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Developing easy-tailorable and high-efficient electromagnetic interference (EMI) shielding textile from waste textile is highly desirable to meet the demand for wearable electronics and economic sustainability for modern society. However, simultaneously featuring with good electrical conductivity and wearability of the derived waste textiles remains a daunting challenge, especially in the absence of conducting additives. Herein, we report the fabrication of a tailorable textile with high flexibility and conductivity to address this challenge via a straightforward graphitization strategy based on a mild reduction procedure. Aided by finite element analysis (FEA) and computer simulation technology (CST) for performance screening in advance, the mechanically-favorable but EMI shielding-unfavorable pores intrinsically produced in interwoven textile call for a low square resistance of the whole textile. The textile with desirable features is fabricated by the Ni-species catalyzed graphitization of cotton cellulose with large-scale production potential. Moreover, the low square resistance of the textile remains stable after immersion in extremely corrosive chemicals or 10000-times bending tests. The textile with a small thickness of 1.4 mm achieves an EMI shielding effectiveness (SE) of 107 dB in 12–18 GHz, 3 fold exceeding the demand for commercial applications (>30 dB). Practical demonstrations show that personal information in a mobile phone or ID card can be prevented from being read by pockets tailored from textiles. This work shows great potential for massive production of high-efficiency EMI shielding textiles for livelihood or military towards the next-generation wearable electronic technology. A flexible textile of high-degree graphitization is achieved from waste cotton by employing Ni-species as the catalyst upon a mild reduction procedure. Featured with favorable conductivity and simultaneously intact interwoven framework, the textile maintains comfortable wearabilities and delivers an excellent electromagnetic shielding efficiency of 107 dB in 12–18 GHz. [Display omitted] [ABSTRACT FROM AUTHOR]

Highlights • We constructed novel KISS1-54 and -10 DNA vaccines with fused tPA signal peptide. • KISS1-54 DNA vaccine could induce stronger humoral response than that KISS1-10 vaccine. • KISS1-54 DNA vaccine could suppress reproductive hormone secretion more effectively than KISS1-10 DNA vaccine. • KISS1-54 DNA vaccine could inhibit fertility more effectively than KISS1-10 DNA vaccine. Abstract Background Most studies on immunocastration currently focused on male animals. However, immunization of male animals does not completely inhibit sexual behavior and fertility. This study aimed to compare the immunocastration effect of KISS1 DNA vaccines encoding different lengths of kisspeptins in female rats for effective castration effects on both male and female rats. Methods Fifteen female rats were randomly divided into three groups. The rats in T1 group or T2 group was orally given respectively KISS1-54 or KISS1-10 DNA vaccines with fused tPA signal peptide, and the control group (Group C) was orally administered with empty vector vaccine, at a dose of 5 × 109 CFU/rat at weeks 0, 3 and 6 of the study. Blood samples were collected by retroorbital bleeding before primary immunization and at weeks 3 and 9 after primary immunization. Results Both KISS1-54 and KISS1-10 DNA vaccines induced the body's humoral immune response, and the anti-kisspeptin antibody titres in the T1 group were significantly higher than that in T2 and C groups (p < 0.05). The rats in T1 group has lower serum kisspeptin and estradiol levels than those in T2 and C groups and smaller litter size of rats than those in the control group after mating (p < 0.05). No significant difference was observed between T2 and C groups. The levels of KISS1 and GPR54 mRNA in the hypothalamus and ovaries of the T1 group were significantly lower than that in control group. However, the levels of KISS1 mRNA in the T2 group were significantly lower than that in the control group only in ovaries (p < 0.05). Conclusion The oral KISS1-54 DNA vaccine with fused tPA signal peptide was more effective than that KISS1-10 DNA vaccine in suppressing fertility of female rats. [ABSTRACT FROM AUTHOR]

Plectropomus leopardus , Promicrops lanceolatus and Cromileptes altivelis are high-value groupers in chinese aquatic product market and are substituted by cheaper ones sometimes due to economic profit. In this study, real-time PCR methods for identification of these groupers were developed. Species-specific primers and probes were designed on the basis of cytochrome oxidase I (COI) mitochondrial DNA sequences of groupers and other fishes. The specificity of the real time PCR assays were tested with a total of 51 specimens of fish, meat and poultry. Amplifications were observed in specific species only. The methods developed were accurate and rapid and offered the potential to detect fraudulent or unintentional mislabeling of these species in routine seafood authentication analysis. [ABSTRACT FROM AUTHOR]

3-Monochloro-1,2-propanediol (3-MCPD) is the most toxic chloropropanols compounds in foodstuff which mainly generated during thermal processing. Kidney is one of the primary target organs for 3-MCPD. Using human embryonic kidney cell (HEK293FT) as an in vitro model, we found that 3-MCPD caused concentration-dependent increase in cytoxicity as assessed by dye uptake, lactatedehydrogenase (LDH) leakage and MTT assays. HEK293FT cell treated with 3-MCPD suffered the decrease of mitochondrial membrane potential and the impairment of mitochondrial oxidative phosphorylation system, especially the reduced amount of mRNA expression and protein synthesis of electron transport chain complex II, complex IV, and complex III. More importantly, energy release (ATP synthesis) was significantly inhibited by 3-MCPD resulting from the down regulation expressions of ATP synthase (ATP6 and ATP8), as well as the loss of transmembrane potential required for synthesis of ATP. The decreased ratio of mitochondrial apoptogenic factors Bax/Bcl-2 and the cytochrome-c release from mitochondria to cytosol followed by the activation of apoptotic initiators caspase 9 and apoptotic executioners (caspase 3, caspase 6 and caspase 7) leading to apoptosis. The activation of caspase 8 and caspase 2 implied that there were probably other factors to induce the caspase-dependent apoptosis. [ABSTRACT FROM AUTHOR]

Patulin (PAT) is one of the most widely disseminated mycotoxins found in agricultural products and could cause renal damage. However, the mechanism of cell damage remains obscure. In this study, the human embryonic kidney cells (HEK293) were treated with PAT (2.5–15 μM). The cytotoxicity was assessed with MTT assay and apoptotic cells were detected by flow cytometry, and further identified by chromatin condensation and nuclear fragmentation with Hoechst 33342 under fluorescence microscope. Reactive oxygen species (ROS) with DCFH-DA was analyzed by fluorometry. The activities of superoxide dismutase (SOD), glutathione (GSH) and catalase (CAT) and malondialdehyde (MDA) content were determined to reveal the potential mechanism of PAT induced apoptosis. The mitochondrial membrane potential was measured by JC-1 probe. The results showed that PAT dose-dependently inhibited the growth of HEK293 cells and resulted in apoptosis in HEK293 cells. Treatment with PAT could induce ROS and MDA accumulation, accompanied by the losses of SOD, CAT, GSH and disruption of the mitochondrial membrane potential. These data suggest that PAT may induce apoptosis in HEK293 cells, in which oxidative stress is involved. [ABSTRACT FROM AUTHOR]

Highlights: [•] Naturally occurring xanthan gum (XG) for preparation of Fe3O4@SiO2–XG composites. [•] Magnetic switchable composites for property of convenient solid/liquid separation. [•] Non-toxic XG immobilized on magnetic Fe3O4 particles through TEOS sol–gel reaction. [•] XG adopted as active sites for adsorptive removal of Pb2+ from aqueous solution. [•] The composites reutilized and Pb2+ reused in battery wastewater by 0.05molL−1 HCl. [Copyright &y& Elsevier]

• Kisspeptin/GPR54 was expressed in Leydig, Sertoli and germ cells of goat testes. • Kisspeptin plays a direct regulation role on testosterone secretion in Leydig cells. • Kisspeptin can directly stimulate Kiss1 / GPR54 mRNA expression in Leydig cells. • Kisspeptins play an autocrine role in goat Leydig cells. Kisspeptin, encoded by the Kiss1 gene, and its receptor GPR54 have a central regulatory role in the male reproduction. However, their functions in peripheral tissues, such as testes, remain unclear. This study investigated the local expressions and function of Kiss1 / GPR54 in goats' testes. The mRNA expression of Kiss1 / GPR54 in pubertal goat Leydig cells was detected through reverse transcriptase PCR (RT-PCR), and its protein expression in Leydig cells or the testis was examined by immunohistochemistry and Western blot analysis. Isolated and cultured Leydig cells were treated with different concentration of kisspeptin (0, 1, 10 and 100 μM) and kisspeptin antagonist for 4, 24 or 72 h. The direct effect of kisspeptin on testosterone secretion and Kiss1 / GPR54 mRNA expression was evaluated by ELISA and RT-PCR. Kiss1 / GPR54 mRNA and protein were expressed in Leydig cells and spermatids, and GPR54 were expressed in Sertoli cells. Kisspeptin treatment significantly stimulated testosterone secretion in Leydig cells, with the highest levels found under 24 h of treatment with 10 μM kisspeptin. Treatment with kisspeptin + kisspeptin antagonist significantly reduced the kisspeptin-stimulated testosterone secretion in Leydig cells. Kisspeptin treatment significantly enhanced the expression of Kiss1 / GPR54 mRNA in Leydig cells. These data suggest the local expressions of Kiss1 / GPR54 in goats' testes and its autocrine role in Leydig cells, which is helpful in understanding the regulation role of kisspeptin/GPR54 system in other peripheral tissues. [ABSTRACT FROM AUTHOR]

A new type of PVC-CPVC-MBS-B44 composite gel polymer electrolyte (GPE), based on LiTFSI and incorporated with nano-silica, is designed. The adhesion of the electrolyte membranes is improved by introducing B44, with its excellent adhesion ability, into the GPEs. The GPE membrane is coated on the anodes by an in-situ dip-coating process for battery assembly, reducing the interfacial resistance of the battery. The PVC-CPVC-MBS-B44 composite GPE exhibits superior electrochemical performance. The electrochemical window is over 4.9 V (vs. Li/Li+), the ion conductivity is 0.96 × 10- 3 S cm−1 at an ambient temperature, and the lithium ion transference number is 0.61. The LiCoO 2 /PVC-CPVC-MBS-B44 composite GPE/graphite cells exhibit maximum discharge capacities of approximately 137.98, 136.5, and 129.4 mAh g−1 at 0.2C, 0.5C, and 1C discharge rates, respectively. The cells with GPE can maintain a high discharge capacity of 116 mAh g−1 and a capacity retention exceeding 82.9% after 200 cycles at 0.5C. Heavy impact, nail penetration, crush test, short-circuit test, drop test and heating test are carried out on 1-Ah GPE pouch cells, and the battery does not ignite nor smoke. A battery prepared using the proposed approach can deliver outstanding safety, high rate capabilities, and superior cycle stability, making it a potential candidate for various applications. • A new PVC-CPVC-MBS-B44 composite GPE based on LiTFSI and doped with nano-SiO 2 is developed. • The GPE membrane is coated in-situ on the anodes by dip-coating. • Excellent electrochemical performance is demonstrated with a Li salt concentration of 2.9%. • The cell with GPE exhibit high rate capabilities, superior cycle stability. • Safety tests reveal that the battery does not ignite or smoke. [ABSTRACT FROM AUTHOR]

This article describes a fabrication approach to Cu 2 ZnSnSe 4 thin films through the direct selenization of precursor films of the metal oxide mixture with elemental selenium at 550 °C for 40 min. The resulting films exhibit a well compacted morphology composed of crystallites of a few micrometers and having reliable photoelectric response in photoelectrochemical determination, suggesting the potential of photovoltaic applications of the films fabricated by this method. To investigate the formation pathway of the Cu 2 ZnSnSe 4 film in this direct selenization method, selenization reactions were carried out with individual Cu, Zn, and Sn oxides under the same conditions, and the results showed that the formation rate of Cu 2 ZnSnSe 4 from a mixture of metal oxides is comparable with that of Cu 2 Se formation, but faster than those of ZnSe and SnSe 2 formation. The facilitated selenization kinetics to form Cu 2 ZnSnSe 4 may be attributed to the oxidation state change of Cu(II) to Cu(I) and Sn(II) to Sn(IV) and the formation of cubic ZnO phase during the preparation of the mixture of metal oxides. [ABSTRACT FROM AUTHOR]

Abstract: Exposure of proestrous Syrian hamsters to a new room, cage, and novel running wheel blocks the luteinizing hormone (LH) surge until the next day in ~75% of hamsters [1]. The studies described here tested the hypotheses that 1) exercise and/or 2) orexinergic neurotransmission mediate novel wheel blockade of the LH surge and circadian phase advances. Female hamsters were exposed to a 14L:10D photoperiod and activity rhythms were monitored with infra-red detectors. In Expt. 1, to test the effect of exercise, hamsters received jugular cannulae and on the next day, proestrus (Day 1), shortly before zeitgeber time 5 (ZT 5, 7h before lights-off) the hamsters were transported to the laboratory. After obtaining a blood sample at ZT 5, the hamsters were transferred to a new cage with a novel wheel that was either freely rotating (unlocked), or locked until ZT 9, and exposed to constant darkness (DD). Blood samples were collected hourly for 2days from ZT 5–11 under red light for determination of plasma LH levels by radioimmunoassay. Running rhythms were monitored continuously for the next 10–14days. The locked wheels were as effective as unlocked wheels in blocking LH surges (no Day 1 LH surge in 6/9 versus 8/8 hamsters, P>0.05) and phase advances in the activity rhythms did not differ between the groups (P=0.28), suggesting that intense exercise is not essential for novel wheel blockade and phase advance of the proestrous LH surge. Expt. 2 tested whether orexin neurotransmission is essential for these effects. Hamsters were treated the same as those in Expt. 1 except that they were injected (i.p.) at ZT 4.5 and 5 with either the orexin 1 receptor antagonist SB334867 (15mg/kg per injection) or vehicle (25% DMSO in 2-hydroxypropyl-beta-cyclodextrin (HCD)). SB-334867 inhibited novel wheel blockade of the LH surge (surges blocked in 2/6 SB334867-injected animals versus 16/18 vehicle-injected animals, P<0.02) and also inhibited wheel running and circadian phase shifts, indicating that activation of orexin 1 receptors is necessary for these effects. Expt. 3 tested the hypothesis that novel wheel exposure activates orexin neurons. Proestrous hamsters were transferred at ZT 5 to a nearby room within the animal facility and were exposed to a new cage with a locked or unlocked novel wheel or left in their home cages. At ZT 8, the hamsters were anesthetized, blood was withdrawn, they were perfused with fixative and brains were removed for immunohistochemical localization of Fos, GnRH, and orexin. Exposure to a wheel, whether locked or unlocked, suppressed circulating LH concentrations at ZT 8, decreased the proportion of Fos-activated GnRH neurons, and increased Fos-immunoreactive orexin cells. Unlocked wheels had greater effects than locked wheels on all three endpoints. Thus in a familiar environment, exercise potentiated the effect of the novel wheel on Fos expression because a locked wheel was not a sufficient stimulus to block the LH surge. In conclusion, these studies indicate that novel wheel exposure activates orexin neurons and that blockade of orexin 1 receptors prevents novel wheel blockade of the LH surge. These findings are consistent with a role for both exercise and arousal in mediating novel wheel blockade of the LH surge. [Copyright &y& Elsevier]

• A high-throughput method is proposed to select a temperature-sensitive material with optimal performance. • A thin-film resistance temperature detector (TFRTD) compatible with the battery assembly process is designed and prepared. • The TFRTD can monitor the internal temperature of the TFRTD integrated battery with stable electrochemical performances. The high-energy-density lithium-ion batteries (LIBs) are susceptible to thermal runaway and lead to safety incidents. Monitoring the internal temperature of LIBs is a promising way to forewarn its thermal runaway. However, the current external temperature sensors show high delay and poor accuracy, and the built-in temperature sensors are incompatible with the assembly process and may damage the battery. Thus, a reliable real-time internal battery temperature monitoring sensor is desired. In this study, a high-throughput selected thin-film resistance temperature detector (TFRTD) is proposed. The TFRTD is integrated between the collectors of the pouch LIB, which is compatible with the battery assembly process. The built-in TFRTD responds 82% faster and measures 33% more accurately than an external RTD, allowing real-time monitoring of internal battery temperature at different current rates. With a discharge rate of 0.5 C, the internal temperature can be monitored to be 0.57 °C higher than the external temperature in a battery with a capacity of only 0.1 Ah. Cycling tests show that the battery with a built-in TFRTD has a capacity retention rate of 92.71% after 100 cycles, and the TFRTD has a limited impact on battery performance. Therefore, the developed novel TFRTD can be used to analyze the battery heating process under different conditions and has some potential for engineering applications. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract Apigenin (API) is a kind of important flavonoid present in temperate and tropical fruit and vegetables, especially the celery. It exerts anticancer, anti-bacterial, anti-viral, anti-inflammatory, anti-oxidation properties. In the present study, the mechanism of protective action of apigenin on 3-chloro-1, 2-propanediol (3-MCPD)-induced renal injury was investigated in rat. Sprague-Dawley (SD) rats were divided into five groups: control group (ultrapure water treated), CMC group (sodium carboxymethylcellulose treated), 3-MCPD treatment group (30 mg/kg body weight/day), 3-MCPD plus API co-treatment group (20, 40 mg/kg body weight/day). The results showed that API significantly reduced renal function markers, serum creatinine and urea nitrogen content. Besides, the renal tissue lesion in 3-MCPD treatment group was restored by API to some extent. We indicated that API exerted renoprotective effect by modulating oxidative phosphorylation especially up-regulated the expressions of ATP6 and ATP8, re-establishing mitochondrial membrane potential (MMP), relieving the increase of Bax/Bcl2 ratio, reducing cytochrome c release, thus inhibiting the activation of Caspase 9 and Caspase 3. In conclusion, apigenin possesses excellent protective effect against 3-MCPD-induced renal injury by modulating mitochondria dependent Caspase cascade pathway. Highlights • Apigenin attenuated 3-MCPD-induced renal injury in vitro. • Apigenin inhibited 3-MCPD-induced disorder of oxidative phosphorylation. • Apigenin protected against 3-MCPD-indcued renal injury via mitochondria dependent Caspase cascade pathway. [ABSTRACT FROM AUTHOR]

Mycotoxins like patulin (PAT) are among the most significant food contaminant with regard to public health. This study aimed to evaluate the protective effect of apigenin (API), one of the most bioactive flavonoids in plant-derived food, on PAT-induced apoptosis in HEK293 cells. Cells were treated under basic conditions, 8 μM PAT without or with API (2.5, 5 and 10 μM) concomitantly for 10 h. API exerted renoprotective effect by inhibiting intracellular reactive oxygen species (ROS) accumulation, modulating oxidative phosphorylation especially elevating the expression of ATP synthase, re-establishing mitochondrial membrane potential (MMP) and maintaining higher intracellular ATP level, accompanied by p53, Bax downregulation and Bcl-2 upregulation. Thereby, cytochrome c release from mitochondria to cytoplasm was reduced, causing inhibition of initiator caspases-9 and executioner caspases (3, 6 and 7) expression and enzyme activities. Results revealed dietary apigenin attenuates patulin-induced apoptosis in HEK293 cells by modulating ROS-mediated mitochondrial dysfunction and caspase signal pathway. [ABSTRACT FROM AUTHOR]

Optimal allocation problem of distribution network (OAPDN), which attracts much attention of electric enterprise, contributes to the flexible and environmental-friendly power supply by rationally introducing distributed generations (DGs) and shunt capacitors (SCs). To smoothly solve OAPDN problems, several effective measures such as advantageous schemes guidance (ASG) mechanism are presented and integrated into the proposed modified gravitational search algorithm with expert experience (MGSA-EE). Multiple OAPDN experiments essentially indicate that the MGSA-EE with higher efficiency and stronger exploration capability reduces the power loss on 33, 69 and 119 node networks by 94.15%, 98.10% and 84.59%, which is superior to most published technologies. Furthermore, multi-objective OAPDN problem which simultaneously considers two or more goals is also studied. Compared with the single-objective one, it is more in line with the diverse demands of actual electricity market, but the difficulty is greatly increased as well. On this basis, this paper extends MGSA-EE to an innovative multi-objective MGSA-EE (MMGSA-EE) algorithm by the suggested non-inferior sorting strategy with constraints-prior. Most typically in multi-objective OAPDN experiments on large scale networks, MMGSA-EE achieves high-quality scheme that concurrently reduces power loss and voltage deviation of 69-node network by 94.07% and 98.69%. Meanwhile, several quantitative indicators also prove that the proposed MMGSA-EE has competitive advantages over the original algorithm in terms of Pareto fronts, node voltage profiles and execution time. In general, MGSA-EE and MMGSA-EE algorithms provide efficient tools for exploring superior DG/SC configuration schemes, and are of great significance to fill research gaps in multi-objective optimizations of distribution network. [ABSTRACT FROM AUTHOR]

3-Chloro-1, 2-propanediol (3-MCPD) is a widespread food contaminant with kidney as the main target organ. The exploration of ingredients as intervention strategy towards 3-MCPD induced nephrotoxicity is needed. Diosgenin (DIO) is a steroidal saponin presented in several plants and foods. Here we assessed whether DIO attenuates nephrotoxicity induced by 3-MCPD using Human embryonic kidney 293 (HEK293) cells and Sprague-Dawley (SD) rats. The results showed that DIO (2, 6, 8 μM) increased cell viability and exerted inhibitory effect on caspase 3 and caspase 9 activities. Histological examination of rats showed that 15 mg/kg bw DIO ameliorated renal pathological changes caused by 3-MCPD (30 mg/kg bw). DIO also induced autophagy and the blockade of autophagy with 3-Methyladenine (3-MA) aggravated mitochondrial apoptosis induced by 3-MCPD in HEK293 cells. Moreover, treatment with DIO caused an increase in p-LKB1/LKB1 and p-AMPK/AMPK expressions and a decrease in p-mTOR/mTOR, p-ULK1(Ser757), p-P70S6K and p-4EBP1 expressions. Additionally, DIO improved mitochondrial dynamics mainly through inhibiting the relocation of DRP1 on mitochondria and enhancing MFN1 and MFN2 expressions. In conclusion, our study demonstrated for the first time that DIO protected against kidney injury induced by 3-MCPD through the induction of autophagy via LKB1-AMPK-mTOR pathway and the improvement of mitochondrial fission and fusion. [Display omitted] • Diosgenin alleviated nephrotoxicity induced by 3-MCPD in vivo and in vitro. • Autophagy induction contributes to the protective effect of diosgenin against 3-MCPD-induced kidney injury. • The improvement of mitochondrial dynamics by diosgenin protected against 3-MCPD-induced kidney injury. [ABSTRACT FROM AUTHOR]

Jujuboside A (JuA) is a triterpenoid saponins isolated from the seed of jujube (semen Ziziphi spinosae) with anti-oxidant, anti-inflammation and anti-apoptosis properties. The present study aimed to investigate the reno-protective effects of JuA on type II diabetes. JuA (20 mg/kg) and Metformin (Met, 300 mg/kg) were administrated to diabetic Sprague Dawley rat for 8 weeks daily. Our results showed that JuA reduced blood glucose and kidney function markers including 24 h urinary protein, urinary β-NAG/urinary creatinine, serum urea nitrogen, serum uric acid and serum creatinine, and relieved renal pathological changes. In addition, JuA decreased O 2 − and H 2 O 2 level, enhanced SOD, CAT and GPx activities, decreased NOX4 expression and improved mitochondrial respiratory chain function through regulating respiratory chain complex expression. Moreover, JuA downregulated the expressions of mitochondrial apoptosis proteins: Bax, CytC, Apaf-1 and caspase 9. Apoptosis mediated by ER stress also been inhibited by JuA via downregulating p-PERK, p-IRE1, XBP1s, ATF4, p-CHOP and caspase 12 expressions. JuA also enhanced autophagy and mitophagy via regulating CaMKK2-AMPK-p-mTOR and PINK1/Parkin pathways. Collectively, these results indicated that JuA protected against type II diabetic nephropathy through inhibiting oxidative stress and apoptosis mediated by mitochondria and ER stress. In addition, autophagy and mitophagy was enhanced by JuA. [Display omitted] • Jujuboside A relieved oxidative stress through inhibiting NOX4 and improving mitochondrial respiratory chain function in DN rat. • Jujuboside A enhanced antioxidant enzyme activities in DN rat. • Jujuboside A inhibited apoptosis induced by ER stress and mitochondria in DN rat. • Autophagy and mitophagy contributed to the protective effect of Jujuboside A on DN rat. [ABSTRACT FROM AUTHOR]

Mitochondrial dynamics and bioenergetics are considered play pivotal roles in the maintenance of mitochondrial function and cell viability. During the widely distributed food contaminant 3-chlorpropane-1,2-diol (3-MCPD) induced nephrotoxicity, mitochondrial morphology and function were impaired, but the specific mechanism responsible for the process has not been fully elucidated. In the present study, using an in vitro human embryonic kidney 293 (HEK293) cell culture model, the role of LKB1/AMPK pathway and mitochondrial fission and fusion dynamics in 3-MCPD-induced cell apoptosis was investigated by using the AMPK inhibitor dorsomorphin and mitochondrial division inhibitor 1 (Mdivi-1), respectively. The results revealed that 3-MCPD significantly decreased the ATP levels, activated the energy-sensing regulator AMPKα and its upstream protein kinase LKB1, disrupted mitochondrial dynamics equilibrium characterized by promoting division and inhibiting fusion, thus inducing cell apoptosis. Notably, suppression of AMPK by dorsomorphin mitigated 3-MCPD-induced cytotoxicity through improvement of the function and dynamics of mitochondria and alleviated apoptosis via the mitochondria-dependent pathway. Moreover, inhibition of mitochondrial fission by Mdivi-1 protected against apoptosis induced by 3-MCPD. Taken together, these results suggest that 3-MCPD triggers apoptosis through activation of LKB1/AMPKα signaling pathway and regulation of mitochondrial fission and fusion dynamics in HEK293 cells. [Display omitted] • 3-MCPD activated LKB1/AMPKα signaling pathway in human embryonic kidney cells. • Suppression of AMPK improved the function and dynamics of mitochondria and alleviated 3-MCPD-evoked renal cell damage. • 3-MCPD led to mitochondrial fusion and fission dynamics disorder. • Inhibition of mitochondrial fission protected against 3-MCPD-induced apoptosis via the mitochondria-dependent pathway. [ABSTRACT FROM AUTHOR]

Patulin (PAT) is a kind of mycotoxins that commonly found in decayed fruits and their products. Our previous studies have shown that PAT induced cell apoptosis and the overproduction of reactive oxygen species (ROS) in human embryonic kidney (HEK293) cells. The present study aimed to further investigate the functional role of NADPH oxidase, one of the main cellular sources of ROS, in PAT-induced apoptosis and oxidative damage in HEK293 cells. We demonstrated that the protein and mRNA expression levels of NADPH oxidase catalytic subunit NOX2 and regulatory subunit p47phox were up-regulated under PAT stress. Inhibiting of NADPH oxidase with the specific antagonist diphenyleneiodonium (DPI) suppressed cytotoxicity and apoptosis induced by PAT as evidenced by the increase of cell viability, the decrease of LDH release and the inhibition of caspase activities. Furthermore, DPI re-established mitochondrial membrane potential (MMP) and enhanced cellular ATP content. Importantly, DPI supplementation elevated endogenous GSH contents as well as the ratio of GSH/GSSG. Meanwhile, the antioxidant-enzyme activities of GPx, GR, CAT and SOD were significantly promoted. Collectively, our results suggested that NADPH oxidase played a critical role in PAT-induced nephrotoxicity, and inhibition of NADPH oxidase by DPI attenuated cell injury and apoptosis via regulation of oxidative damage. • Exposure to PAT induced ROS production through NADPH oxidase in a concentration-dependent manner. • Diphenyleneiodonium (DPI) suppressed cytotoxicity and restored mitochondrial dysfunction induced by PAT. • Supplementation of DPI elevated endogenous GSH contents and the antioxidant-enzyme activities. [ABSTRACT FROM AUTHOR]

3-chlorpropane-1,2-diol (3-MCPD) is a heat-induced food process contaminant that threatens human health. As the primary target organ, the morphological and functional impairment of kidney and the related mechanism such as apoptosis and mitochondrial dysfunction were observed. However, the precise molecular mechanism remains largely unclear. This study aimed to explore the important role of mitochondrial fission and autophagy in the 3-MCPD-caused apoptosis of human embryonic kidney 293 (HEK293) cells. The results showed that blockage of dynamin-related protein-1 (Drp1) by mitochondrial division inhibitor 1 (Mdivi-1, 15 μM) apparently restored 3-MCPD-induced mitochondrial dysfunction, accompanied by prevented the collapse of mitochondrial membrane potential and ATP depletion, and suppressed the occurrence of autophagy. Induction of autophagy occurred following 2.5–10 mM 3-MCPD treatment for 24 h via AMPK mediated mTOR signaling pathway. Meanwhile, enhancement of autophagy by pretreatment with rapamycin (1 nM) alleviated the loss of cell viability and apoptosis induced by 3-MCPD whereas suppression of autophagy by 3-methyladenine (1 mM) further accelerated apoptosis, which was modulated through the mitochondria-dependent apoptotic pathway. Taking together, this study provides novel insights into the 3-MCPD-induced apoptosis in HEK293 cells and reveals that autophagy has potential as an effective intervention strategy for the treatment of 3-MCPD-induced nephrotoxicity. Image 1 • Blockage of Drp1 restored 3-MCPD-induced mitochondrial dysfunction and suppressed autophagy. • Activation of autophagy alleviated 3-MCPD-caused apoptosis via the mitochondria-dependent apoptotic pathway. • 3-MCPD led to autophagy through the AMPK mediated mTOR signaling pathway. [ABSTRACT FROM AUTHOR]