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Pharmaceutical contaminants are causing great attention for the public people, urgently requiring to be eliminated from the environment. Herein, commercial pharmaceutical carbamazepine was chosen as a model to be degraded by a heterogeneous Fenton system using natural pyrite as catalyst. The catalyst was characterized by X-ray diffraction apparatus, high-resolution transmission electron microscopy, and X-ray photoelectron spectroscopy. The elements composition and chemical states of pyrite changed significantly after the Fenton reaction, which promoted the production of active species in the electron transfer process. The degradation efficiency of carbamazepine (2.5?mg/L) can reach 99.71% after 30?min with 0.3?g/L of pyrite and 5?mM of H2O2, respectively. The reaction system was suitable for a wide range of pH (3–9). The environmental adaptability examination of pyrite showed that humic acid (HA) had inhibitory effects on the degradation of carbamazepine. While the changes of degradation efficiency of carbamazepine were inconspicuous in the presence of NO3-and SO42-, indicating strong anti-interference to environment common anions. Free-radical capturers suggested that hydroxyl radical (·OH), superoxide radical (·O2-), and singlet oxygen (1O2) participated in the degradation of carbamazepine. This research has offered a new strategy of “treating wastes with wastes” to use pyrite to remove emerging pollutants.

The assessment of drug toxicity, especially hepatotoxicity, is a critical task in drug development process. To assist with early detection, various in silico approaches have been demonstrated to identify drugs with high hepatotoxicity potential. In this study, based on detailed review on previous reports on drug-induced cholestatic liver injury, we developed a network-based approach to predict cholestatic potential of chemicals using toxicogenomic data. First, the cholestasis network was constructed with 57 relevant genes and 78 connections between genes. Taking only genes in the disease network into account, the evaluation model was trained by genomic data of 17 typical chemicals associated with cholestasis and yielded the prediction accuracy at 88%. The performance of this model was further challenged by an X-permutation test and an external set of 98 chemicals. Among them, 14 chemicals were marked with high risk of inducing cholestasis by our approach. A survey of published literatures confirmed that 71.43% of our predicted chemicals have been shown to induce cholestatic liver injury experimentally and approximately 93% of them have been implicated to promote liver injury to various extents. Together, we concluded that network-based approaches greatly facilitate further understanding of molecular mechanisms for cholestatic liver injury and this concept could be easily generalized to other biological-relevant side-effect assessments.

Metabolic associated fatty liver disease (MAFLD) is a multifactorial systemic disorder that occurs in the absence of excessive alcohol consumption. The disease is characterized by fatty degeneration and fat accumulation in liver parenchymal cells, the incidence of which is increasing annually, particularly in younger adults. MAFLD is caused by genetic and metabolism related disorders, of which mitochondrial dysfunction is the major contributor. Natural products can relieve MAFLD through restoring mitochondrial function. In this article, we describe the relationship between mitochondria and MAFLD and discuss the beneficial effects of natural products as a future anti-MAFLD strategy. Significance Statement. We herein propose that the development of mitochondrial regulators/nutrients from natural products can remedy mitochondrial dysfunction which represents an attractive strategy for the treatment of MAFLD. Furthermore, the mitochondrial regulation of natural products can provide new insight into the underlying mechanisms of action of natural products used for future MAFLD therapeutics.