Rabbit Anti-Human MTOR Polyclonal Antibody

Mercury (Hg) in its all forms, including inorganic Hg (iHg) is an environmental contaminant due to toxicity and diseases in human. However, a little is known about the underlying mechanisms responsible for iHg toxicity. Selenium (Se) is an essential trace element, recognized as an antioxidant and protective agent against metal toxicities. The purpose of this research was to investigate ameliorations of Se counter to iHg-mediated toxicity in PC12 cells. Cytotoxic assays have been shown that iHg (5 mu M) caused oxidative stress and intrinsic apoptosis via ROS generation, oxidizing glutathione, damaging DNA, degrading cell membrane integrity, down-regulating mTOR, p-mTOR, akt and ERK1, and up-regulating cleaved caspase 3 and cytochrome c release in PC12 cells 48 h after incubation. Co-treatment of Se (5 mu M) inhibited intrinsic apoptosis and oxidative stress induced by iHg (5 mu M) via inhibiting ROS formation, boosting GPx contents, increasing reduced glutathione, limiting DNA degradation, improving cell membrane integrity, up-regulating mTOR, p-mTOR, akt, ERK1 and caspase 3, and down-regulating cleaved caspase 3 and cytochrome c leakage in PC12 cells. In conclusion, these results rec-ommended that excessive ROS generation acts a critical role in iHg-influenced oxidative stress and co-treatment of Se attenuates iHg-cytotoxicity through its antioxidant properties.

N-6-methyladenosine (m(6)A) is one of the most common RNA modifications in eukaryotes involved in the regulation of post-transcriptional gene expression, as well as the occurrence and development of diseases related to environmental exposures. Adverse factors produced by environmental exposures, such as reactive oxygen species, inflammation, and cyclobutane pyrimidine dimers, mediate m(6)A modification, thereby regulating downstream gene and protein expression, and signaling pathways, such as FTO/m(6)A RNA/p53 axis, PI3K/AKT/mTOR pathway, and PARP/METTL3/m(6)A RNA/Pol kappa pathway. Moreover, an imbalance in m(6)A methylation levels directly mediates disease pathogenesis. To date, some studies have detailed the mechanisms underlying environmental exposure-mediated global changes in RNA m(6)A methylation. Based on our current understanding, we aimed to elaborate on the molecular mechanisms through which RNA m(6)A methylation regulates gene expression under environmental exposures. In this review, we outline the biogenesis and functions of RNA m(6)A modification. Furthermore, we focus on the effects of environmental exposures on m(6)A levels and highlight the relationships between environmental exposures (doses and time) and m(6)A levels. Although the molecular mechanisms regulating gene expression remains to be elucidated, m(6)A has potential applications as a disease biomarker. (C) 2020 Elsevier Ltd. All rights reserved.