Preparation of a porphyrin-polyoxometalate hybrid and its photocatalytic degradation performance for mustard gas simulant 2-chloroethyl ethyl sulfide

By combining 5,10,15,20-tetra(4-chlorine)phenylporphyrin(TClPP)andα-Keggin polyoxometalate H_(5)PV_(2)Mo_(10)O_(40)(H 5 PVMo)via a simple ion-exchange method,an organic-inorganic hybrid material[C_(44)H_(28)N_(4)Cl_(4)]_(1.5)[H_(2)PMo_(10)V_(2)O_(40)]·2C_(2)H_(6)O(H_(2 )TClPP-H_(2) PVMo)was prepared and thoroughly characterized by a variety of techniques.The homogeneous photocatalytic degradation of 2-chloroethyl ethyl sulfide(CEES)(5μL)by H_(2) TClPP-H_(2) PVMo(1×10^(−6)mol/L)was studied in methanol and methanol-water mixed solvent(v/v=1:1),in which the degradation rate of CEES reached 99.52%and 99.14%,respectively.The reaction followed first-order reaction kinetics,and the half-life and kinetic constant in methanol and the mixed solvent were respectively 33.0min,−0.021 min−1 and 15.7min,−0.043 min−1.Mechanism analysis indicated that under visible light irradiation in the air,CEES was degraded via oxidation and alcoholysis/hydrolysis in methanol and the mixed solvent.O_(2)·−and ^(1)O_(2) generated by H_(2) TClPP-H_(2) PVMo selectively oxidized CEES into a nontoxic sulfoxide.Singlet oxygen capture experiments showed that H_(2) TClPP-H_(2) PVMo(φ=0.73)had a higher quantum yield of singlet oxygen than TClPP(φ=0.35)under an air atmosphere and visible light irradiation.

Histomorphological and Histochemical Alterations Following Short-term Inhalation Exposure to Sulfur Mustard on Visceral Organs of Mice

Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The indanunatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytopasm of hepatocytes and renal parenchymal cells. Renallesions were chazacterized by congestion and hemorrhage. Among visceral tissues, maximum atrophywas observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.

Sulphur Mustard Induced Oxidative Stress and Its Prevention by Sodium 2, 3-Dimercapto Propane Sulphonic Acid (DMPS) in Mice

Sulphur mustard [bis(2 chloro ethyl) sulfide] (SM), a bifunctional alkylating agent has been frequently used as a chemical warfare agent. In the present study, the effects of sodium 2 3 dimercaptopropane sulphonic acid (DMPS) on some biochemical and histological parameters in mice, exposed to 1/4LC 50 concentration of SM vapor (10.5 mg/m\+3) were examined over a period of seven days. Exposure of SM resulted in a significant loss of blood, hepatic and pulmonary glutathione (GSH) and an elevation of hepatic and pulmonary oxidized glutathione (GSSG). These biochemical changes were accompanied by a number of histopathological alterations. The most prominent was congestion and degeneration in viscera and obliteration of chromatin material. These biochemical and histopathological changes were less marked in animals pre administered with DMPS followed by DMPS exposure indicating some protective value of the thiol (DMPS) against SM induced oxidative injury in mice.