Detail of > 69-89-6
- MSDS Download

- CAS Number:
- 69-89-6
- Name:
Xanthine
- Formula:
- C5H4N4O2
- Molecular Structure:

- Synonyms:
- 1H-Purine-2,6-dione,3,7-dihydro-;1H-Purine-2, 6-diol;9H-Purine-2,6-(1H,3H)-dione;3,7-dihydropurine-2,6-dione;Isoxanthine;USAF CB-17;2,6-Dioxo-1,2,3,6-tetrahydropurine;Xanthic oxide;1H-Purine-2,6-diol;2,6(1,3)-Purinedion;XAN;Purine-2,6(1H,3H)-dione;3,5-dihydropurine-2,6-dione;3,7-dihydro-1H-purine-2,6-dione;Pseudoxanthine;Purine-2,6-diol;1H-Purine-2,6-dione, 3,7-dihydro-;Purine-2(3H),6(1H)-dione;Xanthin;1-H-purine-2,6-dione, 3,7-dihydro(9CI);2,6-Dihydroxypurine;
- Molecular Weight:
- 152.11
- EINECS:
- 200-718-6
- Density:
- 1.94 g/cm3
- Melting Point:
- 300 °C
- Boiling Point:
- 834.9 °C at 760 mmHg
- Flash Point:
- 458.7 °C
- Solubility:
- NH4OH: freely soluble
- Appearance:
- White to off-white crystalline powder
- Hazard Symbols:
Xi- Risk Codes:
- 36-43
- Safety:
- 36/37Details
- particular:
- particular
- Deleted CAS:
- 6053-41-4|6050-36-8|42911-15-9|33669-67-9|28522-58-9
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Reference
- Effects of oxygen radicals on cerebral arterioles
- Effects of oxygen radicals on cerebral arterioles. Wei, Enoch P.; Christman, Carole W.; Kontos, Hermes A.; Povlishock, John T. (Dep. Med., Med. Coll. Virginia, Richmond, VA 23298, USA). Am. J. Physiol., 248(2, Pt. 2), H157-H162 (English) 1985. CODEN: AJPHAP. ISSN: 0002-9513. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Xanthine oxidase [9002-17-9] and xanthine [69-89-6], a combination that produces H2O2 and superoxide anion radical, applied topically in anesthetized cats equipped with cranial windows caused arteriolar dilation during application, sustained dilation 1 h after washout, and reduced reactivity to the vasoconstrictive effects of arterial hypocapnia, discrete lesions of the endothelium, and morphol. abnormalities of the vascular smooth muscle by electron microscopy. Similar effects were seen in small, but not in large, arterioles during topical application of H2O2 + FeSO4, a combination that produces free hydroxyl radical. The functional changes caused by xanthine oxidase plus xanthine were inhibited completely by superoxide dismutase plus catalase. Superoxide dismutase or catalase, each by itself, eliminated the residual effects seen after washout and reduced the dilation during application of xanthine oxidase. Thus, superoxide anion radical and H2O2 produced reversible arteriolar dilation; consistent vascular damage is produced in the presence of both superoxide anion radical and H2O2.
- Lipid peroxidation-induced inhibition of g-aminobutyric acid uptake in rat brain synaptosomes: protection by glucocorticoids
- Lipid peroxidation-induced inhibition of g-aminobutyric acid uptake in rat brain synaptosomes: protection by glucocorticoids. Braughler, J. Mark (Upjohn Co., Kalamazoo, MI 49001, USA). J. Neurochem., 44(4), 1282-8 (English) 1985. CODEN: JONRA9. ISSN: 0022-3042. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Incubation of rat brain synaptosomes with xanthine [69-89-6] and xanthine oxidase [9002-17-9] (X/XO) inhibited GABA [56-12-2] uptake. The inhibitory effects of X/XO were temp.- and time-dependent, and were characterized by an increased Km for GABA and a decreased Vmax. Inhibition of GABA uptake by X/XO was assocd. with both the formation of malonyldialdehyde and conjugated dienes, indicating that lipid peroxidn. was involved. Studies with catalase, superoxide dismutase, mannitol and chelated Fe suggested that hydroxyl radical was probably responsible for the initiation of lipid peroxidn. Both the peroxidn. of synaptosomal membranes and the inhibition of GABA uptake by X/XO were enhanced by the addn. of ADP [58-64-0] and FeCl2. The X/XO-induced inhibition of GABA uptake of synaptosomes was prevented by preincubation of synaptosomes with certain glucocorticoids prior to X/XO exposure. , Methylprednisolone Na succinate (MPSS) [2375-03-3], dexamethasone Na phosphate (DMSP) [2392-39-4], and prednisolone Na succinate (PSS) [1715-33-9], all prevented the inhibition of GABA uptake by X/XO. MPSS was most effective at concns. ~100 mM, DMSP was slightly more potent, and PSS was optimal at ~300 mM. Hydrocortisone Na succinate [125-04-2] was ineffective at preventing X/XO-induced inhibition of GABA uptake at concns. £3 mM. The steroids are presumed to work through a mechanism that blocked the formation of lipid peroxides.
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