The hypoxic cell radiosensitizer [2-14C] pimonidazole (2-nitro-alpha-(piperidinomethyl)-l-imidazole ethanol) was injected i.p. into pigmented mice and rats bearing transplanted rhabdomyosarcoma. The injected dose level was 200 mg/kg, and the delivered activity was 96 microCi/kg. Whole-body autoradiography was carried out on all animals. We noted an extensive whole-body distribution of radioactivity. At short intervals, the autoradiograms were characterized by an accumulation of radioactivity in the metabolic and excretory organs (liver, kidney, urinary tract, and intestinal content) as well as in lymphomyeloid tissues (thyroid gland, suprarenal gland, and hypophysis) and salivary glands. In pigmented mice, the uveal and biliary tracts were the highest labelled. The liver and particularly the renal medulla were identified as sites of retention of radioactivity. In the tumor the radioactivity was detected only in peripheral regions, with higher uptake in viable zones than in necrotic islets.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/BF00254237 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Potential Use of Plasma Rich in Growth Factors in Age-Related Macular Degeneration: Evidence from a Mouse Model.
Medicina (Kaunas)
December 2024
BTI Biotechnology Institute, 01005 Vitoria, Spain.
: Age-related macular degeneration (AMD) is the leading cause of low vision and legal blindness in adults in developed countries. Wet AMD can be successfully treated using vascular endothelial growth factor (VEGF) inhibitors; however, dry AMD currently has no effective treatment. The purpose of this study is to analyze the efficacy of intraocular injection of plasma rich in growth factors (PRGF) in an AMD mouse model induced by intraperitoneal administration of sodium iodate.
View Article and Find Full Text PDFInduction of Retinal Ischemia-Reperfusion Injury in a Mouse Eye Model.
J Vis Exp
December 2024
Department of Ophthalmology, Boston University Chobanian & Avedisian School of Medicine;
Ischemia-reperfusion injuries are known to cause a range of retinal pathologies, including diabetic retinopathy, glaucoma, retinal vascular occlusions, and other vaso-occlusive conditions. This manuscript presents a method for inducing ischemia-reperfusion injury in a mouse model. The method utilized anterior chamber cannulation attached to a saline reservoir, generating hydrostatic pressure to raise the intraocular pressure to 90-100 mmHg.
View Article and Find Full Text PDFEffects and mechanisms of theabrownin from black tea in improving hyperuricemia: Evidence from animal study and clinical trial.
Int J Biol Macromol
December 2024
State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Department of Endocrinology, Xiang'an Hospital of Xiamen University, Xiamen University, Xiamen 361102, China.
Article Synopsis
- Hyperuricemia (HUA) is a condition where excess uric acid builds up in the body, and Theabrownin (TB), a compound from black tea, may help improve this condition.
- TB was found to lower uric acid levels and reduce kidney damage in HUA mice by inhibiting an enzyme (xanthine oxidase) and enhancing uric acid transport in the kidneys.
- A clinical trial with HUA patients indicated that consuming TB daily for 12 weeks effectively decreased uric acid levels without negative side effects.
Pleiotropic effects of mutant huntingtin on retinopathy in two mouse models of Huntington's disease.
Neurobiol Dis
December 2024
Department of Physiology & Neuroscience, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Electronic address:
Huntington's disease (HD) is caused by the expansion of a CAG repeat, encoding a string of glutamines (polyQ) in the first exon of the huntingtin gene (HTTex1). This mutant huntingtin protein (mHTT) with extended polyQ forms aggregates in cortical and striatal neurons, causing cell damage and death. The retina is part of the central nervous system (CNS), and visual deficits and structural abnormalities in the retina of HD patients have been observed.
View Article and Find Full Text PDFInterruption of the visual cycle in a novel animal model induces progressive vision loss resembling Stargardts Disease.
Sci Rep
December 2024
INCI-UPR3212-CNRS, 8 Allée du Général Rouvillois, 67000, Strasbourg, France.
Mutations in the gene ABCA4 coding for photoreceptor-specific ATP-binding cassette subfamily A member 4, are responsible for Stargardts Disease type 1 (STGD1), the most common form of inherited macular degeneration. STGD1 typically declares early in life and leads to severe visual handicap. Abca4 gene-deletion mouse models of STGD1 accumulate lipofuscin, a hallmark of the disease, but unlike the human disease show no or only moderate structural changes and no functional decline.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!