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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

Reaction equation

Participants

RoleNameHCIDCharge
Reactant8-(p-Sulfophenyl)theophyllineHCID 1908—
ReactantSodium HydroxideHCID 14798—
ReactantThiobarbituric acidHCID 2723628—
ReactantSodium Lauryl SulfateHCID 3423265—
ReactantHCID 178521059HCID 178521059—
SolventAcetic AcidHCID 176—
SolventWaterHCID 962—
Product8-(p-Sulfophenyl)theophyllineHCID 1908—
ProductAdenosineHCID 60961—

Reaction Conditions

Temperature950 °C

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

DOI10.6084/m9.figshare.5104873.v1
Patent numberUS06103702
Source datasetuspto-grants-2000_08
ORD IDord-fdaab151ce2d44b39c481d43914defbc
Source noteuspto-grants-2000_08