共查询到20条相似文献,搜索用时 15 毫秒
1.
Changes in rat brain monoamine turnover following chronic antidepressant administration 总被引:2,自引:0,他引:2
M F Sugrue 《Life sciences》1980,26(6):423-429
Changes in rat brain monoamine turnover were studied following the chronic administration of five agents which markedly differ in their patterns of monoamine uptake inhibition. Compounds (10 mg/kg, i.p.) were injected once daily for 14 days and experiments undertaken 24 h after the last injection. Chronic administration of desipramine or mianserin elevated brain MOPEG-SO4 content and the α-MT-induced reduction in brain NA levels was enhanced by chronic desipramine. either antidepressant altered turnover of brain DA or 5-HT. Steady state levels of brain 5-HIAA or striatal levels of DOPAC or HVA were also unchanged. Chronically administered Org 6582, a selective inhibitor of 5-HT uptake, decreased basal and attenuated the probenecid-induced increase iin brain 5-HIAA levels. Chronic Org 6582 had no effect on NA or DA turnover and on the levels of MOPEG-SO4, DOPAC or HVA. Neither maprotiline nor chlorimipramine altered turnover of NA, DA or 5-HT or levels of metabolites. Thus, in contrast to the acute situation, chronically administered desipramine increases rat brain NA turnover. Conversely, acute and chronic Org 6582 administration yield similar findings, viz. a decrease in turnover. These observations suggest that rat brain 5-HT systems are more resistant than NA systems to adaptive changes following a prolonged inhibition of monoamine uptake. 相似文献
2.
E A Stone 《Life sciences》1975,16(11):1725-1729
The present study examined the effect of footshock stress on the formation of the two major metabolites of rat brain norepinephrine (NE) - the sulfate conjugates of 3-methoxy-4-hydroxyphenylglycol (MOPEG-SO4) and 3,4-dihydroxyphenylglycol (DOPEG-SO4). Rats receiving intraventricular injections of either 3HNE or Na235SO4 prior to 0.5 hour of footshock showed significant and comparable increases in both sulfated glycols labeled with 3H or 35SO4. Elevations were greatest in the hypothalumus using Na235SO4. In pheniprazine pretreated rats footshock did not increase the production of MOPEG-35SO4 from intraventricular labeled sulfate given alone or in combination with various doses of exogenous MOPEG. The results indicate that neuronally released brain NE is metabolized to form both MOPEG-SO4 and DOPEG-SO4. The increase in these metabolites results from an increased glycol production and not from a stress-induced activation of brain sulfation mechanisms. 相似文献
3.
Eric A. Stone 《Life sciences》1976,19(10):1491-1498
The present study utilized intraventricular injection of Na235SO4 to detect drug induced changes in the formation of the two major metabolites of rat brain norepinephrine (NE) - the sulfate conjugates of 3-methoxy-4-hydroxyphenylglycol (MOPEG-SO4) and 3,4-dihyd (DOPEG-SO4). Assays involved the hypothalamus only. Rats pretreated with clonidine showed a reduced formation of both MOPEG-35SO4 and DOPEG-35SO4 after intraventricular Na235SO4 as well as reduced synthesis of 3H-NE from intraventricular 3H-tyrosine. Phenoxybenzamine (POB) produced increases in the synthesis of both 35S-labeled conjugates and 3H-NE. Neither drug altered the loss of exogenous 3H-MOPEG-SO4 but clonidine increased both the accumulation of labeled sulfate and the sulfation of exogenous MOPEG in pheniprazine treated rats. These results show that the rates of formation of the labeled glycol sulfates are sensitive indicators of changes in brain NE turnover but can also be influenced by factors involved in sulfation that are unrelated to NE turnover. Blockade of NE synthesis with alpha methyltyrosine did not affect resting or POB-elevated levels of the labeled conjugates until stores of NE were reduced by 40%. The latter findings suggest that central noradrenergic neurons can release and metabolize NE at a normal rate despite synthesis blockade so long as adequate stores of NE are available. 相似文献
4.
Regional Distribution and Production Rate of 3-Methoxy-4-Hydroxyphenylethyleneglycol Sulphate (MHPG-SO4 ) in Rat Brain 总被引:1,自引:1,他引:0
Yasuko Kohno Masatoshi Tanaka Ryoichi Nakagawa Nobuo Toshima Nobuyuki Nagasaki 《Journal of neurochemistry》1981,36(1):286-289
The levels of noradrenaline (NA) and 3-methoxy-4-hydroxyphen-ylethyleneglycol sulphate (MHPG-SO4) in 15 brain regions showed a parallel distribution in male Wistar rats. The differences in regional distribution of MHPG-SO4 were similar to those in the rate of NA turnover reported by other investigators. The accumulation rates of MHPG-SO4 during 45 and 90 min after probenecid injection significantly correlated to the steady state levels of MHPG-SO4 in nine regions studied. With the results, the regional levels of MHPG-SO, either in untreated or in probenecid-treated rats, are considered to be a useful index of NA turnover. 相似文献
5.
Immunological study of carbon tetrachloride-mediated induction of tyrosine aminotransferase in rat liver 总被引:1,自引:0,他引:1
Administration of CCl4 (1.0 ml/kg) to rats resulted in a rise of liver tyrosine aminotransferase (l-tyrosine:2-oxoglutarate aminotransferase, EC 2.6.1.5) activity to a maximum of about 3.6 times the normal level 6 hr later. An immunological titration study proved that the phenomenon was due to increased enzyme content. Using an isotopic-immunochemical procedure the half-life of liver tyrosine aminotransferase at 3.5 hr after CCl4 administration was shown to be 11.9 hr in contrast to 2.1 hr in the normal liver. Immunochemical analysis revealed that enzyme synthesis was decreased by CCl4. Thus, in the early stage of CCl4 poisoning, enzyme synthesis proceeded at a moderate rate while degradation was markedly impaired, resulting in the rise of tyrosine aminotransferase in the liver tissue.Several hours after administration of hydrocortisone to adrenalectomized rats, induced tyrosine aminotransferase reached its peak activity and then subsided to the basal level. At any time following hydrocortisone administration, administration of CCl4 consistently caused an elevation of the enzyme activity above the level in controls not treated with CCl4. Actinomycin D (5 mg/kg) also increased the enzyme at an early period of induction cycle but failed to do so at a later period.The CCl4-mediated “superinduction” of hormonally preinduced tyrosine aminotransferase, like the induction of this enzyme by CCl4 at a basal level, was found to be caused by the differential inhibitory effect of CCl4 on the synthesis and degradation of this enzyme. 相似文献
6.
H R Bürki 《Life sciences》1978,23(5):437-441
Rats were pretreated with haloperidol, clothiapine, loxapine, chlorpromazine, thioridazine, NT 104-252, clozapine or perlapine. The animals were decapitated at various times after drug administration, the striata removed and homogenized in tris buffer containing pargyline, ascorbic acid, EGTA and various salts. After centrifugation the homogenates were incubated with 3H-haloperidol, and total and unspecifically bound 3H-haloperidol were measured. Excellent correlations were found between inhibition of specific 3H-haloperidol binding and increases in the striatal concentration of DOPAC induced by the neuroleptics, confirming that DA-receptor blockade provokes an increase in DA-metabolism. No correlation, however, was found with neutoleptic-induced changes in the concentrations of MOPEG-SO4 in the brain stem or of 5-HIAA in the cortex, re-affirming that inhibition of specific 3H-haloperidol binding is due to drug effects on DA-receptors only. 相似文献
7.
The dipeptide aspartame (APM; aspartylphenylalanine methylester), an artificial sweetener, was studied for its ability to influence brain levels of the large neutral amino acids and the rates of hydroxylation of the aromatic amino acids. The administration by gavage of APM (200 mg/kg) caused large increments in blood and brain levels of phenylalanine and tyrosine by 60 minutes. Brain tryptophan level was occasionally reduced significantly, but the brain levels of the branched-chain amino acids were always unaffected. Smaller doses (50, 100 mg/kg) also raised blood and brain tyrosine and phenylalanine, but did not reduce brain tryptophan levels. At the highest dose (200 mg/kg), APM gavage caused an insignificant increase in dopa accumulation (after NSD-1015), and a modest reduction in 5-hydroxytryptophan accumulation. No changes in the brain levels of serotonin, 5-hydroxyindoleacetic acid, dopamine, dihydroxyphenylacetic acid, homovanillic acid, or norepinephrine were produced by APM administration (200 mg/kg). These results thus indicate that APM, even when administered in amounts that cause large increments in brain tyrosine and phenylalanine, produce minimal effects on the rates of formation of monoamine transmitters. 相似文献
8.
Brain concentrations of DOPEG-SO4 were measured fluorometrically 0, 0.5, 1, 2, 4 and 8 hr after i.p. injections of morphine sulfate (20 mg/kg), d-amphetamine sulfate (5 mg/kg), desmethylimipramine HCl (25 mg/kg), or reserpine (5 mg/kg) in order to observe the effects of these drugs on intraneuronal norepinephrine degradation. No change in brain levels of DOPEG-SO4 was found until 8 hr after morphine, at which time the metabolite was significantly (p<.01) decreased. d-Amphetamine and desmethylimipramine significantly (p<.01) decreased the metabolite at all observed timepoints after 0 hr. Brain DOPEG-SO4 after reserpine was significantly (p<.01) increased at 0.5 and 1 hr, and significantly (p<.01) decreased at 4 and 8 hr. DOPEG-SO4 remained unchanged 0–8 hr after saline injections. These results, together with previous measurements of brain 3-methoxy-4-hydroxyphenylethylene glycol sulfate (MOPEG-SO4), indicate that the mechanism of morphine action on noradrenergic neurons differs from those of the other drugs examined and that morphine may cause central norepinephrine release. 相似文献
9.
Selective increase of brain dopamine induced by gamma-hydroxybutyrate: study of the mechanism of action 总被引:2,自引:0,他引:2
Abstract— γ-Hydroxybutyrate (γ-OH) produces a selective accumulation of brain DA not only in normal animals but also in reserpinized animals. This is especially evident after the administration of DOPA; while in parallel experiments γ-OH does not influence significantly the amount of 5-HT present in brain after 5-HTP treatment. γ-OH does not raise DA in rats after inhibition of tyrosine hydroxylase. The accumulation of brain DA is not due to inhibition of MAO or COMT activity. 相似文献
10.
A. Tagliamonte P. Tagliamonte J. Forn J. Perez-Cruet G. Krishna G. L. Gessa 《Journal of neurochemistry》1971,18(7):1191-1196
Cyclic AMP and dibutyryl-cyclic AMP, a derivative of cyclic AMP resistant to phosphodiesterase inactivation, were injected into the lateral ventricles of rats. These nucleotides did not change the level of brain 5-HT but increased the brain level of its principal metabolite, 5-hydroxyindoleacetic acid. Cyclic AMP was less potent than dibutyryl-cyclic AMP. Butyrate and 5′-AMP were inactive. The effect of dibutyryl cyclic AMP on 5-HT metabolism was studied both in vivo and in vitro. The rate of synthesis of 5-HT was measured by the rate of accumulation of 5-hydroxyindoleacetic acid after the transport of this acid out of the brain was blocked with probenecid. The rate of synthesis of brain 5-HT increased from 0-38 μg/g/h in control rats to 0-65 μg/g/h after dibutyryl-cyclic AMP. In addition cyclic AMP and dibutyryl-cyclic AMP markedly increased brain tryptophan, while AMP was inactive. Since brain tryptophan hydroxylase has a Km for its substrate that is much higher than the concentrations of tryptophan normally present in the brain, it is likely that the increase in the rate of synthesis of brain 5-HT is secondary to the cyclic AMP induced increase in the levels of brain tryptophan. In vitro studies revealed that dibutyryl-cyclic AMP increased the uptake of radioactive labelled tryptophan into slices of rat brain stem and the formation of 5-HT and 5-hydroxyindoleacetic acid. 相似文献
11.
A Yuwiler 《Journal of neurochemistry》1973,20(4):1099-1109
Abstract— Intraperitoneal administration of both D- or L-tryptophan elevated the levels of serotonin and 5-hydroxyindoleacetic acid in the brains of hypophysectomized and intact rats. In intact rats, the increase in brain 5-hydroxyindoles was slower after D-tryptophan than after L-tryptophan. Similarly, brain tryptophan rose more slowly after administration of D-tryptophan. The uptake of L-tryptophan from blood into brain was at a rate about one-third that of 3H2O. D-tryptophan uptake was at 1/25 that of 3H2O. Brain and liver tryptophan aminotransferase activities were stereospecific for the L-isomer and no evidence could be found for a tryptophan racemase in brain. Evisceration prevented the increase in brain 5-hydroxyindoles following peripheral administration of D-tryptophan administration but not that after L-tryptophan. The serotonin ratios between the two brain regions examined remained constant following administration of either D- or L-tryptophan. On the basis of these results we concluded that the increase in brain 5-hydroxyindoles following administration of L-tryptophan was not dependent upon stress-induced changes in pituitary hormones and that the elevations after D-tryptophan were dependent upon its prior conversion to L-tryptophan via peripheral deamination and subsequent transamination. 相似文献
12.
Disposition of fucose in brain 总被引:6,自引:4,他引:2
Abstract— Labelled fucose administered to rats in vivo was rapidly incorporated into brain glycoproteins, but not into any other brain constituents, including glycolipids and acid mucopolysaccharides. Maximum incorporation of tritium-labelled fucose into brain glyco-proteins occurred 3–6 h after intraperitoneal injection in young or adult rats, and the half-time for the turnover of glycoprotein-fucose in young rats was approximately 2 weeks. Within 3 h after the administration of either [1-3H]fucose or fucose generally labelled with tritium, 75 per cent of the total acid-soluble radioactivity in plasma and brain was found to be volatile, and by 24 h after injection more than 90 per cent of the acid-soluble radioactivity was volatile. The tritium in labelled fiicose appears to undergo arapid exchange reaction with hydrogen atoms in body water, although the tritium in fucose glycosidically- linked to glycoproteins is biologically stable. The rapid disappearance of labelled free fucose from the plasma and tissues of the rat precludes the possibility of any significant degree of reutilization of labelled precursor, and provides support for other data indicating that the turnover of fucose in brain glycoproteins is relatively slow in comparison to that of hexosamine and sialic acid. Activities of α-L-fucosidase in rat brain, with pH optima at 40 and 6.0, had essentially the same Km (4 × 10?4 M and 3.2 × 10?4 M, respectively) with p-nitrophenyl-α-L-fucopyranoside as substrate. Activities of both were competitively inhibited by L-fucose. However, the Kt measured at pH 4 (1.9 × 10?2) was almost ten times greater than that measured at pH 6 (1.5 × 10?4). 相似文献
13.
Spinal cord section brings about early and late changes in rat liver tyrosine-alpha-ketoglutarate aminotransferase activity. Early effects (4 h after surgery): spinal cord section at C7 level causes an unreactiveness of rat liver tyrosine-alpha-ketoglutarate aminotransferase both to endogenously and exogenously elevated plasma glucocorticoid levels. Induction of tyrosine–alpha-ketoglutarate aminotransferase by hydrocortisone administration is almost completely inhibited. This unreactiveness of the rat liver enzyme to hydrocortisone is not due to delayed resorption of hydrocortisone by the peritoneum as tested with [3H]hydrocortisone, to changes in the secretion of hypophyseal hormones or to changes in the levels of glucose in blood or liver. L3 level section of the spinal cord or sham operation results in a stress-like enzyme pattern (an increase at 4 h with return to normal level at 24 h). The stress elevation of tyrosine–alpha-ketoglutarate aminotransferase at 4 h after the operation is absent in C7 level sectioned rats. This effect is not due to a decreased plasma corticosterone level since it is 4.1-fold higher in C7 level sectioned rats and 2.7-fold higher in sham-operated controls (as measured 2.5 h after the operation). Late effects (24 h after the surgery): C7 level section of the spinal cord brings about a nine-fold increase in a tyrosine–alpha-ketoglutarate aminotransferase activity in animals with intact adrenals and three-fold increase in adrenalectomized rats at 24 h after the operation. This increase is abolished almost completely by cycloheximide, irrespective of the time of administration. Experiments with actinomycin D, injected at different times after C7 level section have shown that there exists a period of higher sensitivity of the amino-transferase toward the antibiotic (lasting about 3 h), followed by a period of lower sensitivity (lasting 16 h or longer). These results can be explained by assuming the existence of two tyrosine-alpha-ketoglutarate aminotransferase mRNAs with different lifetime. A direct participation of the CNS in the changes in enzymic activity observed after section of the spinal cord above the segments innervating the liver is suggested. 相似文献
14.
Susana Cabrerizo José Pedro De La Cruz Juan Antonio López-Villodres Javier Muñoz-Marín Ana Guerrero José Julio Reyes María Teresa Labajos José Antonio González-Correa 《The Journal of nutritional biochemistry》2013,24(12):2152-2157
The aim of this study was to analyze the mechanism of the neuroprotective effect of hydroxytyrosol (HT) in an experimental model of hypoxia-reoxygenation in rat brain slices. After reoxygenation the increase in lactate dehydrogenase efflux was inhibited by HT in a concentration-dependent manner and dose-dependent inhibition after oral administration to rats for 7 days (1, 5 and 10 mg/kg per day). Maximum inhibition was 57.4% in vitro and 38.7% ex vivo. Hydroxytyrosol reduced oxidative stress parameters: it inhibited lipid peroxidation and increased enzymatic activities related with the glutathione system both in vitro and after oral administration to rats. The increase in prostaglandin E2 and interleukin 1β after reoxygenation were inhibited after incubation of brain slices with HT and after oral administration. The accumulation of nitric oxide in brain slices was reduced in a concentration-dependent manner. In conclusion, HT exerts a neuroprotective effect in a model of hypoxia-reoxygenation in rat brain slices, both in vitro and after 7 days of oral administration to rats. HT exerts an antioxidant activity and lowered some inflammatory markers in this model. 相似文献
15.
One of the many pharmacological targets of ethanol is the GABA inhibitory system, and chronic ethanol (CE) is known to alter
the polypeptide levels of the GABAA receptor subunits in rat brain regions. In the present study, we investigated the regulation of the tyrosine kinase phosphorylation
of the GABAA receptor α1-, β2- and γ2-subunits in the rat cerebellum, cerebral cortex and hippocampus following chronic administration of ethanol to the rats.
We observed either down-regulation or no change in the tyrosine kinase phosphorylation of the α1 subunit, whereas there was an up-regulation or no change in the case of β2- and γ2-subunits of the GABAA receptors depending on the brain region following chronic administration of ethanol to the rats. These changes reverted back
to the control level following 48 h of ethanol-withdrawal. These results suggest that tyrosine kinase phosphorylation of GABAA receptors may play a significant role in ethanol dependence. 相似文献
16.
R W Fuller H D Snoddy K W Perry B W Roush B B Molloy F P Bymaster D T Wong 《Life sciences》1976,18(9):925-933
Quipazine, 2-(1-piperazinyl)-quinoline, is a drug that has been reported to stimulate serotonin receptors in brain. We therefore studied the effect of quipazine on several parameters of serotonin metabolism in rat brain. Quipazine caused a slight, dose-related elevation of serotonin levels and decrease in 5-hydroxyindoleacetic acid levels for 2–4 hrs after it was administered. The decrease in 5-hydroxyindoleacetic acid levels was probably due primarily to a depression of 5-hydroxyindole synthesis, since quipazine also decreased the rate of 5-hydroxytryptophan accumulation after NSD 1015, the rate of serotonin decline after α-propyldopacetamide, and the rate of 5-hydroxyindoleacetic acid accumulation after probenecid. The elevation of serotonin was probably due to weak inhibition of monoamine oxidase. Quipazine reversibly inhibited the oxidation of serotonin by rat brain monoamine oxidase and protected against the irreversible inactivation of the enzyme . Quipazine also was a potent inhibitor of serotonin uptake into brain synaptosomes and attained concentrations in brain higher than the IC50. However, quipazine did not prevent the depletion of brain serotonin by p-chloroamphetamine . In addition to stimulating serotonin receptors in brain, quipazine may inhibit monoamine oxidase and serotonin reuptake . 相似文献
17.
Ogasawara Y Sakamoto T Ishii K Takahashi H Tanabe S 《Biological trace element research》2002,86(3):269-278
An experimental rat model of aluminum accumulation in the brain was developed to aid in determining neurotoxity of aluminum
(Al). Al was administered orally, intravenously, and intraperitoneally, in the absence or presence of citric acid or maltol.
Oral administration of Al hydroxide [Al (OH)3] or aluminum chloride (AlCl3) with citric acid for 7 wk was not found to increase brain Al levels. Similarly, a single intravenous injection of AlCl3 in the presence or absence of either citric acid or maltol did not alter brain Al levels after 48 h. Only daily intraperitoneal
injections of AlCl3 (8 mg Al/kg body weight) and an equimolar amount of maltol over a 14-d period enhanced accumulation of Al in rat brain. No
significant increases were observed for the experimental groups receiving intraperitoneal AlCl3 alone or with citric acid. This result suggests that the chemical form of Al strongly influences its bioavailability and
that intraperitoneal administration of the Al-maltol complex appears to be useful in creating subacute model of Al accumulation
in brain tissue. 相似文献
18.
S A Borisenko 《Biulleten' eksperimental'no? biologii i meditsiny》1989,107(3):312-314
Probenecid at a dose 100 and 200 mg/kg, i.v. has been found to decrease in a dose-dependent manner the level of radioactivity of cerebrospinal fluid (CSF) measured at 1, 15, 30 and 60 min. after the intravenous injection of 14C-tyrosine, 14C-tryptophan and 14C-DOPA. Ethanol at a dose 2 and 4 g/kg, i. p. has not changed the level of radioactivity of the CSF. It is suggested that mentioned in the literature an increased accumulation of the labeled tyrosine, tryptophan and DOPA in the brain structures after their intravenous injection is not related to the inhibitory effect of ethanol on the excretory function of the choroid plexus of the brain. On the other hand, it is concluded that probenecid is able to inhibit the excretion from the brain of some acid compounds including tyrosine, tryptophan and DOPA. 相似文献
19.
Owing to its lipophilic property, carbon tetrachloride (CCl4) is rapidly absorbed by both the liver and brain. We investigated the protective effects of crocin against brain damage caused by CCl4. Fifty rats were divided into five groups of ten: control, corn oil, crocin, CCl4 and CCl4 + crocin. CCl4 administration decreased glutathione (GSH) and total antioxidant status (TAS) levels, and catalase (CAT) activity, while significant increases were observed in malondialdehyde (MDA) and total oxidant status (TOS) levels and superoxide dismutase (SOD) activity. The cerebral cortex nuclear lamina developed a spongy appearance, neuronal degeneration was observed in the hippocampus, and heterochromatic and pyknotic neurons with increased cytoplasmic eosinophilia were observed in the hippocampus after CCl4 treatment. Because crocin exhibits strong antioxidant properties, crocin treatment increased GSH and TAS levels and CAT activities, and decreased MDA and TOS levels and SOD activity; significant improvements also were observed in histologic architecture. We found that crocin administration nearly eliminated CCl4 induced brain damage by preventing oxidative stress. 相似文献
20.
Cholinesterase activities in rat forebrain, erythrocytes, and plasma were assessed after a single oral administration of metrifonate
or dichlorvos. In 3-month-old rats, the dichlorvos (10 mg/kg p.o.)-induced inhibition of cholinesterase reached its peak in
brain after 15–45 min and after 10–30 min in erythrocytes and plasma. Cholinesterase activity recovered rapidly after the
peak of inhibition, but did not reach control values in brain and erythrocytes within 24 h after drug administration. The
recovery of plasma cholinesterase activity, in contrast, was already complete 12 h after dichlorvos treatment. Metrifonate
(100 mg/kg p.o.) had qualitatively similar inhibition kinetics as dichlorvos, albeit with a slightly delayed onset. Peak values
were attained 45–60 min (brain) and 20–45 min (blood), after drug administration. Apparently complete recovery of cholinesterase
activity was noted in both tissues 24 h after treatment. The dose-dependence of drug-induced inhibition of cholinesterase
in rat blood and brain was determined at the time of maximal inhibition, i.e., 30 min after dichlorvos treatment and 45 min
after metrifonate treatment. The oral ED50 values obtained for dichlorvos were 8 mg/kg for brain and 6 mg/kg for both erythrocyte and plasma cholinesterase. The corresponding
oral ED50 values for metrifonate were 10 to 15 times higher, i.e., 90 mg/kg in brain and 80 mg/kg in erythrocytes and plasma. In rats
deprived of food for 18 h before drug treatment, the corresponding ED50 values for metrifonate were 60 and 45 mg/kg, respectively, indicating an about two-fold higher sensitivity of fasted rats
to metrifonate-induced cholinesterase inhibition compared to non-fasted rats. Compared to 3-month-old rats, 19-month-old rats
showed a higher sensitivity towards metrifonate and dichlorvos. At the time of maximal inhibition, there was a strong correlation
between the degree of cholinesterase inhibition in brain and blood. These results demonstrate that single oral administration
of metrifonate and dichlorvos induces an inhibition of blood and brain cholinesterase in the conscious rat in a dose-dependent
and apparently fully reversible manner. While the efficiency of a given dose of inhibitor may vary with the satiety status
or age of the animal, the extent of brain ChE inhibition can be estimated from the level of blood ChE activity. 相似文献