Chloroform was bound covalently to DNA, RNA and proteins of rat and mouse organs in vivo after i.p. injection. Covalent Binding Index values of rat and mouse liver DNA classify chloroform as a weak initiator. Labelings of RNA and proteins from various organs of both species were higher than that of DNA. In an in vitro cell-free system, chloroform was bioactivated by cytochrome P450-dependent microsomal fractions, by cytosolic GSH-transferases from rat and mouse liver, and particularly by the latter enzymes from mouse lung. This observation suggests that GSH plays a role in the binding of chloroform metabolites to DNA. The presence of both microsomal and cytosolic enzymatic systems in the standard incubation mixture generally led to an additive or synergistic bioactivating effect for rat and mouse, respectively.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1177/030089169107700401 | DOI Listing |
Biomed Mater
January 2025
School of Food Science and Technology, Dalian Polytechnic University, SKL of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Dalian 116034, People's Republic of China.
Bone morphogenetic protein 2 (BMP-2) and a polysaccharide (SUP) were embedded in the calcium phosphate cement (CPC) scaffold, and the bone repair ability was evaluated. The new scaffolds were characterized using x-ray diffraction, Fourier transform-infrared, scanning electron microscopy, and energy dispersive spectroscopy analyses. CPC-BMP2-SUPH scaffold promoted the BMP-2 release by 1.
View Article and Find Full Text PDFHepat Oncol
December 2024
Advanced Imaging Research Center, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.
The aim of this study was to assess the utility of weighted amide proton transfer (APT) MRI in three different rodent models of hepatocellular carcinoma (HCC). APT MRI was evaluated in models of diethylnitrosamine (DEN) induced HCC, N1S1 syngeneic orthotopic xenograft and human HepG2 ectopic xenograft. All models of HCC showed a higher APT signal over the surrounding normal tissues.
View Article and Find Full Text PDFSci Rep
January 2025
Key Laboratory for Stem Cells and Tissue Engineering Ministry of Education, Guangdong Provincial Key Laboratory of Brain Function and Disease, Institute of Spinal Cord Injury, Department of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Neuromuscular diseases usually manifest as abnormalities involving motor neurons, neuromuscular junctions, and skeletal muscle (SkM) in postnatal stage. Present in vitro models of neuromuscular interactions require a long time and lack neuroglia involvement. Our study aimed to construct rodent bioengineered spinal cord neural network-skeletal muscle (NN-SkM) assembloids to elucidate the interactions between spinal cord neural stem cells (SC-NSCs) and SkM cells and their biological effects on the development and maturation of postnatal spinal cord motor neural circuits.
View Article and Find Full Text PDFCell Signal
January 2025
Department of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou 510120, PR China. Electronic address:
Intervertebral disc degeneration (IVDD) is a leading cause of low back pain, primarily driven by inflammatory processes within the disc, particularly involving the infiltration and activity of macrophages. High Mobility Group Box 1 (HMGB1) has been identified as a crucial mediator in this inflammatory cascade, yet its precise role in macrophage-induced disc degeneration remains unclear. In this study, we employed a combination of in vivo and in vitro models, including genetically engineered mice with macrophage-specific overexpression of HMGB1, a rat model of IVDD, and cultured macrophages and nucleus pulposus cells (NPCs), to elucidate the role of HMGB1 in IVDD.
View Article and Find Full Text PDFCell Rep Med
January 2025
Biomaterials Research Center, School of Biomedical Engineering, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China; Department of Cardiology, Guangzhou Institute of Cardiovascular Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, China; Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China; School of Basic Medical Science, Guangzhou Medical University, Guangzhou, Guangdong 510182, P.R. China. Electronic address:
C-C chemokine receptor type 2 (CCR2) cardiac-resident macrophages (CCR2 cRMs) are known to promote cardiac repair after myocardial infarction (MI). However, the substantial depletion and slow recovery of CCR2 cRMs pose significant barriers in cardiac recovery. Here, we construct a functional conductive cardiac patch (CCP) that can provide exogenously elastic conductive microenvironment and induce endogenously reparative microenvironment mediated by CCR2 cRMs for MI repair.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!