mediated MIT. In conclusion, this nanosystem achieved efficient PTT and MIT for HCC by exploiting the cascade effect among PDA, AgNPs, and GOx, providing a novel idea for the design of multimodal tumor therapeutic systems with cascade regulation.

Integrative Metabolomics, Enzymatic Activity, and Gene Expression Analysis Provide Insights into the Metabolic Profile Differences between the Slow-Twitch Muscle and Fast-Twitch Muscle of Pseudocaranx dentex.

The skeletal muscles of teleost fish encompass heterogeneous muscle types, termed slow-twitch muscle (SM) and fast-twitch muscle (FM), characterized by distinct morphological, anatomical, histological, biochemical, and physiological attributes, driving different swimming behaviors. Despite the central role of metabolism in regulating skeletal muscle types and functions, comprehensive metabolomics investigations focusing on the metabolic differences between these muscle types are lacking. To reveal the differences in metabolic characteristics between the SM and FM of teleost, we conducted an untargeted metabolomics analysis using Pseudocaranx dentex as a representative model and identified 411 differential metabolites (DFMs), of which 345 exhibited higher contents in SM and 66 in FM. KEGG enrichment analysis showed that these DFMs were enriched in the metabolic processes of lipids, amino acids, carbohydrates, purines, and vitamins, suggesting that there were significant differences between the SM and FM in multiple metabolic pathways, especially in the metabolism of energy substances. Furthermore, an integrative analysis of metabolite contents, enzymatic activity assays, and gene expression levels involved in ATP-PCr phosphate, anaerobic glycolysis, and aerobic oxidative energy systems was performed to explore the potential regulatory mechanisms of energy metabolism differences. The results unveiled a set of differential metabolites, enzymes, and genes between the SM and FM, providing compelling molecular evidence of the FM achieving a higher anaerobic energy supply capacity through the ATP-PCr phosphate and glycolysis energy systems, while the SM obtains greater energy supply capacity via aerobic oxidation. These findings significantly advance our understanding of the metabolic profiles and related regulatory mechanisms of skeletal muscles, thereby expanding the knowledge of metabolic physiology and ecological adaptation in teleost fish.

Mitochondria: An Emerging Unavoidable Link in the Pathogenesis of Periodontitis Caused by Porphyromonas gingivalis.

Porphyromonas gingivalis (P. gingivalis) is a key pathogen of periodontitis. Increasing evidence shows that P. gingivalis signals to mitochondria in periodontal cells, including gingival epithelial cells, gingival fibroblast cells, immune cells, etc. Mitochondrial dysfunction affects the cellular state and participates in periodontal inflammatory response through the aberrant release of mitochondrial contents. In the current review, it was summarized that P. gingivalis induced mitochondrial dysfunction by altering the mitochondrial metabolic state, unbalancing mitochondrial quality control, prompting mitochondrial reactive oxygen species (ROS) production, and regulating mitochondria-mediated apoptosis. This review outlines the impacts of P. gingivalis and its virulence factors on the mitochondrial function of periodontal cells and their role in periodontitis.

Inorganic polyphosphate and the regulation of mitochondrial physiology.

Inorganic polyphosphate (polyP) is an ancient polymer that is well-conserved throughout evolution. It is formed by multiple subunits of orthophosphates linked together by phosphoanhydride bonds. The presence of these bonds, which are structurally similar to those found in ATP, and the high abundance of polyP in mammalian mitochondria, suggest that polyP could be involved in the regulation of the physiology of the organelle, especially in the energy metabolism. In fact, the scientific literature shows an unequivocal role for polyP not only in directly regulating oxidative a phosphorylation; but also in the regulation of reactive oxygen species metabolism, mitochondrial free calcium homeostasis, and the formation and opening of mitochondrial permeability transitions pore. All these processes are closely interconnected with the status of mitochondrial bioenergetics and therefore play a crucial role in maintaining mitochondrial and cell physiology. In this invited review, we discuss the main scientific literature regarding the regulatory role of polyP in mammalian mitochondrial physiology, placing a particular emphasis on its impact on energy metabolism. Although the effects of polyP on the physiology of the organelle are evident; numerous aspects, particularly within mammalian cells, remain unclear and require further investigation. These aspects encompass, for example, advancing the development of more precise analytical methods, unraveling the mechanism responsible for sensing polyP levels, and understanding the exact molecular mechanism that underlies the effects of polyP on mitochondrial physiology. By increasing our understanding of the biology of this ancient and understudied polymer, we could unravel new pharmacological targets in diseases where mitochondrial dysfunction, including energy metabolism dysregulation, has been broadly described.

Polypropylene microplastics affect the physiology in Drosophila model.

Microplastics (MPs) pollution has been a hot research topic in recent years. MPs are ubiquitous throughout the ecological environment and are eventually accumulated in organisms through inhalation or ingestion. However, given that MPs are inert pollutants, their effects on organisms are not clear. In previous study, we have investigated the effects of polyethylene terephthalate MPs on physiology of Drosophila. What is the effect of polypropylene microplastics (PP-MPs)? The results of our experiments show that being exposed to high concentration of PP-MPs have significant effect on Drosophila. PP-MPs exposure can significantly increase locomotor activity and shorten the time of group sleep in Drosophila. In the presence of high concentrations of PP-MPs, the triglyceride content was reduced in females and their ability of egg production was affected. However, there was no significant effect on the level of protein and carbohydrate, or on the food intake. Our experimental results can provide some preliminary data for assessing the potential hazard of PP-MPs to other organisms.

Microplastics increases the heat tolerance of Daphnia magna under global warming via hormetic effects.

The ecological risk assessment of microplastics under global warming receives increasing attention. Yet, such studies mostly focused on increased mean temperatures (MT), ignoring another key component of global warming, namely daily temperature fluctuations (DTF). Moreover, we know next to nothing about the combined effects of multigenerational exposure to microplastics and warming. In this study, Daphnia magna was exposed to an environmentally relevant concentration of polystyrene microplastics (5 µg L-1) under six thermal conditions (MT: 20 â„ƒ, 24 â„ƒ; DTF: 0 â„ƒ, 5 â„ƒ, 10 â„ƒ) over two generations to investigate the interactive effects of microplastics and global warming. Results showed that microplastics had no effects on Daphnia at standard thermal conditions (constant 20 °C). Yet, microplastics increased the fecundity, heat tolerance, amount of energy storage, net energy budget and cytochrome P450 activity, and decreased the energy consumption when tested under an increased MT or DTF, indicating a hormesis effect induced by microplastics under warming. The unexpected increase in heat tolerance upon exposure to microplastics could be partly explained by the reduced energy consumption and/or increased energy availability. Overall, the present study highlighted the importance of including DTF and multigenerational exposure to improve the ecological risk assessment of microplastics under global warming.

Hyperleptinemia as a contributing factor for the impairment of glucose intolerance in obesity.

Obesity has emerged as a major risk factor for insulin resistance leading to the development of type 2 diabetes (T2D). The condition is characterized by high circulating levels of the adipose-derived hormone leptin and a state of chronic low-grade inflammation. Pro-inflammatory signaling in the hypothalamus is associated with a decrease of central leptin- and insulin action leading to impaired systemic glucose tolerance. Intriguingly, leptin not only regulates body weight and glucose homeostasis but also acts as a pro-inflammatory cytokine. Here we demonstrate that increasing leptin levels (62,5 µg/kg/d, PEGylated leptin) in mice fed a high-fat diet (HFD) exacerbated body weight gain and aggravated hypothalamic micro- as well as astrogliosis. In contrast, administration of a predetermined dose of a long-acting leptin antagonist (100 µg/kg/d, PESLAN) chosen to block excessive leptin signaling during diet-induced obesity (DIO) showed the opposite effect and significantly improved glucose tolerance as well as decreased the total number of microglia and astrocytes in the hypothalamus of mice fed HFD. These results suggest that high levels of leptin, such as in obesity, worsen HFD-induced micro-and astrogliosis, whereas the partial reduction of hyperleptinemia in DIO mice may have beneficial metabolic effects and improves hypothalamic gliosis.

Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

Anti-Fatigue Effects of Lycium barbarum Polysaccharide and Effervescent Tablets by Regulating Oxidative Stress and Energy Metabolism in Rats.

The purpose of this study was to investigate the anti-fatigue effect of natural Lycium barbarum polysaccharide (LBP) during exercise, develop a functional anti-fatigue effervescent tablet by applying LBP to practical products, and help patients who have difficulty swallowing conventional tablets or capsules. LBP was extracted with water, and DEAE-52 cellulose was used for purification. The chemical structure and monosaccharide composition of LBP by Fourier transform infrared spectroscopy (FI-IR) and ion chromatography (IC). Lycium barbarum polysaccharide effervescent tablets (LBPT) were prepared by mixing LBP and an excipient. Animal experiments showed that LBP and LBPT significantly increased the exhaustive swimming time in rats. LBP and LBPT improved biochemical markers in rat serum, such as lactic acid and creatine kinase, enhanced the antioxidant capacity of rat muscle, and reversed the decrease in serum glucose, ATP and glycogen content caused by exercise. Transmission electron microscopy showed that LBP and LBPT increased the density of mitochondria in rat liver. In addition, molecular experiments showed that LBP and LBPT could improve oxidative stress caused by exercise by regulating the Nrf2/HO-1 signaling pathway and regulating energy metabolism via the AMPK/PGC-1α signaling pathway.

Microplastics (Polystyrene) Exposure Induces Metabolic Changes in the Liver of Rare Minnow (Gobiocypris rarus).

Microplastics are environmental contaminants and an emergent concern. Microplastics are abundant in freshwater and can cause biochemical stress in freshwater organisms. In the current study, rare minnows (Gobiocypris rarus) were exposed to 1µm polystyrene microplastics at 200 µg/L concentration. We observed various sublethal effects after four weeks of exposure but no mortality. Numerous cellular and tissue alterations were observed in the liver. Differential metabolites and differentially expressed genes between control and exposure groups were identified and mapped to pathways in the Kyoto Encyclopedia of Genes and Genomes. The combination of transcriptomic and metabolomic analyses revealed significantly varied metabolic pathways between the two groups. These pathways were involved in glucolipid, amino acid, and nucleotide metabolism. Results demonstrated that MP exposure induced immune reaction, oxidative stress, and disturbed glycolipid and energy metabolism. The current study provided novel insights into the molecular and metabolic mechanisms of microplastic ecotoxicology in rare minnow.

Citrate-based materials fuel human stem cells by metabonegenic regulation.

A comprehensive understanding of the key microenvironmental signals regulating bone regeneration is pivotal for the effective design of bioinspired orthopedic materials. Here, we identified citrate as an osteopromotive factor and revealed its metabonegenic role in mediating citrate metabolism and its downstream effects on the osteogenic differentiation of human mesenchymal stem cells (hMSCs). Our studies show that extracellular citrate uptake through solute carrier family 13, member 5 (SLC13a5) supports osteogenic differentiation via regulation of energy-producing metabolic pathways, leading to elevated cell energy status that fuels the high metabolic demands of hMSC osteodifferentiation. We next identified citrate and phosphoserine (PSer) as a synergistic pair in polymeric design, exhibiting concerted action not only in metabonegenic potential for orthopedic regeneration but also in facile reactivity in a fluorescent system for materials tracking and imaging. We designed a citrate/phosphoserine-based photoluminescent biodegradable polymer (BPLP-PSer), which was fabricated into BPLP-PSer/hydroxyapatite composite microparticulate scaffolds that demonstrated significant improvements in bone regeneration and tissue response in rat femoral-condyle and cranial-defect models. We believe that the present study may inspire the development of new generations of biomimetic biomaterials that better recapitulate the metabolic microenvironments of stem cells to meet the dynamic needs of cellular growth, differentiation, and maturation for use in tissue engineering.

The ontogenesis of catabolic abilities and energy metabolism during endogenous nutritional periods of tongue sole, Cynoglossus semilaevis.

The ontogenesis of catabolic abilities and energy metabolism during endogenous nutritional periods of tongue sole was investigated. In this work, trypsin-like proteases (TRY) and triglyceride lipase (LIP) activities were measured to assess the capacities to catabolize proteins and lipids, respectively. Meanwhile, specific enzymes including pyruvate kinase (PK), glutamic oxalo acetic transaminase (GOT) and glutamate dehydrogenase (GDH), and hydroxyacyl CoA dehydrogenase (HOAD) as well as their ratios were assayed to evaluate the abilities to use energy substrates of carbohydrates, amino acids and fatty acids, respectively, for energy production. In addition, activities of citrate synthase (CS) and lactate dehydrogenase (LDH) and LDH/CS ratio were calculated to analyse the evolution of aerobic and anaerobic pathways. The study found that hatching occurred at 38.8 h after fertilization (HAF), mouth-opening day of eleuteroembryo appeared at 3 days after hatching (DAH), and the most rapid embryonic growth was observed in blastula stage before hatching. Enzymatic assay revealed that except for PK which appeared in cleavage stage onwards, all the other enzymes functioned after fertilization, preparing well for the coming embryogenesis of tongue sole. By comparing the average specific activity of enzyme in each period, it can be found that the highest value occurred at 3 DAH (for TRY, LIP, PK and LDH), 2 DAH (for GDH), fertilized egg (for GOT) and segmentation stage (for HOAD and CS), and the lowest value occurred at fertilized egg (for HOAD, CS and GDH), cleavage stage (for TRY, PK and LDH), gastrula stage (for GOT) and hatching day (for LIP). Based on the changeable patterns of metabolic enzymatic activities and ratios, it is concluded that metabolic capacities on three energy substrates displayed stage-specific traits, and the dominant energy substrate was fatty acids before segmentation stage, amino acids until hatching day and carbohydrate during eleuteroembryo period. As for energy production mode, aerobic pathway appeared to increase greater in fertilized egg and gastrula stage, whereas anaerobic pathway played a predominant role during cleavage stage, blastula stage, segmentation stage and eleuteroembryo stage. These results are valuable to elucidate the nutritional requirements of embryonic stages in tongue sole and to further understand their energy metabolic mechanisms.

Validation of saliva and urine use and sampling time on the doubly labelled water method to measure energy expenditure, body composition and water turnover in male and female cats.

Less invasive protocols are necessary to study energy expenditure (EE) of cats living in homes for expressing their normal living conditions. The present study compared sampling times and the use of saliva, urine and blood to measure 2H and 18O to apply the doubly labelled water method. In the first study, four cats were used to evaluate the enrichment (2, 4, 6, 7 and 8 h) and elimination (2, 4, 6, 8, 10, 12, 14, 16, 18 and 20 d) of 2H and 18O (subcutaneously injected). The maximum enrichment was after 5 h (R2 0·82) of injection, with an Ln linear elimination of both isotopes (P < 0·001; R2 0·99). The results of EE were similar, regardless of the sampling time used (P = 0·999). In the second study, seven male cats and seven female cats were used. Before and after isotope injection (5 h, 7 d, 10 d and 14 d), blood, saliva and urine were collected. Isotope enrichment was lower in urine (P < 0·05) and at the similar level in blood and saliva. Isotope elimination was similar for all fluids (P < 0·473). The EE calculated with blood and saliva was similar but higher for urine (P = 0·015). According to Bland-Altman statistics, blood and saliva presented low bias and high correlation (P < 0·001), but this was not observed for urine (P = 0·096). Higher EE was observed for male cats (384 (se 39) kJ/kg0·67 per d) than for female cats (337 (se 34) kJ/kg0·67 per d; P < 0·05). The sampling time for the method is flexible, and saliva can be used as a substitute for blood.

Creatine nanoliposome reverts the HPA-induced damage in complex II-III activity of the rats' cerebral cortex.

Phenylketonuria (PKU) is a metabolic disorder accumulating phenylalanine (Phe) and its metabolites in plasma and tissues of the patients. Regardless of the mechanisms, which Phe causes brain impairment, are poorly understood, energy deficit may have linked to the neurotoxicity in PKU. It is widely recognized that creatine is involved in maintaining of cerebral energy homeostasis. Because of this, in a previous work, we incorporated it into liposomes and this increased the concentration of creatine in the cerebral cortex. Here, we examined the effect of creatine nanoliposomes on parameters of oxidative stress, enzymes of phosphoryl transfer network, and activities of the mitochondrial respiratory chain complexes (RCC) in the cerebral cortex of young rats chemically induced hyperphenylalaninemia (HPA). HPA was induced with L-phenylalanine (5.2 µmol/g body weight; twice a day; s.c.), and phenylalanine hydroxylase inhibitor, α-methylphenylalanine (2.4 µmol/g body weight; once a day; i.p.), from the 7th to the 19th day of life. HPA reduced the activities of pyruvate kinase, creatine kinase, and complex II + III of RCC in the cerebral cortex. Creatine nanoliposomes prevented the inhibition of the activities of the complexes II + III, caused by HPA, and changes oxidative profile in the cerebral cortex. Considering the importance of the mitochondrial respiratory chain for brain energy production, our results suggesting that these nanoparticles protect against neurotoxicity caused by HPA, and can be viable candidates for treating patients HPA.

Comparative Proteomic and Morpho-Physiological Analyses of Maize Wild-Type Vp16 and Mutant vp16 Germinating Seed Responses to PEG-Induced Drought Stress.

Drought stress is a major abiotic factor compromising plant cell physiological and molecular events, consequently limiting crop growth and productivity. Maize (Zea mays L.) is among the most drought-susceptible food crops. Therefore, understanding the mechanisms underlying drought-stress responses remains critical for crop improvement. To decipher the molecular mechanisms underpinning maize drought tolerance, here, we used a comparative morpho-physiological and proteomics analysis approach to monitor the changes in germinating seeds of two incongruent (drought-sensitive wild-type Vp16 and drought-tolerant mutant vp16) lines exposed to polyethylene-glycol-induced drought stress for seven days. Our physiological analysis showed that the tolerant line mutant vp16 exhibited better osmotic stress endurance owing to its improved reactive oxygen species scavenging competency and robust osmotic adjustment as a result of greater cell water retention and enhanced cell membrane stability. Proteomics analysis identified a total of 1200 proteins to be differentially accumulated under drought stress. These identified proteins were mainly involved in carbohydrate and energy metabolism, histone H2A-mediated epigenetic regulation, protein synthesis, signal transduction, redox homeostasis and stress-response processes; with carbon metabolism, pentose phosphate and glutathione metabolism pathways being prominent under stress conditions. Interestingly, significant congruence (R2 = 81.5%) between protein and transcript levels was observed by qRT-PCR validation experiments. Finally, we propose a hypothetical model for maize germinating-seed drought tolerance based on our key findings identified herein. Overall, our study offers insights into the overall mechanisms underpinning drought-stress tolerance and provides essential leads into further functional validation of the identified drought-responsive proteins in maize.

Glucose metabolism from mouth to muscle: a student experiment to teach glucose metabolism during exercise and rest.

We developed an experiment to help students understand basic regulation of postabsorptive and postprandial glucose metabolism and the availability of energy sources for physical activity in the fed and fasted state. Within a practical session, teams of two or three students (1 subject and 1 or 2 investigators) performed one of three different trials: 1) inactive, in which subjects ingested a glucose solution (75 g in 300 ml of water) and rested in the seated position until the end of the trial; 2) prior activity, in which the subject performed 15 min of walking before glucose ingestion and a subsequent resting phase; and 3) postactivity, in which the subject ingested glucose solution, walked (15 min), and rested afterwards. Glucose levels were drawn before trials (fasting value), immediately after glucose ingestion (0 min), and 5, 10, 15, 20, 25, 30, 40, 50, and 60 min thereafter. Students analyzed glucose values and worked on 12 tasks. Students evaluated the usefulness of the experiment; 54.2% of students found the experiment useful to enable them to gain a further understanding of the learning objectives and to clarify items, and 44.1% indicated that the experiment was necessary to enable them to understand the learning objectives. For 6.8% the experiment was not necessary but helpful to check what they had learned, and 3.4% found that the experiment was not necessary. The present article shows the great value of experiments within practical courses to help students gain knowledge of energy metabolism. Using an active learning strategy, students outworked complex physiological tasks and improved beneficial communication and interaction between students with different skill sets and problem-solving strategies.

[Metabolomics study of tris(2-chloroethyl) phosphate induced hepaotoxicity and nephrotoxicity in Sprague-Dawley rats].

Objective: To discuss the potential toxic target organ and the toxic effects and mechanisms of tris (2-chloroethyl) phosphate (TCEP) on SD rats. Methods: 40 female SD rats weaning from milk for 21 days, weighted (50±2.3)g were selected as subjects and marked by the weight. They were randomly divided into 4 groups, namely control group, 50 (L), 100 (M) and 250 (H) mg·kg(-1)·d(-1) dose of TCEP group. Each group has 10 rats, and administrated the corresponding dose of drug or vehicle by mouth, quaque die for 60 days. All rats were sacrificed after the last administration. The livers and kidneys were dyed by HE for pathological observation; and the blood samples were collected to analyze the biochemical index. H(1)-Nuclear Magnetic Resonance ((1)H-NMR)-based metabolomics methods coupling with histopathogy examination were used to investigate the toxic effects of TCEP. Results: Inflammatory cell infiltration and hepatic necrosis were observed in the liver of TCEP-treated rats. Inflammatory cells invaded and calcification/ossification foci were also found in renal of TCEP-treated rats and tumor hyperplasia were existed in renal tubule in H group. The level of HDL-C in the L, M and H group were separately (1.7±0.09) , (1.5±0.07) and (1.3±0.1) µmol/L, which were all significantly lower than that of control group ( (1.9±0.2) µmol/L) (P<0.05) . The activity of cholinesterase (CHE) in the L, M and H group were separately (918±14.8) , (828±28.6) and (674±36.5) U/L, which were all significantly lower than that of control group ((1056±28.8) µmol/L) (P<0.05). Moreover, The level of creatinine (CRE) in the L, M and H group were separately (29.8±4.6) , (28.9±5.3) and (25.8±6.2) µmol/L, which were all significantly lower than that of control group ((30.2±3.9) µmol/L) (P<0.05). In the H group, the enzyme activities of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), alkaline phosphatase (ALP) and the contents of total bilirubin (TBIL), glucose (GLU) and uric acid (UA) were all significantly higher than the results in control group. The results of (1)H-NMR metabolomics showed that the contents of lactate, glycine, high-density lipoprotein, low-density lipoprotein and phosphatidylcholine in blood of rats would decrease by TCEP exposure, while N-acetylglycoprotein, acetate, alanine, glucose, lipids, lipoproteins and fatty acids would increase. Conclusion: TCEP caused disorders in endogenous energy metabolism, leading to the pathological changes of inflammatory cells infiltration and necrosis in liver and kidney, caused enzyme activity changes of ALT, ALP and the content changes of other liver and kidney injury-related markers.

The Effect of Marginal Zn2+ Excess Released from Titanium Coating on Differentiation of Human Osteoblastic Cells.

Composite coatings based on chitosan and zinc nanoparticles (ZnNPs) were successfully produced on Ti13Zr13Nb substrates by cathodic electrophoretic deposition (EPD). The unfavorable phenomenon of water electrolysis-induced nonuniformity was reduced by applying a low voltage (20 V) and a short deposition time (1 min). Surface analysis (roughness and hydrophilicity) reveals the potential of these coatings for enhancing cell attachment and bone-implant integration. However, there is a concern about adhesion and strength; therefore, incorporating ZnNPs shows promise for enhancing mechanical properties, suggesting opportunities for further optimization of the process. The aim of this work was to investigate whether Zn2+ released from coating yields overt cellular impairment. hFOB1.19 osteoblastic cells were used as a model in this study. A subtoxic, 0.125 mmol/L, Zn concentration did not cause significant negative changes in cultured osteoblastic cells, as there was no significant change in their viability and their mitochondrial metabolism. Moreover, the alkaline phosphatase and lactate dehydrogenase activities were aggravated. However, a high, over 0.175 mmol/L, Zn2+ concentration caused total cell death. This was caused by the inhibition of mitochondrial enzymes' activities. Our data indicate that composite coatings releasing Zn2+ may be used as the differentiating factor toward osteoblastic cells.

Polystyrene microplastics with absorbed nonylphenol induce intestinal dysfunction in human Caco-2 cells.

Due to the massive production and use of plastic, the chronic and evolving exposure to microplastics in our daily lives is omnipresent. Nonylphenol (NP), a persistent organic pollutant, may change toxicity when it co-exists with microplastics. In this study, polystyrene microplastics (PS-MPs), either alone or with pre-absorbed NP, generated oxidative stress and inflammatory lesions to Caco-2 cells, as well as affecting proliferation via the MAPK signaling pathway and causing apoptosis. Damage to cell membrane integrity and intestinal barrier (marked by lower transepithelial electric resistance, greater bypass transport, and tight junction structural changes) leads to enhanced internalization risk of PS-MPs. Some important intestinal functions including nutrient absorption and xenobiotic protection were also harmed. It is worth noting that the exposure of PS-MPs with a diameter of 0.1 µm improved intestinal functions quickly but acted as a chemosensitizer for a long time, inhibiting cell perception of other toxic substances and making the cells more vulnerable.