Protective effect of adenosine triphosphate against cisplatin-induced necrotic and degenerative oral mucositis in rats.

Background: Inflammation, oxidative damage, and adenosine triphosphate (ATP) depletion play a role in the pathogenesis of cisplatin (CIS)-induced oral mucositis.

Objective: The purpose of this research is to examine the impact of ATP against potential oral mucositis development in cisplatin-treated rats. Methodology All rats were randomly assigned to four groups, namely healthy control group (HG), ATP group (ATPG), Cisplatin group (CISG), and ATP + Cisplatin group (ATCS).

Investigation of Behavior of Forced Degradation of Lidocaine HCl by NMR Spectroscopy and GC-FID Methods: Validation of GC-FID Method for Determination of Related Substance in Pharmaceutical Formulations.

The forced degradation study of lidocaine HCl was carried out according to the ICH guideline Q1A (R2). The degradation conditions were assessed to be hydrolysis, oxidation, photolysis and dry heat during 24 h, 48 h and 72 h and then the samples were investigated by GC-FID method and nuclear magnetic resonance (NMR) spectroscopy. According to these results, the degradation products were not observed in all reaction conditions during the 72 h period.

Secondary/tertiary benzenesulfonamides with inhibitory action against the cytosolic human carbonic anhydrase isoforms I and II.

Carbonic anhydrase inhibitors of primary sulfonamide type, RSO(2)NH(2), have clinical applications as diuretics, antiglaucoma, antiepileptic, antiobesity and antitumor drugs. Here we investigated inhibition of two human cytosolic isozymes, hCA I and II, with a series of secondary/tertiary sulfonamides, incorporating tosyl moieties (CH(3)C(6)H(4)SO(2)NR1R2). Most compounds inhibited both isoforms in low micromolar range, with inhibition constants between 0.

Sulfapyridine-like benzenesulfonamide derivatives as inhibitors of carbonic anhydrase isoenzymes I, II and VI.

The inhibition of two human cytosolic carbonic anhydrase (hCA, EC 4.2.1.