Comparative biochemistry and physiology. C, Comparative pharmacology and toxicology最新文献

1. In Sprague-Dawley (SD) rats treated for 7 days with malotilate (MAL:250 mg/kg, p.o.), cytochrome P-450 and b5 contents, aminopyrine N-demethylase and heme oxygenase activities were significantly increased. In Wistar rats, cytochrome b5 content and heme oxygenase and delta-aminolevulinic acid synthetase activities were found to be significantly increased. 2. Among the antipyrine metabolites excreted in urine during the 24 hr after antipyrine (100 mg/kg, i.p.) administration, norantipyrine increased significantly in Sprague-Dawley rats, while a significant increase of 4-hydroxyantipyrine was observed in Wistar rats. 3. The serum dimethadione/trimethadione ratio was only found to be significantly increased in Sprague-Dawley rats. 4. These results indicate that malotilate may have inducible effects on hepatic drug metabolizing enzymes, and that it affects the various cytochrome P-450 isozymes from different strains of rat in different ways.

1. The effects of some synthetic alpha 2-adrenoceptor agonists on the mechanical activity and on contractile responses to catecholamines were examined in smooth muscle strips isolated from rainbow trout stomach. 2. Contractile responses to noradrenaline and adrenaline in the rainbow trout stomach strips were due to alpha 2-adrenoceptor activation. 3. Clonidine, p-aminoclonidine, naphazoline and guanabenz caused no mechanical response but concentration-dependently inhibited the contractile responses to noradrenaline and adrenaline without affecting the responses to acetylcholine, carbachol, 5-hydroxytryptamine and methionine-enkephalin. The order of potency was naphazoline greater than p-aminoclonidine greater than clonidine greater than guanabenz. 4. It is suggested that in the smooth muscle preparation of the trout stomach, some synthetic compounds (clonidine, p-aminoclonidine, naphazoline and guanabenz), which act on mammalian preparations as alpha 2-adrenoceptor agonists, show an antinoradrenaline (-adrenaline) effect; those compounds can be classified as alpha 2-adrenoceptor antagonists.

1. A neurotoxic peptide was isolated from the venom of the scorpion Buthus martensi Karsch collected in Henan Province, China. 2. This toxin showed the highest neurotoxic potency to crickets amongst all components in the venom examined. 3. The amino acid composition of the toxin was similar to that of insect toxin 1 of Leiurus quinquestriatus quinquestriatus. 4. The partial primary sequence of the toxin at the N-terminal was very similar to that of an insect toxin of Androctonus australis Hector. 5. We conclude that the neurotoxin we isolated is indeed an insect toxin and thus named it as BmK IT.

1. Crithidia fasciculata was grown in a serum-free medium. 2. Twenty-six hours after addition of 2, 5, 20, 50, and 150 microM acivicin to logarithmically growing organisms, cell counts were decreased to 46, 23, 14, 9.1, and 8.6% of the control, respectively. 3. Guanosine plus cytidine (0.1 mM each) provided complete protection against growth inhibition by 5 microM acivicin. 4. Cells exposed to 10 microM acivicin showed a time-dependent, irreversible inactivation of L-glutamine-dependent carbamoyl-phosphate synthetase II activity; ammonia-dependent synthetase II activity was increased up to 34% of the control. 5. Glutamine (20 mM) protected the enzyme from inactivation in vivo. 6. These results indicate that acivicin acts as an affinity analog of L-glutamine in vivo as it does in vitro.

1. Recent concept of postsynaptic modulation is reviewed on the basis of literature data and the results of our investigation using conventional intracellular and voltage-clamp recording methods, in vitro. 2. Experimental evidence provided that the sensitivity of nicotinic ACh receptors endowed on the postsynaptic membrane of the bullfrog sympathetic ganglia and of the frog skeletal muscle end-plate is either facilitated or inhibited by other neurotransmitters or neurohormones. 3. We propose that one neurotransmitter not only initiates its own postsynaptic potential but also regulates the efficacy of synaptic transmission mediated by a distinct neurotransmitter, as an endogenous "antagonist" or "sensitizer".

1. Melanin-aggregation response of the medaka melanophores to a series of adrenergic drugs were examined. 2. Concentration-response curves for the drugs indicated that the melanin-aggregating effects of alpha 2 adrenergic agonists, naphazoline, tramazoline and clonidine, were more than 100-fold greater than that of alpha 1 agonists, phenylpropanolamine, phenylephrine, oxymetazoline and methoxamine. 3. The inhibitory effect of alpha 2 antagonist, yohimbine, on the cell responses to the agonists were also about 100-fold greater than that of alpha 1 antagonists, corynanthine and prazosin. 4. These results indicate that adrenergic receptors which mediate melanin-aggregation response of the cells are alpha 2 in nature.

The treatment of rats with propylthiouracil (PTU) resulted in an induction of not only cationic but also anionic glutathione (GSH) transferases. DE-52 column chromatography of the anionic GSH transferases divided into five main peaks (I-V). Peaks I-IV had a high activity toward 1-chloro-2,4-dinitrobenzene (CDNB). Peak V, which is a new form of the enzyme, showed high activity to ethacrynic acid. PTU induced peaks I and V, whereas phenobarbital increased the activity of only peak I.

1. Adenosine and its derivatives induced dispersion of leucosomes in leucophores of the medaka, Oryzias latipes. 2. Among the purines used, 5'-N-ethylcarboxiamideadenosine was the most effective and its potency was far greater than that of adenosine, N6-L-phenylisopropyladenosine and N6-cyclohexyladenosine. 3. Methylxanthines inhibited the purine action competitively, but beta adrenergic antagonists and dipyridamole did not. 4. Beta adrenergic agonists and forskolin synergistically augmented the purine action, while Li+ blocked it competitively. 5. The results suggest that medaka leucophores possess A2 adenosine receptors on the cell membranes, the stimulation of which induces leucosome-dispersion response by increasing the cellular level of cyclic AMP through activation of adenylate cyclase activity.

1. The purpose of the study was to investigate the effect of ethanol and acetaldehyde on the erythrocyte and leucocyte system of Wistar rats. 2. Administration of the ethanol or acetaldehyde caused a considerable drop in the number of erythrocytes, haemoglobin level and haematocrit value in rats. 3. The mean erythrocyte volume was smaller after only 0.5 hr of exposure to ethyl alcohol. 4. The solutions used caused changes in the leucocyte system expressed in distinct neutrophilic leucocytosis. 5. Changes in the leucogram were reflected in the increase in the leucocyte index. 6. The degree of intensity of changes in both the erythrocyte and leucocyte system point to the greater toxicity of ethyl alcohol intoxication than is the case of acetaldehyde in a toxically corresponding dose (i.e. 0.5 and 5 g/kg body wt respectively).