ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01932.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01933.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01934.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractNicardipine has been shown to have an anti‐atherogenic effect in rabbits given a 2% cholesterol diet. Current evidence suggests that lipid peroxidation plays an important role in atherogenesis. This study examines the effect of nicardipine on lipid peroxidation in rabbits given a 2% cholesterol diet, 8 of these rabbits given nicardipine 0.5 mg/kg twice daily intramuscularly for ten weeks while the remaining untreated 6 were controls. After ten weeks, serum malondialdehyde in the control group was significantly higher compared to their baseline levels (P<0.05). However, there was no increase in serum malondialdehyde in the nicardipine group after 10 weeks. The area of Sudan IV positive intimal lesions (atherosclerotic plaques) were significantly decreased (P<0.01) in the treated group compared to the control group. The aortic tissue content of cholesterol and diene conjugates were also decreased in the nicardipine group (P<0.01). These findings suggest a possible link between nicardipine and lipid peroxidation in mediating its antiatherogenic effect

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01907.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractThe effects of induction of various forms of cytochromes P450 by chemicals like phenobarbital on the hepatic oxidative desulfuration and acute toxicity of the phosphorothioate insecticide parathion have been well‐characterized. However, the effects of these chemicals on the metabolism and acute toxicity of the active metabolite paraoxon are less understood. In the present study, daily pretreatment of mice with phenobarbital (intraperitoneally 75 mg/kg) for up to eight days resulted in a transient increase in hepatic microsomal A‐esterase activity, with a corresponding transient decrease in serum A‐esterase activity (A‐esterase was defined as hydrolysis of paraoxon which could be inhibited by EDTA). These alterations could be accounted for by a temporary decrease in the rate of secretion of A‐esterase from liver. However, the same pretreatment resulted in a sustained protective effect against the acute toxicity of paraoxon. These data suggest that alterations in A‐esterase activity as a result of phenobarbital pretreatment cannot account for the observed antagonism of the acute toxicity of paraoxon. Furthermore, these data demonstrate that the protective effect of phenobarbital pretreatment on phosphorothioate insecticides like parathion cannot be attributed exclusively to alterations in oxidative desulfuration of thes

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01908.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01936.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstractγ‐spectrometry and autoradiography were used to examine the axoplasmic flow of manganese in the olfactory nerves and to study the uptake of the metal in the brain after application of54Mn2+in the olfactory chambers of pikes. The results show that the54Mn2+is taken up in the olfactory receptor cells and is transported at a constant rate along the primary olfactory neurones into the brain. The maximal velocity for the transported54Mn2+was 2.90±0.21 mm/hr (mean±S.E.) at 10°, which was the temperature used in the experiments. The54Mn2+accumulated in the entire olfactory bulbs, although most marked in central and caudal parts. The metal was also seen to migrate into large areas of the telencephalon, apparently mainly via the secondary olfactory axons present in the medial olfactory tract. A transfer along fibres of the medial olfactory tract probably also explains the labelling which was seen in the diencephalon down to the hypothalamus. The results also showed that there is a pathway connecting the two olfactory bulbs of the pike and that this can carry the metal. Our data further showed a marked accumulation of54Mn2+in the meningeal epithelium and in the contents of the meningeal sacs surrounding the olfactory bulbs. It appears from our study that manganese has the ability to pass the synaptic junctions between the primary and the secondary olfactory neurones in the olfactory bulbs and to migrate along secondary olfactory pathways into the telencephalon and the diencephalon. Manganese is a neurotoxic metal which in man can induce an extrapyramidal motor system dysfunction associated with occupational inhalation of manganese‐containing dusts or fumes. We propose on basis of our results that the neurotoxicity of inhaled manganese may be related to an uptake of the metal into the brain via the olfactory neurones. The manganese can thereby circumvent the blood‐brain barrier and gain direct access to the central nervo

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01909.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01937.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01938.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

AbstractDiclofenac (0.5–2 mM) dose‐ and time‐dependently reduces the viability of isolated hepatocytes. This effect cannot be counteracted by the calcium channel blockers diltiazem (0.05–0.1 mM) and verapamil (0.05–0.5 mM), the calmodulin antagonist calmidazolium (0.01 mM) or Quin 2‐AM (0.1 mM), an intracellular calcium chelating agent. On the contrary, verapamil even accentuates the toxic effects of diclofenac. It is concluded from these results, that diclofenac causes cell damage by other mechanisms than calci

ISSN:0901-9928    

DOI:10.1111/j.1600-0773.1995.tb01910.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY