Search

Di-2-ethylhexyl phthalate (DEHP), as a common endocrine disrupting chemicals, can induce toxicity to reproductive system. However, the mechanism remains to be explored. In our study, DEHP exposure induced testicular injury in rats. The high throughput transcriptional sequencing was performed to identify differentially expressed genes (DEGs) between the treatment and control groups. KEGG analysis revealed that DEGs were enriched in apoptosis, PPARα, and ER stress pathway. DEHP up-regulated the expression of PPARα, Bax, Bim, caspase-4. GRP78, PERK, p-PERK, eIF2α, p-eIF2α, ATF4 and CHOP. This view has also been confirmed in TM3 and TM4 cells. In vitro, after pre-treatment with GW6471 (an inhibitor of PPARα) or GSK (an inhibitor of PERK), the apoptosis was inhibited and mitochondrial dysfunction was improved. Moreover, the improvement of mitochondrial dysfunction decreased the expression of PERK pathway by using SS-31(a protective agent for mitochondrial function). Interestingly, ER stress promoted the accumulation of ROS by ERO1L (the downstream of CHOP during ER stress), and the ROS further aggravated the ER stress, thus forming a feedback loop during the apoptosis. In this process, a vicious cycle consisting of PERK, eIF2α, ATF4, CHOP, ERO1L, ROS was involved. Taken together, our results suggested that mitochondrial dysfunction and ER stress-ROS feedback loop caused by PPARα activation played a crucial role in DEHP-induced apoptosis. This work provides insight into the mechanism of DEHP-induced reproductive toxicity. [Display omitted] • DEHP induced apoptosis in rat testis. • MEHP induced apoptosis in TM3 and TM4 cells. • PPARα was activated to induce mitochondrial dysfunction through CPT1A pathway. • Apoptosis was via PPARα regulated mitochondrial disorder and ER stress interaction. • the ER stress-ROS feedback loop was discovered during apoptosis. [ABSTRACT FROM AUTHOR]

To obtain diesel fuels with high combustion properties from hydrotreatment of vegetable oils, inhibiting the formation of multibranched isomers (MuBI) is highly desirable. A core@shell structural ZSM-22@SiO 2 zeolite was designed to passivate external acid sites and promote the formation of monobranched isomers (MoBI), which have much higher cetane numbers than MuBI (>85 vs. <60). A series of ZSM-22@SiO 2 zeolites with different amounts of shell silica were synthesized through a facile crystal growth method. External acid sites could be successfully inactivated using the proposed method. Synthesized zeolites were used as supports for bifunctional catalysts in hydrodeoxygenation of methyl palmitate. The effects of the shell silica amount and SiO 2 /Al 2 O 3 ratio of the core zeolite were investigated. The MoBI percentage in total isomers increased from 71% to 95% at a reaction temperature of 300 °C. However, deoxygenation activity and isomerization selectivity decreased gradually with increasing amount of shell silica. Fourier transform infrared spectroscopy of CO adsorption combined with transmission electron microscopy demonstrated that Pt particles exposed more Pt(1 0 0) facets than Pt(1 1 1) facets in silica-coated catalysts. This could be the most likely reason for the decreased deoxygenation activity. The decrease in the number of Brønsted acid sites could be responsible for the lowered isomerization selectivity. Catalytic performance could be enhanced by reducing the SiO 2 /Al 2 O 3 ratio of core ZSM-22. Catalysts with lower SiO 2 /Al 2 O 3 ratios favored smaller Pt particles and exposed more active Pt(1 1 1) corner sites. Additionally, acid sites played an important role in the adsorption of oxygenates. [ABSTRACT FROM AUTHOR]

Arsenic exposure is related to insulin resistance (IR). However, the underlying mechanism is still uncertain. NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome is a key driving factor of IR. We found that NaAsO 2 caused hepatic IR, activated NLRP3 inflammasome, and inhibited glycolysis pathway in vivo. We also found that tricarboxylic acid cycle (TCA cycle) was inhibited, and the content of hepatic lactate was upregulated with the treatment of arsenic. Consistent with these findings, we found that NLRP3 inflammasome and glycolysis were involved in the development of IR in L-02 cells. Besides, inhibiting NLRP3 inflammasome upregulated aerobic glycolysis and inhibited anaerobic glycolysis. Moreover, we demonstrated that NLRP3 inflammasome could bind to pyruvate kinase, liver and RBC (PKLR). Simultaneously, insulin signaling rather than NLRP3 inflammasome activation was altered by overexpressing PKLR. In summary, after treatment with NaAsO 2 , NLRP3 inflammasome blocked the glycolytic pathway via binding to PKLR, which in turn caused hepatic IR. This study shed new light on the molecular mechanism underlying arsenic-induced IR. • NLRP3 inflammasome was involved in arsenic-induced hepatic insulin resistance (IR). • NaAsO2 blocked the glycolytic pathway in hepatic insulin resistance. • NLRP3 inflammasome modulated glycolysis pathway via binding to PKLR. [ABSTRACT FROM AUTHOR]

Semiconductor photocatalysis can carry out selective chemical transformations under ambient conditions, mitigating the associated environmental consequences. However, a single semiconductor photocatalyst usually cannot perform the transformations satisfactorily from the aspects of light-absorption, efficiency, and selectivity, etc. To address these challenges, cadmium sulfide (CdS)/titanate hybrid was fabricated by simultaneously growing titanate and CdS and had been comprehensively characterized. The optimized CdS/titanate hybrid can power the highly selective oxidative homocoupling of amines under the irradiation of green light-emitting diodes (LEDs). Specifically, CdS with a narrow bandgap captures green light; the conduction band of titanate activates molecular oxygen (O 2). The valence band of CdS could ensure the selective oxidative homocoupling of amines in methanol (CH 3 OH). The hybridization between CdS and titanate accounts for the expeditious oxidative homocoupling of amines into imines and the improved stability. Reactive oxygen species (ROS) quenching experiments and in situ electron paramagnetic resonance (EPR) tests suggest that superoxide anion (O 2 −) and benzylamine radical are intermediates en route to imines. This work highlights the viability of hybridization of dual semiconductor nanostructures in implementing visible light-powered selective conversions. [ABSTRACT FROM AUTHOR]

Exposure to arsenic is a risk factor for nonalcoholic steatohepatitis (NASH). Ferroptosis is a form of regulated cell death defined by the accumulation of lipid peroxidation. In the current study, we observed the occurrence of ferroptosis in arsenic-induced NASH by assessing ferroptosis related hallmarks. In vitro , we found that ferrostatin-1 effectively attenuated the executing of ferroptosis and NASH. Simultaneously, the expression of ACSL4 (acyl-CoA synthetase long-chain family member 4) was upregulated in rat's liver and L-02 cells exposed to arsenic. While, suppression of ACSL4 with rosiglitazone or ACSL4 siRNA remarkably alleviated arsenic-induced NASH and ferroptosis through diminishing 5-hydroxyeicosatetraenoic acid (5-HETE) content. Additionally, Mitofusin 2 (Mfn2), a physical tether between endoplasmic reticulum and mitochondria, has rarely been explored in the ferroptosis. Using Mfn2 siRNA or inositol-requiring enzyme 1 alpha (IRE1α) inhibitor, we found NASH and ferroptosis were obviously mitigated through reducing 5-HETE content. Importantly, Co-IP assay indicated that Mfn2 could interact with IRE1α and promoted the production of 5-HETE, ultimately led to ferroptosis and NASH. Collectively, our data showed that ferroptosis is involved in arsenic-induced NASH. These data provide insightful viewpoints into the mechanism of arsenic-induced NASH. • Ferroptosis is involved in NaAsO 2 -induced nonalcoholic steatohepatitis. • NaAsO 2 -induced ferroptotic cell death depends on the interaction of Mfn2 and IRE1α. • The ACSL4 plays a leading role in the progression of ferroptosis induced by NaAsO 2 via manipulating 5-HETE content. [ABSTRACT FROM AUTHOR]