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1.
The tissue distribution and excretion of [14CH3S]methamidophos was followed in female Sprague-Dawley rats after intravenous injection at a toxic, but nonlethal, dose (8 mg/kg). Radiolabel was rapidly distributed to all tissues at approximately equal concentrations. Peak tissue levels were achieved within 1–10 min except in the central and peripheral nervous system where peak levels (40 nmol/g) were found between 20 and 60 min, corresponding to peak signs of toxicity. Within 24 hr of dosing, 47% of the radioactivity was recovered in the urine and 34% as 14CO2 with <5% in the feces over 7 days. Cholinesterase (ChE) inhibition was measured in erythrocytes, plasma, and various regions of the central nervous system (CNS) at selected times after administration of methamidophos at 8 mg/kg. The degree of acetylcholinesterase (AChE) inhibition in the three CNS regions was similar, reaching a minimum of 15–20% of control values at 30–60 min, when toxicity was most severe. The degree of erythrocyte AChE inhibition was less than that of the CNS although the time course was similar. Plasma ChE inhibition was more rapid than that of the CNS or erythrocytes and reactivation was slower. When similar concentrations of methamidophos to those found in vivo were incubated with CNS homogenates, plasma, or erythrocytes in vitro (5 × 10?5M) a similar degree of inhibition occurred over the same time course. It is, therefore, concluded that the cholinergic toxicity produced by methamidophos is a result of the in vivo stability of this compound combined with its entry into the nervous system in sufficiently high concentrations to inhibit AChE.  相似文献   

2.
At 37°C and pH 7.4–8.0, five higher O-alkyl analogs of methamidophos and four O-alkyl O-2,5-dichlorophenyl phosphoramidates all were more potent progressive inhibitors of hen brain AChE and neuropathy target esterase (NTE) than was methamidophos itself. For AChE, ka increased from 7.2 × 102 to 1.0 × 105 M−1 min−1 between methyl and n-hexyl S-methyl esters and from 9.3 × 103 to 8.9 × 105 M−1 min−1 between ethyl and n-hexyl dichlorophenyl analogs. For NTE, the ranges were from 16 to 7.9 × 104 for S-methyl esters, and were 9.7 × 104 to 7.8 × 106 M−1 min−1 for dichlorophenyl. S-methyl esters were more active against AChE than against NTE and all the dichlorophenyl esters were more active against NTE than against AChE. Spontaneous reactivation of 75–100% activity without aging of AChE was found after 19 hr incubation at 37°C after inhibition by all nine straight-chain alkyl analogs. After inhibition by O-isopropyl S-methyl phosphorothioamidate, some spontaneous reactivation with complete aging of all remaining inhibited AChE occurred during 19 hr. No spontaneous reactivation or aging of inhibited NTE was detected. It was concluded that the molecular structures of the inhibited enzymes obtained from equivalent compounds in the two series of inhibitors were identical and that the leaving groups were, therefore, S-methyl and O-2,5-dichlorophenyl, respectively. Although hen brain NTE inhibited by methamidophos in vitro did not age, cases of delayed neuropathy in man have been reported and, presumably, require aging as well as inhibition of NTE. Possible explanations of this apparent discrepancy include (i) the fact that methamidophos consists of two chiral forms and that the form seen to be active in vitro may be disposed of preferentially in vivo, (ii) the possibility of activation in vivo to a different inhibitor, (iii) differences between conformation and ease of aging of inhibited NTE in vitro and in vivo, and (iv) species differences.  相似文献   

3.
The toxicity and LD50 of O,S,S-trimethyl phosphorodithioate were reexamined in the rat. Animals treated orally (single dose) with this compound exhibited early cholinergic signs followed at approximately 5 hr by delayed toxic signs, with an LD50 of 43 mg/kg. Contamination of O,S,S-trimethyl phosphorodithioate by as much as 5% (w/w) O,O,O-trimethyl phosphorothioate provided only limited antagonism to the dithioate's toxicity. In contrast, the addition of 5% O,O,S-trimethyl phosphorodithioate to O,O,S-trimethyl phosphorothioate gave protection against the toxic effects of the latter compound up to 80 mg/kg of toxicant. Pretreatment of rats with as little as 5% O,O,O-trimethyl phosphorothioate, 24 hr prior to treatment with 200 mg/kg O,O,S-trimethyl phosphorothioate, gave complete protection against the toxic effects of this compound. Conversely, administration of 10% (w/w) O,O,O-trimethyl phosphorothioate 4 or 24 hr after treatment with 60 or 80 mg/kg of O,O,S-trimethyl phosphorothioate provided only partial protection at 4 hr and no protection from the effects of the toxicant at 24 hr. The ability of O,O,O-trimethyl phosphorothioate to antagonize the toxicity of this compound depended markedly on the route of administration (oral, intravenous, or intraperitoneal). At 4 hr past treatment with toxicant, only oral administration of the antagonist provided full protection. Intraperitoneal and intravenous administration of antagonist 4 hr after treatment with toxicant were partially effective and completely ineffective, respectively, in halting the toxic effects of this compound.  相似文献   

4.
Oral administration of O,O,S-trimethyl phosphorothioate (OOS), an impurity in several technical organophosphorus insecticides, causes delayed toxicity in rats with death occurring up to 28 days after the treatment. The oral LD50 was determined to be 60 mg/kg. The effect of a single nonlethal dose of OOS (20 mg/kg) on in vivo protein synthesis in different organs was determined by measurement of the incorporation of [14C]leucine at 6 hr to 28 days after treatment. As early as 6 hr after OOS treatment the incorporation of [14C]leucine into the liver, lung, thymus, kidney, and spleen was elevated and remained elevated for up to 7 days. With the exception of the lung, organ weights were significantly decreased during the same time period. On Day 28 after treatment, the amount of [14C]leucine incorporation had decreased to the control level in all of the organs studied. Treatment with OOS at 20 mg/kg caused a significant increase in hematocrit on Days 3,5, and 7, and as early as 6 hr after treatment at 60 mg/kg. The clinical biochemistry of plasma indicated that there was no significant change from control values in the glutamic pyruvic transaminase, glutamic oxalic transaminase, lactate dehydrogenase, or alkaline phosphatase activities with the 20 mg/kg dose. The analysis of the intermediary metabolites indicated that the redox state of cytosol was more reduced on Day 5, whereas that of mitochondria was not affected by OOS. Data obtained at selected times after oral administration of a 60 mg/kg dose of OOS and that obtained from animals starved for 3 days are also discussed.  相似文献   

5.
A study of the toxico‐kinetics, recovery percentage from different substrates, cytotoxicity and role of cytochrome P450 and b5 of liver microsome in the metabolism of deltamethrin were carried out in female black Bengal goat. The ALD50 value of deltamethrin in goat by intravenous route lies between 0.2 and 0.6 mg kg?1. Intravenous disposition kinetics using a dose of 0.2 mg kg?1 showed that the maximum blood concentration of deltamethrin was recorded at 0.5 min, followed by rapid decline, and a minimum concentration was detected at 6 min after administration. The following values were obtained : Vdarea 0.148 (± 0.02) litre kg?1; t1/2 (α) 0.22 (± 0.02) min; t1/2 (β) 2.17 (± 0.37) min; Kel 1.05 (± 0.24) min?1; AUC 4.30(± 0.45) µg min ml?1; ClB 0.05 (± 0.006) litre kg?1 min?1; T～B 1.93 (± 0.58); fc 0.40(± 0.05). After 10 min, liver retained the maximum residue, and heart, adrenal gland, kidney, spleen, fat and brain also held the insecticide; liver, fat, heart and spleen retained residue after 30 min, and bone, liver and fat retained residue after 60 min of intravenous administration. Oral absorption of deltamethrin was poor and inconsistent, and approximately 65% of administered dose was recovered from faeces and gastrointestinal contents. The excretion of deltamethrin through urine was meagre, and only 0.01 and 0.013% of the administered dose was recovered after 3 and 5 days of oral administration respectively. All the tissues retained the residue after 3 days; while fat, rumen, reticulum, omasum, abomasum, large and small intestine and bone retained the residue after 5 days of oral administration; and the percentage recoveries were 1.73 and 0.027 respectively. Deltamethrin reduced the level of cytochrome P450 content of liver microsomal pellet of goat after 5 days of oral administration. Histopathological examination of liver, kidney, heart, spleen brain and lung sections of treated goats did not reveal any pathological changes. © 2001 Society of Chemical Industry  相似文献   

6.
The oral toxicity of 5-benzyl-3-furylmethyl-(1R, cis)-chrysanthemate (cismethrin) to female rats decreased as their environmental temperature was raised. Acute oral LD50 values increased from 157 mg/kg at 4°C to 197 mg/kg at 20°C and to > 1000 mg/kg at 30°C. Cismethrin was much more toxic given intravenously when the LD50 was 4.5 mg/kg. This value did not change at different environmental temperatures. Irrespective of the environmental temperature, or route of adminstration, following the respective LD50's cismethrin caused tremors in rats when brain levels of 0.5–1.0 μg/g were reached and, at death, brain concentrations were 3.9–5.1 μg/g. These results suggested that the accumulation of cismethrin by the brain could be used as a model for the nervous system as a whole. The isomeric 5-benzyl-3-furylmethyl-(1R, trans)-chrysanthemate (bioresmethrin) was about 50 times less toxic to rats than cismethrin. After an intravenous LD50, tremors started when brain concentrations were 4–5 μg/g. At death, brain levels were 25–35 μg/g. Plasma esterases were about equally active in hydrolysing cismethrin and bioresmethrin, whereas liver microsomal esterases hydrolyzed bioresmethrin over 10 times more rapidly than cismethrin. It is suggested that the lower toxicity of bioresmethrin is not only due to its faster metabolism but to an intrinsically lower toxicity at the critical site of action in the nervous system.  相似文献   

7.
As preliminary probes to determine the mode of delayed toxic action of O,O,S-trimethyl phosphorothioate (I) in the rat, the effect of I on rat tissue and organs, and on blood, urine, and pharmacokinetic parameters was investigated. Following oral administration, 30 to 200 mg/kg I caused liver necrosis as a major pathological effect. Morphological changes were also observed in the heart, adrenal, tissues of the small intestine, and kidney. Most animals treated with I developed bronchopneumonia after 3 days. Blood samples taken from rats poisoned with 60 mg/kg I showed severe hemoconcentration; however, serum Na+, Cl?, albumin, and total carbonate/bicarbonate varied only slightly. Na+ and Cl? concentrations in the urine showed a steady decline with time following poisoning but K+ levels remained relatively constant. Pharmacokinetic studies showed that 14C levels in the blood following intraperitoneal or intravenous administration of 60 mg/kg [CH3O14C]I were not affected when the animals were cotreated with 5% of the antagonist O,O,O-trimethyl phosphorothioate. However, lower levels of 14C were found in antagonized animals following oral administration.  相似文献   

8.
Some inhibition kinetic properties and in vivo inhibition of the plasma juvenile hormone esterase from the cabbage looper (Trichoplusia ni Hübner) by one phosphoramidothioate and two trifluoromethylketones were examined. O-ethyl,S-phenyl phosphoramidothioate was shown to react irreversibly with the enzyme in a time-dependent manner, and the inhibition reaction can be factored into a reversible step with a dissociation constant, Kd, of 4.55 × 10?5M followed by a phosphorylation step with a rate constant, k2, of 1.98 min?1. The phosphorylated enzyme did not show spontaneous recovery after 48 hr of dialysis. On the other hand, the two trifluoromethylketones were shown to act as reversible inhibitors, as their inhibited enzyme was regenerated completely after dialysis. However, 1,1,1,-trifluoro-3-thiooctylpropan-2-one, in contrast to 1,1,1-trifluorotetradecan-2-one, showed progressive time-dependent inhibition, and its reaction with the enzyme followed characteristic bimolecular second-order kinetics with a rate constant, ki, of 3.37 × 107M?1 min?1. The in vivo inhibition data of topically treated larvae at equimolar amounts of the tested compounds indicated rapid penetration, and the stability of the inhibition was higher for the phosphoramidothioate than for the trifluoromethylketones. The relationship of the mechanism of inhibition and the in vivo inhibition of these compounds to the understanding of the interactions between juvenile hormone and juvenile hormone esterase is discussed.  相似文献   

9.
The ameliorative effect of daily administrated dose of green tea extract (60 mg polyphenols/animal/day) was investigated on albino rats Rattus norvegicus (150-180 gm) intoxicated with 1/30 and 1/60 LD50 fenitrothion organophosphate insecticide for 28 days. Blood samples were taken at 14 and 28 days for further biochemical parameters. Histopathological studies were carried out in the liver and kidney at the end of the experiment. Significant inhibition in plasma cholinesterase (ChE), a biomarker of Ops, was recorded. Damage in the liver and kidney tissues was observed and confirmed with elevation of plasma alanine aminotransferase (ALT), aspartate aminotaransferase (AST), albumin, urea and creatinine, as well as an elevation in the oxidative stress (OS) marker malondialdehyde (MDA). Decrease in total glutathione (GSH) content in erythrocytes and fluctuation in glutathione S-transferase (GST) activity in plasma was also observed. Green tea supplementation (60 mg/animal/day) partially counteracts the toxic effect of fenitrothion on oxidative stress parameters and repairs tissue damage in the liver and kidney, especially when supplemented to 1/60 LD50 intoxicated animals depending on the duration. It seems that enzyme and metabolite markers of these organs need more time to be restored to the control level.  相似文献   

10.
The effects of pyrethroids on the on-going electrical activity of the axons of neurosecretory cells from the brain of fifth instar Rhodnius prolixus have been studied using extracellular electrodes. Low concentrations of the pyrethroids decamethrin, bioresmethrin, permethrin, and bioallethrin all produce dramatic increases in the overall frequency and dramatic changes in the pattern of electrical activity when applied directly to the exposed brain and corpora cardiaca in an otherwise intact insect. This change in activity was brought about by a recruitment in active units and the production of phasic acivity. A doubling of frequency over that of controls was brought about by low doses of the pyrethroids, namely decamethrin, 1 × 10?10M; bioresmethrin, 2 × 10?10M; permethrin, 1 × 10?9M; and bioallethrin, 2 × 10?7M. Similar hyperactivity of this system occurred during intoxication of intact insects following topical application of LD95 bioresmethrin. The enhanced sensitivity shown by neurosecretory cells over that of other cell types is discussed, as is the possibility that the increases in electrical activity of neurosecretory axons may result in massive neurohormonal release and thereby contribute to the eventual poisoning of the insect.  相似文献   

11.
The reactivation of the rat brain muscarinic acetylcholine receptor (mACh-R) binding with dimercaptosuccinic acid (DMSA) after in vitro and in vivo inhibition by mercuric chloride (HgCl2) and methylmercuric chloride (MeHg) was investigated. Receptor binding was estimated by the potent and specific antagonist l-[3H]quinuclidinyl benzilate ([3H]QNB). Rat brain synaptosomal membranes were exposed to HgCl2 and MeHg. At 1 × 10?4M. HgCl2 caused complete inhibition of the [3H]QNB binding. The inhibition of [3H]QNB binding by HgCl2 was still higher than 50% at 1 × 10?8M. MeHg caused less inhibition of [3H]QNB binding than HgCl2. The inhibited receptors showed a significant degree of reactivation when treated with DMSA. The recovery was almost complete after MeHg inhibition or with the lower HgCl2 concentrations. Generally, the reactivation was dependent on the concentration of DMSA. When rats injected with either early or delayed doses of DMSA following administration with five consecutive daily doses (8 mg/kg body wt, Gavage method) of MeHg or HgCl2, the inhibition of [3H]QNB binding was less than untreated ones. The early treatment with DMSA decreased the inhibition of [3H]QNB binding due to MeHg or HgCl2 intoxication. However, DMSA was more effective in reducing HgCl2 inhibition than MeHg either in vitro or in vivo treatment. The ability of DMSA to reactivate the mACh-R after inhibition with the mercurials emphasizes the involvement of essential sulfhydryl groups in [3H]QNB binding sites, and also shows that these sulfhydryl groups are the primary target for the MeHg and HgCl2 inhibition of the rat brain muscarinic receptors.  相似文献   

12.
The inhibition of eel acetylcholinesterase by the 4-nitrophenyl esters of 2-furyl(methyl)-, methyl(2-thienyl)-, di-2-furyl-, and di-2-thienylphosphinic acid (I, II, III, and IV, respectively) was investigated at pH 6.90 in 0.067 M phosphate buffer (25.0°C) using stopped-flow instrumentation and automated data processing. Our evaluation of the dissociation constant, Kd, the unimolecular bonding rate constant, k2, and the bimolecular reaction constant, ki, are the first reported values for these constants for alkyl/heteroaryl and diheteroaryl esters of phosphinic acids. The largest ki value (19,330 M?1 sec?1) was observed for the reaction of I with the enzyme. The order for the remaining three is II > IV > III. There is no direct relationship between the hydrolysis rates of the esters and their anticholinesterase activities on eel acetylcholinesterase. Likewise, there is no direct relationship between their anticholinesterase activities and the LD50 values in rats.  相似文献   

13.
Homogenates of three strains of Myzus persicae, A, R, and E, with an LD50 for topically applied parathion of 9, 93, and 263 ng per aphid, showed an in vitro hydrolytic degradation of paraoxon of 2.3, 4.7, and 8.6 pmol/mg aphid/h, respectively. These values represent Vmax; Km was <10?7M. The three strains showed a malaoxon degradation of 2.4, 11.9, and 18.8 pmol/mg/h at 10?6M substrate concentration. Vmax for R and E was 21 and 27 pmol, respectively and Km 7 and 4 × 10?7M. Activity in strain A was too low to estimate these entities. The breakdown product of paraoxon was mainly diethyl phosphoric acid, that of malaoxon mainly dimethyl phosphoric acid. No hydrolysis of the carboxylester groups of malaoxon was found. Hydrolysis of paraoxon and malaoxon was inhibited by isopropyl and n-propyl paraoxon and by the salioxon-analog K2. The two latter compounds were shown to act as synergists with parathion when added in amounts that caused little mortality when given alone. The hydrolytic enzyme is soluble and retains its activity during incubations of several hours. It is likely that it is responsible for at least part of the resistance. Resistance was maintained without selection over a period of three years. There was no correlation between degree of resistance and carboxylesterase activity of the strains.  相似文献   

14.
The toxicity (72 hr) of acephate and methamidophos to fourth-instar larvae of the tobacco budworm, Heliothis virescens (F.), was nearly equivalent. In contrast, toxicity (72 hr) of methamidophos to adult boll weevils, Anthonomus grandis grandis (Boheman), was substantially greater than that of acephate. The internal accumulation of acephate was greater for A. grandis grandis than for H. virescens at 24 and 48 hr post-treatment, as was excretion. Acephate was metabolized to methamidophos both in vivo and in vitro by H. virescens but not by A. grandis grandis. In vitro acetylcholinesterase inhibition by methamidophos was greater than that of acephate, but less than that of paraoxon for H. virescens, A. grandis grandis, and the electric eel. Treatment of H. virescens larvae with acephate resulted in increased in vivo acetylcholinesterase inhibition between 24 and 72 hr post-treatment, which was associated with a large increase in mortality. H. virescens treated with methamidophos showed greater mortality and greater acetylcholinesterase inhibition at earlier time periods than those treated with acephate. However, by 72 hr post-treatment, in vivo acetylcholinesterase inhibition by LD50 doses of acephate and methamidophos were approximately equivalent. These results indicate that, for H. virescens, toxicity of acephate is directly related to its metabolism to methamidophos and subsequent acetylcholinesterase inhibition. Likewise, the differential toxicity of acephate and methamidophos to A. grandis grandis adults appears to be due to their inability to metabolize acephate to methamidophos.  相似文献   

15.
The in vivo metabolism of [14CH3S]- and [14CH3O]O,O,S-trimethyl phosphorothioate (OOS) was followed in rats after oral administration of threshold or LD50 toxic doses of 20 or 60 mg/kg. Similar metabolic studies were conducted with coadministration of 1% O,O,O-trimethyl phosphorothionate (OOO), which prevented all signs of delayed toxicity, including weight loss. When administered alone, OOS was metabolized mainly (50–60%) via removal of the CH3S moiety, which was largely converted to expired CO2. Approximately 20% of the compound was O-demethylated, presumably by conjugation with glutathione, and then further metabolized to CO2. Major urinary products were identified as O,O-dimethyl phosphoric acid (50–60%) and O,S-dimethyl phosphorothioic acid (～20%). Coadministration of OOO caused a slight decrease (～5%) in the cleavage of the CH3S moiety, indicated by a reduction in 14CO2 from [14CH3S]OOS and a quantitatively similar increase in the formation of O,S-dimethyl phosphoric acid. Limited pharmacokinetic studies indicated that OOS was rapidly absorbed and distributed throughout the body. Coadministration of 1% OOO caused a slight increase in the blood half-life of parent OOS when administered at 60 mg/kg. It was concluded that a small proportion of the cleavage of the CH3S moiety from OOS is involved in the intoxication process, and that this intoxication reaction is specifically inhibited by OOO.  相似文献   

16.
Development and phenobarbital (PB) induction of microsomal cytochrome P-450, cytochrome P-450 reductase, two epoxidation, and two O-demethylation activities were examined in chronologically timed populations of insecticide-susceptible (NAIDM) and -resistant (Rutgers) house flies. Measurements of these enzymes started with the pharate adult stage and ended 5 days following eclosion. Untreated insects of both strains had comparable reductase levels, whereas cytochrome P-450 and associated monooxygenase activities were 1.5-fold or more higher in Rutgers. Maximum induction, as well as toxicity, occurred at a lower PB concentration in NAIDM than Rutgers. The drug caused consistently higher increases in enzymes and activities within 12 hr of starting treatment in both strains. When PB was withdrawn from treated flies (both strains) 48 hr after treatment began, specific activities (product min?1 mg protein?1) in all enzymes returned to control values in 24 hr while metabolic capacity (product min?1 insect?1) achieved control values within 48 hr. The changes in turnover numbers (pmol product min?1 pmol P-450?1), in conjunction with the differences in the monooxygenation of the four substrates, suggest that PB treatment induced both a quantitative and qualitative change in NAIDM monooxygenation but only a quantitative change in Rutgers monooxygenation.  相似文献   

17.
The tissue distribution and excretion of 14C-labeled propham and chlorpropham were investigated in the adult female rat after a single oral dosage. The average 3-day urinary excretions of radioactivity were 55.9%, 82.6%, 79.5%, and 85.4% of an oral dose of chain [14C] chlorpropham, ring [14C] chlorpropham, chain [14C] propham, and ring [14C] propham, respectively. With chain [14C] chlorpropham 35.4 ± 7.5% of the administered radioactivity appeared in the respired air, whereas only 5.0 ± 0.8% was found in CO2 from chain [14C] propham. There was no significant difference in the rate of excretion or the route of elimination among rats receiving different oral dosages, ranging from less than 4 mg/kg to 200 mg/kg. The radioactivity was distributed in all tissues with highest concentration found in the kidney. The average biological half-life of 14C from chlorpropham and propham in most organs was short, ranging between 3 and 8 hr; however, in brain, fat, and muscle, the half-life was about twice the value for other organs.Both compounds were metabolized by hydrolytic and oxidative mechanisms and the resulting metabolites were excreted either as free forms or as conjugates.Subcellular distribution of 14C in the rat liver and kidney after an oral administration of chlorpropham and propham was investigated. The percentage distribution of 14C in the particulate and soluble fractions was dependent on the elapsed time after dosing.  相似文献   

18.
The toxicities, to a laboratory susceptible strain and to a resistant strain of Oryzaephilus surinamensis (L.), of water-dispersible powder formulations of pirimiphos-methyl, fenitrothion or chlorpyrifos-methyl under constant conditions of 25°C and 70% r. h. were compared to the toxicities when the insects were exposed to a diurnal cycle of 12.5–20–12.5°C and 70–50–70% r. h. to simulate grain store conditions in the UK during spring and autumn. All the insecticides were more effective at 25°C and 70% r. h. The LD50 values for the susceptible strain were low, being 4.4 and 1.4 mg m?2 at 12.5-20°C and 25°C, respectively, for chlorpyrifos-methyl, 18.3 and 4.1 mg m?2, respectively, for pirimiphos-methyl, and 4.0 and < 1.O mg m?2, respectively, for fenitrothion. The LD50 values obtained from the two sets of environmental conditions for a resistant strain (484) differed by factors of 1.8 for chlorpyrifos-methyl, 4.8 for pirimiphos-methyl, and 7.3 for fenitrothion. Toxicity studies were also made with chlorpyrifos-methyl under various constant conditions of temperature and humidity from 5–30°C (5°C intervals) and 30, 50, 70 and 90% r. h., and also at O°C and 60% r. h. Chlorpyrifos-methyl was very effective and there was little or no cross resistance to chlorpyrifos-methyl in the resistant strain. From 15 to 30°C, mortality was high, and differences in mortality at the LD50 level for the various humidities were slight, but there was a decrease in mortality with decreasing humidity at any one temperature, in particular, at 5°C, 50 and 70% r. h., and 10°C and 50% r. h. Chlorpyrifosmethyl was more toxic to both strains at the highest humidity (90%) throughout the whole temperature range. The LD50 values for each strain decreased at each temperature as the water vapour concentration was increased. At O°C and 60% r. h., all the insects from both strains died but the cause of death was not clear.  相似文献   

19.
The present study was undertaken to investigate the potential of monocrotophos (MCP), a widely used organophosphorus insecticide, to induce hyperglycemia and its interactive ability to accentuate the early diabetic outcomes and associated complications in experimentally rendered diabetic rats. Rats were rendered diabetic with an acute dose (60 mg/kg b.w, i.p) of streptozotocin. MCP was orally administered at a sublethal dose (1/20 LD50, 0.9 mg /kg b.w./d, 5 days) to both normal and diabetic rats. While MCP per se moderately increased (by 25%) the blood glucose levels in normal rats, it significantly aggravated the hyperglycemic outcome in diabetic rats (56% above diabetic rats). Further, experimentally-induced diabetes was associated with only a marginal increase in total and HDL-cholesterol levels, while serum triglyceride levels were significantly enhanced. Although MCP per se did not affect these parameters, it caused a marked increase in triglyceride levels in serum of diabetic rats (54% above diabetic control). Furthermore, MCP-induced higher activity levels of serum transaminases viz., ALT and AST (51% and 71% higher as compared to diabetic control) suggestive of enhanced hepatic damage. Collectively, our findings provide evidence that MCP on repeated exposure has the propensity to augment the secondary complications associated with diabetes in a rat model.  相似文献   

20.
Following intraperitoneal administration to male mice of trichlorphone, 4 mg/animal = 160 mg/kg and butonate, 5 and 10 mg/animal = 200 and 400 mg/kg, labeled by 14C in the OCH3-groups, nucleic acids taken from different organs and urine were analyzed for [7-14C]methylguanine. The limit of detection was 2 × 10?8, calculated as 14C relative to the total dose. The maximum of 14C in 7-methylguanine was 2 × 10?7 in lung, kidney, and testicles and 3 × 10?6 in liver. The excretion rate of 7-MeG from nucleic acids is very rapid, a halflife of 2.0 hr was measured in liver from butonate and of < 24 hr was calculated in the whole body from trichlorphone, contrary to the excretion rate of 3.0–3.5 days following administration of strongly genotoxic agents. The relative amounts of [7-14C]methylguanine excreted in the urine were determined and compared with data for dichlorvos, dimethyl sulfate, and methyl methanesulfonate from the literature. Following intraperiotoneal administration, the methylating capability towards N-7 of guanine in nucleic acids is given by the ratio of about 100:10:25 for dichlorvos, butonate, and trichlorphone, respectively.  相似文献   

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