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  • 1
    Electronic Resource
    Electronic Resource
    Solid-phase extraction and reversed-phase high-performance liquid chromatographic determination of sulphur mustard in blood
    Amsterdam : Elsevier
    Journal of Chromatography B: Biomedical Sciences and Applications 661 (1994), S. 341-345 
    Details
    ISSN: 0378-4347
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0378-4347(94)00375-0
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  • 2
    Electronic Resource
    Electronic Resource
    Does methyl isocyanate interaction with normal hemoglobin alter its structure and function? (1992)
    Springer
    Bulletin of environmental contamination and toxicology 48 (1992), S. 77-82 
    Details
    ISSN: 1432-0800
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00197486
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  • 3
    Electronic Resource
    Electronic Resource
    Acute toxicity of methyl isocyanate in rabbit: In vitro and in vivo effects on rabbit erythrocyte membrane (1992)
    Springer
    Archives of environmental contamination and toxicology 22 (1992), S. 300-304 
    Details
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract Methyl isocyanate (MIC) interaction with the rabbit erythrocyte membrane increased the fluidity of the membrane and decreased the osmotic fragility of erythrocytes both in vitro and in vivo in rabbits intoxicated with MIC subcutaneously. MIC inhibited both acetylcholinesterase (AChE) and adenosine triphosphatase (ATPase) activities of erythrocytes dose-dependently in vitro, while in vivo a decreased trend in ATPase activity with unaltered AChE activity was observed. MIC also caused significant decrease in plasma sodium level with corresponding increase in potassium level in rabbits. The observed effects are due to MIC, per se, as the hydrolysis products of MIC, methylamine and N,N′-dimethylurea did not affect the erythrocyte fluidity and enzymes activities both in vitro and in vivo while they increased the osmotic fragility of erythrocytes in vivo in rabbits administered subcutaneously in equimolar concentration to MIC dosage. Inhibition of Na+-K+-dependent ATPase with altered permeability to cations and also probably water transport of plasma membrane due to MIC interaction are envisaged.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00212090
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  • 4
    Electronic Resource
    Electronic Resource
    In vitro and in vivo effects of methyl isocyanate on rat brain mitochondrial respiration (1994)
    Springer
    Archives of environmental contamination and toxicology 27 (1994), S. 272-275 
    Details
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract The present study deals with the in vitro and in vivo effects of methyl isocyanate (MIC) on rat brain mitochondrial function. Addition of MIC to tightly coupled brain mitochondria in vitro resulted in a mild stimulation of state 4 respiration, abolition of respiratory control, decrease in ADP/O ratio, and inhibition of state 3 oxidation. The oxidation of NAD+-linked substrates (glutamate + malate) was more sensitive (fourfold) to the inhibitory action of MIC than succinate while cytochrome oxidase was unaffected. Administration of MIC subcutaneously at a lethal dose affected respiration only with glutamate + malate as the substrate (site I) and caused a 20% decrease in state 3 oxidation leading to a significant decrease in respiratory control index while state 4 respiration and ADP/O ratio remained unaffected. As both the malondialdehyde and iron contents of brain mitochondria were not altered, it may be inferred that the observed in vivo inhibition of state 3 oxidation is induced by MIC through systemic stagnant hypoxia leading to ischemia of brain, which further contributes to the cerebral hypoxia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00214274
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  • 5
    Electronic Resource
    Electronic Resource
    Acute toxicity of methyl isocyanate in mammals. II. Induction of hyperglycemia, lactic acidosis, uraemia, and hypothermia in rats (1990)
    Springer
    Archives of environmental contamination and toxicology 19 (1990), S. 314-318 
    Details
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract When rats were administered methyl isocyanate (MIC) by inhalation or subcutaneous route it produced severe hyperglycemia, clinical lactic acidosis, highly elevated plasma urea, and reduced plasma cholinesterase activity with unaltered erythrocytc acetyl cholinesterase activity. Irrespective of the route of administration, MIC also caused severe hypothermia, which was not ameliorated by prior administration of atropine sulphate. Acute toxic effects of MIC are essentially similar by either route except for the intensity of the effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01054971
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  • 6
    Electronic Resource
    Electronic Resource
    Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in rats II Pulmonary histopathology in the subacute and chronic phases (1994)
    Springer
    Archives of toxicology 69 (1994), S. 45-51 
    Details
    ISSN: 1432-0738
    Keywords: Key words Methyl isocyanate toxicity ; Methylamine toxicity ; Pulmonary pathology ; Long-term effects ; Fibrosis ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This paper describes the long-term (subacute and chronic) histopathological effects in the lungs of rats subjected to a single exposure to methyl isocyanate (MIC) by both the inhalation and subcutaneous (s.c.) routes as well as the role of methylamine (MA) and N,N′-dimethylurea (DMU), the hydrolytic derivatives of MIC in eliciting the observed changes. At the subacute phase, the intra-alveolar and interstitial edema were prominent only in the inhalation group as against the more pronounced inflammatory response in the s.c. route. With the progress of time the evolution of lesions appeared to be similar, culminating in the development of significant interstitial pneumonitis and fibrosis. MA, one of the hydrolytic derivatives of MIC, also caused interstitial pneumonitis progressing to fibrosis, albeit to a lesser extent than MIC, indicating its contribution to the long-term pulmonary damage. The diffuse interstitial pulmonary fibrosis observed at 10 weeks after a single exposure to MIC by either route is of greater significance in the context of the occurrence of pulmonary fibrosis in the late autopsies of Bhopal gas victims and also clinical sequelae in some of the survivors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050136
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of methyl isocyanate on rabbit cardiac Na+, K+-ATPase (1995)
    Springer
    Archives of toxicology 69 (1995), S. 694-697 
    Details
    ISSN: 1432-0738
    Keywords: Key words Methyl isocyanate toxicity ; Na+ ; K+-ATPase inhibition ; Circular dichroism of Na+ ; K+-ATPase ; Kinetics ; Rabbit myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study describes the effect of methyl isocyanate (MIC) on rabbit cardiac microsomal Na+, K+-ATPase. Addition of MIC in vitro resulted in dose-dependent inhibition of Na+, K+-ATPase, Mg2+-ATPase and K+-activated p-nitrophenyl phosphatase (K+-PNPPase). Activation of Na+, K+- ATPase by ATP in the presence of MIC showed a decrease in Vmax with no change in Km. Similarly, activation of K+ PNPPase by PNPP in the presence of MIC showed a decrease in Vmax with no change in Km. The circular dichroism spectral studies revealed that MIC interaction with Na+, K+-ATPase led to a conformation of the protein wherein the substrates Na+ and K+ were no longer able to bind at the Na+- and K+-activation sites. The data suggest that the inhibition of Na+, K+-ATPase was non-competitive and occurred by interference with the dephosphorylation of the enzyme-phosphoryl complex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050234
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  • 8
    Electronic Resource
    Electronic Resource
    Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in rats I Pulmonary histopathology in the acute phase (1994)
    Springer
    Archives of toxicology 69 (1994), S. 39-44 
    Details
    ISSN: 1432-0738
    Keywords: Key words Methyl isocyanate toxicity ; Histopathology ; Lungs ; Methylamine toxicity ; N ; N′-Dimethyl urea toxicity ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study describes the acute histopathological changes induced by methyl isocyanate (MIC) in the lungs of rats at 24 h after a single exposure to varied concentrations/doses of MIC by inhalation and subcutaneous (s.c.) routes and also delineates the effects due to the hydrolytic derivatives of MIC, viz., methylamine (MA) and N,N′-dimethyl urea (DMU). MIC, either inhaled or administered s.c., resulted in a wide range and extent of histopathological changes in the lungs, proportional to the exposure concentration/dose. The salient, effects of inhaled MIC are acute necrotizing bronchitis of the entire respiratory tract accompanied by varying degrees of confluent congestion, hyperemia and interstitial and intra-alveolar edema, while MIC administered s.c. led to prominent vascular endothelial damage, congestion and severe interstitial pneumonitis with apparently normal bronchial epithelium; and intra-alveolar edema only with the high dose. The only noteworthy lesion produced by MA and DMU (to some extent) was interstitial pneumonitis, suggesting their possible involvement in the subsequent inflammatory response of MIC. Except, for the endothelial changes, the overall spectrum of the histopathological lesions is quite comparable to those observed in the lungs of Bhopal victims during the acute phase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050135
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