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- Bookeditor, Curtis D. Klaassen, PhD, DABT, ATS, FAASLD, University Distinguished Professor and Chair (Retired), Department of Pharmacology, Toxicology and Therapeutics, School of Medicine, University of Kansas, Kansas City, Kansas.Summary: "The gold-standard text on the science of poisons updated to capture the latest breakthroughs and developments Casarett & Doull's Toxicology: The Basic Sciences of Poisons is the most trusted all-in-one overview of the biomedical and environmental aspects of toxicology. Presented in full color, it delivers a skill-building review of the basic components of toxicology, including general principles, modes of action, and chemical-specific toxicity. Spanning the entire field, Casarett & Doull's is considered to be the ultimate authority in toxicology. The Ninth Edition has been extensively updated by each chapter author and is enhanced by the addition of all-new chapters on timely topics such as computational toxicology and auditory toxicology. The extensive use of tables, illustrations, and other visuals make the information easy to understand and remember"-- Provided by publisher.
Contents:
Unit I: General principles of toxicology
Unit II: Disposition of toxicants
Unit III: Non-organ directed toxicity
Unit IV: Target organ toxicity
Unit V: Toxic agents
Unit VI: Environmental toxicology
Unit VII: Applications of toxicology.Digital Access AccessPharmacy 2019 - ArticleLarsson C.Contrib Nephrol. 1978;12:82-91.The renal prostaglandins (PGs) are formed mainly in the endoplasmatic reticulum from locally available precursor, arachidonic acid (C20:4). Although the main PG formation occurs in the papilla, significant amounts of PGs are also formed in the cortex. PGs are not stored, but at once released to the cytosol and metabolized by soluble enzymes, 15-OH-PG-dehydrogenase (PGDA), delta13-PG-reductase and PGE-9-keto-reductase. PG metabolism by the PGDH pathway occurs predominantly in cortex. C20:4 can be used to study the biological effects of the renal PG system. C20:4 given to rabbits increases renal biosynthesis of PGs, renal blood flow, predominantly in the juxtamedullary cortex, and plasma renin activity. These effects are inhibited by PG synthesis inhibitors like indomethacin.