The effect of sulphur mustard (0.5 LD50, percutaneous) on antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)) in blood cells (erythrocytes (RBC), leucocytes (WBC) and platelets) and body tissues (liver, kidney, spleen and brain) of rats has been investigated 24 h post exposure. The SOD activity was significantly decreased in WBC, platelets, spleen and brain as compared to control. The CAT activity was significantly inhibited in RBC, WBC and spleen as compared to control. The GSH-Px activity was signficantly depressed in WBC, spleen and liver as compared to control. It is concluded that sulphur mustard at a sublethal dose inhibited antioxidant enzyme activities in WBC and spleen. Thus, antioxidant enzymes in lymphatic tissues may be used as suitable models for assessing mustard toxicity. The study suggests the formation of reactive oxygen species in sulphur mustard intoxication.

Administration, Topical↗

PubMedDate not supplied

Diisopropylphosphorofluoridate-induced depression of compound action potential of frog sciatic nerve in vitro is mediated through the inhibition of cholinesterase activity.

Effect of diisopropylphosphorofluoridate (DFP), an irreversible cholinesterase (ChE) inhibitor, on compound action potential (CAP) of sciatic nerve in vitro was examined. Further, the role of cholinesterase reactivator (1 acetyl-4-hydroxy imino methyl pyridinium bromide; SPK-3) in reversing DFP-induced changes was also evaluated. Diisopropylphosphorofluoridate produced a dose-dependent depression of the CAP. A concentration as low as 0.01 microM DFP produced a 5% depression (P < 0.05) and the maximal depression (30% of control) was observed with 1 microM. The SPK-3 (up to 10 microM) had no effect on the CAP; SPK-3 (10 microM) antagonized the DFP-induced depression of the CAP partially but not after 1 microM DFP. However, the inhibitory concentration of DFP to produce 50% of the maximal depression (IC50) was 0.38 +/- 0.025 microM in the presence of SPK-3 (10 microM; n = 4), against 0.15 +/- 0.05 microM for DFP alone (n = 7). These IC50 values were significantly different (P < 0.05, Student's t-test). The DFP decreased nerve ChE activity by 41% in the absence of SPK-3 and by 31% in the presence of SPK-3. Although SPK-3 could not completely reactivate the inhibited enzyme, it seems reasonable to conclude that the DFP-induced depression of the action potential of sciatic nerve was mediated by inhibiting the ChE activity.

Action Potentials↗

PubMedDate not supplied

Beryllium-induced biochemical alterations and their prevention following co-administration of meso-2,3-dimercaptosuccinic acid or 2,3-dimercaptopropane sulphonate in rats.

The effects of meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercaptopropane sulphonate (DMPS) on body beryllium burden, hepatic lipid peroxidation, glutathione, alkaline and acid phosphatase and some biochemical variables of porphyrin metabolism were studied in beryllium-poisoned rats. It was observed that beryllium poisoning is associated with a slight increase in lipid peroxidation, significant depletion of alkaline phosphatase and elevation of acid phosphatase activities in the liver and increased beryllium concentration in blood and other soft organs. Evidence is presented that both DMSA and DMPS during concomitant administration prevented most of the above beryllium-induced biochemical alterations. Tissue beryllium concentration and histopathological lesions in liver and kidneys were also significantly less marked following simultaneous administration of DMPS compared to beryllium-exposed controls; DMSA was comparatively less effective.

Animals↗

PubMedDate not supplied

Route-specific cardiorespiratory and neuromuscular changes following organophosphorous poisoning in rats.

Organophosphorous compounds cause a variety of physiological effects. The effect of various routes of administration of these compounds on the pathophysiology is still an open question. The present study addresses the effect of two organophosphorous compounds, namely diisopropyl fluorophosphate and methylisopropyl phosphonofluoridate, given by two different routes (i.v. and s.c.), on physiological parameters in anaesthetized and artificially ventilated rats. Both organophosphorous compounds produced a dose-dependent rise in blood pressure, bradycardia and twitch potentiation after i.v. administration. These effects are mediated by muscarinic as well as alpha-adrenoreceptors and are not affected by adrenalectomy. However, after s.c. administration, both organophosphorous compounds produced a dose-dependent transient hypotension and bradycardia, mediated by muscarinic receptors, without affecting other physiological parameters. The results indicate the route-specific effects of these compounds on the cholinergic-catecholaminergic interactions in rats.

Adrenalectomy↗