Search

Ochratoxin A (OTA) is a mycotoxin commonly found in food and feed. It presents a serious threat to human and animal health while also posing a risk as a potential aquatic contaminant. Although many research efforts have been placed on OTA contamination and detoxification, systematic and in-depth studies on summarizing its primary sources, formation mechanisms, toxicological effects, and control technologies remain essential. This review systematically analyzed the sources of OTA contamination, including the main toxin-producing strains and their specific colonization environments, in which the biosynthetic pathways and key regulatory factors of OTA were outlined. On this basis, the principle, merits, disadvantages, and application potential of OTA control technologies, including the physical, chemical, and biological detoxification techniques, were comparatively evaluated. The applications of genetic engineering with an emphasis on newly identified degradative enzymes and their potential in OTA removal were carefully elucidated. Considering the stringent global OTA regulatory standards and food safety handling requirements, this review highlights the necessity of comprehensive control measure development and emphasizes the importance of rigorous technical evaluation and regulatory approval. The aim is to provide theoretical support for effective OTA control and to guide future OTA contamination management in complex environments. [ABSTRACT FROM AUTHOR]

Research has revealed the involvement of mitochondrial autophagy and iron death in the pathogenesis of myocardial fibrosis. The objective of this study is to investigate whether the mitochondrial-targeted H 2 S donor AP39 inhibits mitochondrial autophagy and antagonizes myocardial cell iron death through the PINK1/Parkin pathway, thereby improving myocardial fibrosis in rats with myocardial infarction. A rat model of myocardial infarction was created by intraperitoneal injection of a high dose of isoproterenol, and H9c2 myocardial cells were subjected to hypoxic injury induced by CoCl 2. Western blot, RT-PCR, transmission electron microscopy, immunohistochemistry, as well as echocardiography, and studies on isolated hearts were employed. In the hearts of rats with myocardial infarction, there was a significant accumulation of interstitial collagen fibers, accompanied by downregulation of CSE protein expression, activation of the PINK1/Parkin signaling pathway, and activation of mitochondrial autophagy. Intervention with AP39 resulted in a significant improvement of the aforementioned changes, which could be reversed by the addition of PAG. Similar results were observed in vitro experiments. Furthermore, the addition of CCCP reversed the antagonistic effect of AP39 on myocardial cell iron death, while the addition of RSL3 reversed the inhibitory effect of AP39 on collagen production in myocardial cells. The mitochondrial-targeted H 2 S donor AP39 can inhibit mitochondrial autophagy through the PINK1/Parkin pathway, antagonize myocardial cell iron death, and improve myocardial fibrosis in rats with myocardial infarction. [Display omitted] • Mitochondria-targeted hydrogen sulfide donor AP39 inhibited mitophagy and ferroptosis in myocardial infarcted rat cardiomyocytes. • AP39 reduces the level of reactive oxygen species and inhibits ferroptosis by suppressing hypoxia-induced mitophagy in cardiomyocytes. • AP39 ameliorates myocardial fibrosis in rats with myocardial infarction by inhibiting the PINK1/Parkin pathway. [ABSTRACT FROM AUTHOR]

Hypothyroidism alone can lead to myocardial fibrosis and result in heart failure, but traditional hormone replacement therapy does not improve the fibrotic situation. Hydrogen sulfide (H 2 S), a new gas signaling molecule, possesses anti-inflammatory, antioxidant, and anti-fibrotic capabilities. Whether H 2 S could improve hypothyroidism-induced myocardial fibrosis are not yet studied. In our study, H 2 S could decrease collagen deposition in the myocardial tissue of rats caused by hypothyroidism. Furthermore, in hypothyroidism-induced rats, we found that H 2 S could enhance cystathionine-gamma-lyase (CSE), not cystathionine β-synthase (CBS), protein expressions. Finally, we noticed that H 2 S could elevate autophagy levels and inhibit the transforming growth factor-β1 (TGF-β1) signal transduction pathway. In conclusion, our experiments not only suggest that H 2 S could alleviate hypothyroidism-induced myocardial fibrosis by activating autophagy and suppressing TGF-β1/SMAD family member 2 (Smad 2) signal transduction pathway, but also show that it can be used as a complementary treatment to conventional hormone therapy.

Myocardial fibrosis is a key link in the occurrence and development of diabetic cardiomyopathy. Its etiology is complex, and the effect of drugs is not good. Cardiomyocyte apoptosis is an important cause of myocardial fibrosis. The purpose of this study was to investigate the effect of gaseous signal molecule sulfur dioxide (SO 2 ) on diabetic myocardial fibrosis and its internal regulatory mechanism. Masson and TUNEL staining, Western-blot, transmission electron microscopy, RT-qPCR, immunofluorescence staining, and flow cytometry were used in the study, and the interstitial collagen deposition, autophagy, apoptosis, and changes in phosphatidylinositol 3-kinase (PI3K)/AKT pathways were evaluated from in vivo and in vitro experiments. The results showed that diabetic myocardial fibrosis was accompanied by cardiomyocyte apoptosis and down-regulation of endogenous SO 2 -producing enzyme aspartate aminotransferase (AAT) 1/2 . However, exogenous SO 2 donors could up-regulate AAT1/2, reduce apoptosis of cardiomyocytes induced by diabetic rats or high glucose, inhibit phosphorylation of PI3K/AKT protein, up-regulate autophagy, and reduce interstitial collagen deposition. In conclusion, the results of this study suggest that the gaseous signal molecule SO 2 can inhibit the PI3K/AKT pathway to promote cytoprotective autophagy and inhibit cardiomyocyte apoptosis to improve myocardial fibrosis in diabetic rats. The results of this study are expected to provide new targets and intervention strategies for the prevention and treatment of diabetic cardiomyopathy.