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Per- and polyfluoroalkyl substances (PFAS), widely utilized in consumer products, have been linked to an increased risk of cardiovascular disease (CVD). With the increasing prevalence of high-fat diet, a common risk factor for CVD, the PFAS exposed populations who consume a high-fat diet will inevitably grow and may have a higher CVD risk. However, the potential toxic effect and mode of action remain elusive. We constructed a mouse model orally exposed to perfluorooctane sulfonate (PFOS), a prototypical PFAS, and fed a high-fat diet. PFOS exposure induced cardiomyopathy and structural abnormalities in the mice heart. Moreover, a characteristic of energy metabolism remodeling from aerobic to anaerobic process was observed. Interestingly, PFOS was rarely detected in heart but showed high level in serum, suggesting an indirect route of action for PFOS-caused cardiac toxicity. We further demonstrated that PFOS-caused circulating inflammation promoted metabolic remodeling and contractile dysfunction in cardiomyocytes. Wherein, PFOS stimulated the release of IL-1β from circulating proinflammatory macrophages mediated by NF-κB and caspase-1. This study provides valuable data on PFAS-induced cardiac risks associated with exposed populations with increasing high-fat diet consumption, highlighting the significance of indirect pathways in PFOS's impact on the heart, based on the distribution of internal exposure., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Airborne fine particles, generating from human activities, have drawn increasing attention due to their potential lung health hazards. The currently available toxicological data on fine particles is still not sufficient to explain their cause-and-effect. Based on well reported critical role of ATP on maintaining lung structure and function, the alterations of ATP production and energy metabolism in lungs of rats exposed to different dosages of seasonal PM 2.5 were investigated. Haze dosage PM 2.5 exposure was demonstrated to reduce the ATP production. Activity of critical enzymes in TCA cycle, such as malate dehydrogenase (MDH) and citrate synthase (CS), and expression of mitochondrial respiration chain genes were attenuated in groups exposed to haze dosage PM 2.5 . In contrast, there was prominent augment of glycolytic markers at haze dosage PM 2.5 , including metabolite contents (pyruvate and lactic acid), enzyme activities (hexokinase (HK) and pyruvate kinase (PKM)), along with mRNA levels of PKM and LDH. Consequently, sub-chronic exposure to seasonal haze PM 2.5 caused reduction in ATP generation and metabolic rewiring from TCA cycle to glycolysis. Our findings can help better understand the toxicological mechanism of lung disease caused by particulate air pollution., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Fine particulate matter is one of the leading threats to cardiovascular health worldwide. The exploration of novel and sensitive biomarkers to detect damaging effect of fine particulate matter on cardiac tissues is of great importance in the better understanding of haze-caused myocardial injury. A link between heart failure and PPARα-regulated energy metabolism has been confirmed previously. Herein, the study intends to reveal the critical biomarkers of fine particulate matter induced myocardial damage from the PPARα-regulated energy metabolism. Ambient fine particulate matter induced severe pathological alterations in cultured cells, accompanied by the decrease in ATP content. Additionally, the expressions of CPT1/CPT2 and levels of CS and MDH, crucial members in β-oxidation and the TCA cycle, were significantly decreased. In direct contrast, fine particulate matter increased the biomarkers of glycolysis, as measured by the accumulation of pyruvate and lactate contents, and the enhanced activities of HK and PKM1/2. Importantly, fine particulate matter-exposed cardiomyocytes exhibited the reduced PPARα level, that increased when cardiomyocytes were co-incubation with WY-14643 and fine particulate matter. Simultaneously, the adverse impact of fine particulate matter on critical biomarkers were observed in β-oxidation, TCA cycle and glycolysis, associated with WY-14643 additional complement. Fine particulate matter caused the myocardial energy metabolism transformation through the regulation of PPARα expression and translation, which provided novel and critical biomarkers for haze particles-caused myocardial damage. Image 1 • Fine particulate matter contributed to the attenuation of myocardial ATP. • Fine particulate matter decreased the expressions of critical members in β-oxidation and TCA cycle. • Fine particulate matter increased the levels of biomarkers in glycolysis. • Fine particulate matter-caused transformation of energy metabolism was mediated by the regulation of PPARα. This study provided novel and critical biomarkers involved in myocardial energy metabolism for haze particles-caused myocardial damage. [ABSTRACT FROM AUTHOR]

• TBBPA exhibited the strongest enhancing effect on cell migration among other tested treatments. • The process of migration was accompanied by the invasion instead of EMT. • NOX-driven ROS in lieu of energy metabolism was sensitive to TBBPA stimulation. • Molecular docking suggested a link between TBBPA ligand and NOX receptor. Due to the extensive applications and deleterious effects of Tetrabromobisphenol A (TBBPA), the health risk and possible mechanisms have been a topic of concern. However, the knowledge on carcinogenic risk of TBBPA and corresponding mechanisms remains scarce. In this study, endometrial cancer cells were exposed to low doses of TBBPA and its main derivatives including TBBPA bis (2,3-dibromopropyl ether) (TBBPA-BDBPE) and TBBPA bis (2-hydroxyethyl ether) (TBBPA-BHEE). The data from wound healing and transwell assays demonstrated that TBBPA treatment exhibited the strongest enhanced effect on cell migration among other tested treatments. Of note, the process of invasion rather than epithelial-mesenchymal transition (EMT) was accompanied by the occurrence of migration elevated by TBBPA. Furthermore, the levels of several metabolite indicators were measured to assess the underlying mechanisms involved in TBBPA-induced cell migration. The findings suggested that NADPH oxidase (NOX)-driven ROS instead of energy metabolism was sensitive to TBBPA stimulation. In addition, molecular docking supported a link between TBBPA ligand and NOX receptor. Accordingly, this study has provided new insights for TBBPA-induced carcinogenic effects and may arise peoples' vigilance to environmental pollution of brominated flame retardant. [ABSTRACT FROM AUTHOR]