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  • 1
    Electronic Resource
    Electronic Resource
    Interaction of organophosphorus compounds with carboxylesterases in the rat (1996)
    Springer
    Archives of toxicology 70 (1996), S. 444-450 
    Details
    ISSN: 1432-0738
    Keywords: Key words Organophosphorus compounds ; Carboxylesterases ; Detoxication of organophosphates ; Soman ; Sarin ; Dichlorvos
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Carboxylesterases (CarbE) are involved in detoxication of organophosphorus compounds (OPC) through two mechanisms: hydrolysis of ester bonds in OPC which contain them and binding of OPC at the active site of CarbE which reduces the amount of OPC available for acetylcholinesterase inhibition. This study of the interaction of rat plasma and liver CarbE with dichlorvos, soman and sarin in vitro and in vivo was undertaken in order to contribute to better understanding of the role of CarbE in detoxication of OPC. The results obtained have shown that inhibitory potency (I50) of dichlorvos, sarin and soman towards rat liver CarbE was 0.2 μM, 0.5 μM and 4.5 μM, respectively, for 20-min incubation at 25°C. Second-order rate constants (ka) for liver CarbE inhibition were 2.3×105 M-1 min-1, 6.9×104 M-1 min-1 and 1.1× 104 M-1 min-1 for dichlorvos, sarin and soman, respectively. The corresponding values for plasma CarbE could not be calculated because of dominant spontaneous reactivation of inhibited CarbE. CarbE inhibited with these OPC in vitro spontaneously reactivate with half-times of 18, 143 and 497 min for sarin, dichlorvos and soman in plasma and 111, 163 and 297 min for sarin, soman and dichlorvos in liver, respectively. These results were also confirmed in experiments in vivo in which rats were subcutaneously treated with 0.5 LD50 of these agents. The half-times of spontaneous reactivation of rat plasma CarbE in vivo were 1.2, 2.0 and 2.7 h for dichlorvos, sarin and soman, respectively. These findings have changed current understanding of the mechanism of interaction of CarbE with OPC and involvement of the enzymes in detoxication of OPC, suggesting an active and important role of the enzymes in metabolic conversions of OPC to their less toxic metabolites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050297
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  • 2
    Electronic Resource
    Electronic Resource
    Repeated low doses of O-(2-chloro-2,3,3 trifluorocyclobutyl) O-ethyl S-propyl phosphorothioate (KBR-2822) do not cause neuropathy in hens (1997)
    Springer
    Archives of toxicology 72 (1997), S. 93-96 
    Details
    ISSN: 1432-0738
    Keywords: Key words Neuropathy ; Promotion ; Organophosphate-induced delayed polyneuropathy (OPIDP) ; Neuropathy target esterase (NTE)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Certain esterase inhibitors such as O-(2-chlo-ro-2,3,3-trifluorocyclobutyl) O-ethyl S-propyl phosphorothioate (KBR-2822) and phenylmethanesulfonyl fluoride (PMSF) cause exacerbation (promotion) of toxic and traumatic axonopathies. Although these chemicals are capable of inhibiting neuropathy target esterase (NTE), which is the target for organophosphate induced delayed neuropathy, the target for promotion is unlikely to be NTE. Experiments were aimed to ascertain if neuropathy is caused by repeated dosing with a promoter not causing NTE inhibition and in the absence of deliberate injury to axons. Hens were treated with KBR-2822 (0.2 or 0.4 mg/kg per day) by gavage for 90 days and observed for clinical signs up to 21–23 days after treatment when histopathological examination was carried out. NTE and acetylcholinesterase (AChE) were measured at intervals and mean percentages of inhibition at steady state of inhibition/resynthesis (on day 20) were as follows: mean inhibition NTE was ≤8% in the 0.2 mg/kg group and between 15 and 18% in the 0.4 mg/kg group in brain, spinal cord and peripheral nerve; mean AChE inhibition in brain was 31 and 57% in the two experimental groups, respectively. Controls treated with paraoxon (not neuropathic or a promoter and given at 0.05 mg/kg per day by gavage) showed 45% mean AChE inhibition and no NTE inhibition. Neither clinical nor morphological signs of neuropathy were observed in any group. To ascertain whether sub-clinical lesions were produced by the repeated treatment with KBR-2822, hens were given KBR-2822 (0.2 mg/kg per day) for 21 days by gavage followed by PMSF (120 mg/kg s.c. 24 h after the last dose of KBR-2822). A control group of hens was treated with the neuropathic DFP (0.03 mg/kg s.c. daily for 21 days causing 40–50% NTE inhibition) followed by PMSF (120 mg/kg s.c.). After PMSF, the KBR-2822 treated hens did not develop neuropathy whereas DFP treated hens did. Lack of neuropathy after repeated treatment with KBR-2822 indicates that a continuous promoting `pressure' on hen axons is harmless in the absence of a concurrent biochemical or neurotoxic injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050473
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Detection of apoptosis and phagocytosis in vitro in C6 rat glioma cells treated with tiazofurin (1998)
    Springer
    Apoptosis 3 (1998), S. 345-352 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; phagocytosis ; rat glioma ; tiazofurin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Tiazofurin, an anticancer drug which inhibits IMP dehydrogenase activity and decreases GTP concentration in various malignant cells, induced inhibition of growth and apoptosis in C6 rat glioma in vitro. The effects of tiazofurin were significantly blocked by addition of exogenous guanosine, suggesting the role of decreased GTP in triggering specific signal transduction pathways involved in apoptosis of C6 cells. The most interesting result of this study was the evidence of phagocytosis of apoptotic cells in vitro by neighbouring cells, a phenomenon considered to occur only in apoptosis in vivo. The possibility of observing phagocytosis in C6 glioma cells suggests that this cell system could be a good model for studying mechanisms of phagocytosis in vitro.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009677021374
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    Paper (German National Licenses)
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