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Experimental Stomatology
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
Administration of excessive amounts of iodide to hamsters leads to damage to the epithelial cells lining the distal part of the collecting ducts of the submandibular gland. In contrast, the parotid and sublingual glands are unaffected. To establish whether the variations in response are related to the iodine concentrating capacity of the three major salivary glands, Follis41 looked into the reparative process of iodine-induced hamster sialadenitis, the effects of certain pharmacologic agents on the gland response, and the reactivity of the salivary glands of other species to excess iodine intake. For the reparative studies, three groups of adult male hamsters were given 20 mg potassium iodide i.p. for 2, 4, or 8 days. On days 3, 5, and 9, the right submandibular gland was excised and examined microscopically. Groups of animals were serially sacrificed 2 to 62 days later, at which time the left gland was removed and processed for microscopic examination. For the pharmacologic studies, animals were first given an injection of either (1) atropine sulfate — 0.5 mg in two doses separated by a 4-hr interval, (2) pilocarpine nitrate — 5 mg on the same schedule as atropine, (3) thiouracil — one 50 mg dose, or (4) potassium thiocyanate — one 50 mg dose. All of the animals received potassium iodide i.p. 10 min after the first drug injection and were sacrificed 24 hr later. For the studies of species differences, rats, mice, rabbits, cats, and dogs were given potassium iodide i.p. at a level of 500 mg/kg body weight.
Radioactivity and Radiotracers
Published in Graham Lappin, Simon Temple, Radiotracers in Drug Development, 2006
The second example, shown in Figure 2.6 is more complex and illustrates a cyclization reaction as a step in the synthesis of cephalosporin antibiotic.4 Note that the radiolabeled intermediate is simply potassium thiocyanate (KS14CN).
The Tissue Plasminogen Activator — A Historical Account
Published in Cornelis Kluft, Tissue-Type Plasminogen Activator (t-PA): Physiological and Clinical Aspects, 1988
A systematic study was now initiated of fibrinolytically active solutions (blood, secretions, etc.) — mostly done by Sten Müllertz and summarized by him in 1956.53 It is not intended here to deal with these aspects, except to mention that streptokinase was found to act on human blood by generating an activator of plasminogen able also to convert bovine plasminogen to plasmin, despite the resistance of the latter plasminogen to streptokinase.54 This was an important finding which explained the intense — and until then enigmatic — lytic effect of streptokinase on human plasma or euglobulin in comparison with that of the tissue activator. Saline extracts of active tissues contained only a minute fraction of the total activity, and this was caused by an activator of plasminogen55 and not by a protease proper, as had been suggested.32 Among several proteases, only trypsin exerted an activating effect on plasminogen, suggesting that activation of plasminogen depends upon a partial proteolytic splitting of the plasminogen molecule.55 Work on the tissue plasminogen activator progressed slowly during this period, despite the availability of improved methods of assay. Continued studies of tissues from various mammalian species and different organs then showed the presence in the bovine lung of large amounts of an inhibitor of fibrinolysis,56 and this inhibitor could be extracted by solutions of potassium thiocyanate. It was later purified and found similar to the pancreatic inhibitor of Kunitz now called aprotinin.57 This extraction procedure was then tried on the active but insoluble tissue preparations, and this resulted in a complete extraction of the tissue plasminogen activator from the bulk of cellular material and the recovery of the activator by precipitation with acetone.58 With the resolution problem solved, the road was now open for a closer examination of the tissue plasminogen activator59 and the development of an assay method,60 allowing systematic studies of the distribution of the activator in various tissues or animal species beginning with those by Ole K. Albrechtsen.61–64
Synthesis, kinetic studies and in-silico investigations of novel quinolinyl-iminothiazolines as alkaline phosphatase inhibitors
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Muhammad Naeem Mustafa, Pervaiz Ali Channar, Muhammad Sarfraz, Aamer Saeed, Syeda Abida Ejaz, Mubashir Aziz, Fatmah Ali Alasmary, Hanadi Yaqob Alsoqair, Hussain Raza, Song Ja Kim, Asad Hamad
Potassium thiocyanate (1 mmol) was added in dry acetone (15 ml) in two necks round bottom flask fitted with reflux condenser and stirred for 5 min. The acetone solution of suitably substituted acid chlorides (1 mmol) was added dropwise to dissolve the potassium thiocyanate with stirring. The resulting mixture was heated to reflux the temperature for time of 3–4 h to afford the isothiocyanate. After cooling, an acetone solution of 3-aminoquinoline (1 mmol) was introduced dropwise and temperature of resulting solution was kept 60 °C for 12–14 h to afford the acyl thioureas on addition with ice cooled water. The resultant product was purified by recrystallization in acetone or ethanol.
Thiocyanate toxicity: a teaching case
Published in Clinical Toxicology, 2022
C. James Watson, Daniel L. Overbeek, Gabriella Allegri-Machado, Mark D. Kellogg, Al Patterson, J. Brian McAlvin, Michele M. Burns
Used into the mid-twentieth century for hypertension, thiocyanate is currently recognized as the endogenous product of the cyanide antidote sodium thiosulfate, as well as a byproduct of infusions of nitroprusside. Historically, thiocyanate was associated with renal impairment, delirium, and death. Contemporary literature on thiocyanate toxicity is limited, and includes reports on laboratory interference caused by thiocyanate. We present the case of an adolescent with an intentional potassium thiocyanate ingestion.