HuagongsheHuagongshe Chemistry Print Report · For research reference only
HRID 1871209Generated: November 1, 2026
8-(p-Sulfophenyl)theophylline → 8-(p-Sulfophenyl)theophylline
https://huagongshe.com/reaction/1871209
Participants
| Role | Name | HCID | Charge |
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| Reactant | 8-(p-Sulfophenyl)theophylline | HCID 1908 | — |
| Reactant | Sodium Hydroxide | HCID 14798 | — |
| Reactant | Thiobarbituric acid | HCID 2723628 | — |
| Reactant | Sodium Lauryl Sulfate | HCID 3423265 | — |
| Reactant | HCID 178521059 | HCID 178521059 | — |
| Solvent | Acetic Acid | HCID 176 | — |
| Solvent | Water | HCID 962 | — |
| Product | 8-(p-Sulfophenyl)theophylline | HCID 1908 | — |
| Product | Adenosine | HCID 60961 | — |
Reaction Steps
Concentrations of the products of lipid peroxidation [thiobarbituric acid reactive substances (TBARS)] were measured using the thiobarbituric acid reaction from representative samples of jejunum tissue of septic and control rats at 24 and 72 hours after sepsis induction. Tissue homogenate samples (0.2 ml; 10% w/v) were combined with 0.2 ml 8.1% sodium dodecyl sulfate, 1.5 ml of 20% acetic acid (the solution adjusted to pH 3.5 with NaOH), and 1.5 ml of 0.8% aqueous solution of thiobarbituric acid. Distilled water was added to bring the total volume up to 4 ml, then heated in an oil bath at 950° C. for 60 min. After cooling, 1 ml distilled water and 5 ml n-butanol/pyridine (15:1 v/v) was added. After shaking 30 sec, followed by centrifugation at 4000 rpm for 10 min, absorbance of the organic layer was measured at 532 nM. Data from tissue obtained from non-septic rats, and septic rats treated with saline (No Rx), 8-SPT, or pentostatin are expressed as nmols TBARS per mg protein in FIG. 6 Elevated TBARS were found as early as 24 hours after sepsis induction. Adenosine receptor blockade (8-SPT) resulted in exacerbation of the sepsis-induced elevation in TBARS. Inhibition of adenosine deaminase with pentostatin resulted in diminution of tissue TBARS during sepsis. These data confirm the presence of oxidative damage in this model of sepsis, and the ability to reduce oxidative damage by inhibiting adenosine deaminase. The data demonstrating exacerbation of oxidative damage with adenosine receptor blockade points to the primary role for endogenous adenosine in these responses.
Provenance & Evidence
| DOI | 10.6084/m9.figshare.5104873.v1 |
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| Patent number | US06103702 |
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| Source dataset | uspto-grants-2000_08 |
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| ORD ID | ord-fdaab151ce2d44b39c481d43914defbc |
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| Source note | uspto-grants-2000_08 |
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