Intestinal metabolism and absorption of carbaryl studied with a portal fistula

These data were obtained by use of a total and continuous portal vein fistula which virtually eliminated vascular redistribution of compounds absorbed from the gastrointestinal tract to nondigestive tissues (i.e., liver). The method allows direct measurement of the compounds absorbed, which is especially important in metabolism studies of ingested toxic compounds. These studies demonstrated that in vivo metabolism did occur within the intestine during the process of absorption of the pesticide carbaryl (naphthyl N-methylcarbamate) and naphthol, the hydrolysis product of the pesticide. Portal absorption of naphthol from a liquid diet (46 ± 4% of dose/120 min) was slower than from Ringer medium (75 ± 1%/120 min); portal absorption accounted for 82 ± 8 and 83 ± 4%, respectively, of the ¹⁴C absorbed from the intestine. The proportion of hydrophilic ¹⁴C-metabolites (water soluble) in portal blood varied from 6 to 89% and was a function of the substrate, dose vehicle (liquid diet vs Ringer), and time of portal fluid collection. Metabolism in the small intestine before absorption was confirmed for both substrates. The principal lipophilic constituent in portal fluid was the unmetabolized substrate for both carbaryl and naphthol; the principal ampholyte metabolite was naphthyl glucuronide. Although these in vivo data are qualitatively similar to evidence from previous in vitro studies, this in vivo evidence demonstrated that the extent of metabolism (and possibly detoxication) was considerably less than would be predicted from in vitro studies and indicates that the hazard of ingestion of carbaryl and other lipophilic toxic agents may be greater than realized.     

Alternate pathways of metribuzin metabolism in soybean: Formation of N-glucoside and homoglutathione conjugates

Metribuzin [4-amino-6-tert-butyl-3(methylthio)-1,2,4-triazin-5(4H)-one] metabolism was studied in soybean [Glycine max (L.) Merr. Tracy]. Pulse treatment studies with seedlings and excised mature leaves showed that [5-¹⁴C]metribuzin was absorbed rapidly and translocated acropetally. In seedlings, >97% of the root-absorbed ¹⁴C was present in foliar tissues after 24 hr. In excised leaves, 50–60% of the absorbed ¹⁴C remained as metribuzin 48 hr after pulse treatment, 12–20% was present as polar metabolites, and 20–30% was present as an insoluble residue. Metabolites were isolated by solvent partitioning, and were purified by adsorption, ion-exchange, thin-layer, and high-performance liquid chromatography. The major metabolite (I) was identified as a homoglutathione conjugate, 4-amino-6-tert-butyl-3-S-(γ-glutamyl-cysteinyl-β-alanine)-1,2,4-triazin-5(4H)-one. Metabolite identification was confirmed by qualitative analysis of amino acid hydrolysis products, fast atom bombardment (FAB), and chemical ionization (CI) mass spectrometry, and by comparison with a reference glutathione conjugate synthesized in vitro with a hepatic microsomal oxidase system from rat. Minor metabolites were identified as an intermediate N-glucoside conjugate (II), a malonyl N-glucoside conjugate (III), and 4-malonylamido-6-tert-butyl-1,2,4-triazin-3,5(2H,4H)-dione (N-malonyl DK, IV) by CI and FAB mass spectrometry. Alternative pathways of metribuzin metabolism are proposed.     

Metabolism of dibutyl-14C-labeled dibutylaminosulfenyl derivative of carbofuran in the cotton plant

The fate of the di-n-butylaminosulfenyl moiety in 2,3-dihydro-2,2-dimethyl-7-benzofuranyl (di-n-butylaminosulfenyl)(methyl)carbamate (DBSC or Marshal) was studied in the cotton plant at 1, 3, 6, and 10 days following foliage treatment with [di-n-butylamino-¹⁴C]DBSC. Dibutylamine and two major radioactive metabolites were obtained following extraction of the plant tissue with a methanol-buffer containing N-ethylmaleimide (NEM), a sulfhydryl scavenger which was added to prevent the cleavage of the NS bond during the workup procedure. The most adundant radioactive material recovered from plants was identified as a product arising from the reaction between NEM and dibutylamine. Extraction of plant tissue with straight methanol-buffer solution or with methol-buffer containing other sulfhydryl scavengers resulted in 57–86% of the applied radioactivity being recovered as dibutylamine in the organosoluble fraction. When [¹⁴C]dibutylamine was applied to cotton leaves, most of the radioactivity, i.e., 96% of the total recovered radioactivity, was found in the organosoluble fraction as dibutylamine. Dibutylamine is the major metabolite of [di-n-butylamino-¹⁴C]DBSC in the cotton plant.     

Metribuzin metabolism in tomato: Isolation and identification of N-glucoside conjugates

Metribuzin [4-amino-6-tert-butyl-3-(methylthio)-1,2,4-triazin-5(4H)-one] metabolism was studied in tomato (Lycopersicon esculentum Mill. “Sheyenne”). Pulse-treatment studies with seedlings and excised leaves showed that [5-¹⁴C]metribuzin was rapidly absorbed, translocated (acropetal), and metabolized to more polar products. Foliar tissues of 19-day-old seedlings metabolized 96% of the root-absorbed [¹⁴C]metribuzin in 120 hr. Excised mature leaves metabolized 85–90% of the petiole-absorbed [¹⁴C]metrubuzin in 48 hr. Polar metabolites were isolated by solvent partitioning, and purified by adsorption, thin-layer, and high-performance liquid chromatography. A minor intermediate metabolite (I) was identified as the polar β-d-(N-glucoside) conjugate of metribuzin. The biosynthesis of (I) was demonstrated with a partially purified UDP-glucose: metribuzin N-glucosyltransferase from tomato leaves. A possible correlation between foliar UDP-glucose: metribuzin N-glucosyltransferase activity levels and differences in the tolerance of selected tomato seedling cultivars to metribuzin was suggested. The major polar metabolite (II) was identified as the malonyl β-d-(N-glucoside) conjugate of metribuzin.     

A total-continuous portal vein fistula in gastrointestinal and toxicology research

A method for the total collection of portal vein blood over extended periods has been developed. The method has been applied in gastrointestinal toxicology research involving rats. The method facilitated quantitative recovery of portal vein blood for 120 min for measurement and identification of absorbed radiolabeled components derived from a toxic lipphilic pesticide placed in the lumen of the small intestine. The method can be applied to any substance—nutrient, anutrient, xenobiotic chemical, or endocrine factor—absorbed into the portal vein from the gastrointestinal tract. The method (a) provides for collection of compounds absorbed from the gastrointestinal tract before distribution to nondigestive tissues (i.e., liver), (b) allows measurement of the compounds absorbed without the need to monitor flow rate, and (c) facilitates accumulation of sufficient material from the total portal circulation for analyses when submicrogram quantities are absorbed. The latter two features are important but impossible to attain with small samples of portal blood and are crucial in research with minute quantities of substrate. These features become requirements in metabolism and toxicology research. The method involves replacement of the portal blood with a suspension of perfluorohydrocarbons to substitute for the major functions of natural blood. The total-continuous portal vein fistula makes it possible to investigate metabolic and transport phenomena in live animals which previously could be explored only by in vitro methods. The method may be applied to conscious animals with further refinements.     

The biochemical mechanism of action of the dinitroaniline herbicide oryzalin

Dinitroaniline herbicides such as oryzalin (3,5-dinitro-N⁴,N⁴-dipropylsulfanilamide) disrupt mitosis in the meristematic cells of seedling plants by inhibiting the formation of microtubules. For further understanding of the biochemical mechanism of action of oryzalin, laboratory analyses with isolated plant tubulin must be employed. Plant tubulin from flagella of the alga Chlamydomonas was isolated and purified. This tubulin was incubated with [¹⁴C]oryzalin, and free oryzalin was separated from oryzalin bound to plant tubulin by miniature DEAE-cellulose chromatography. Scatchard analysis predicts a molar ratio of oryzalin bound to plant tubulin of 1.0 ± 0.1 when oryzalin is incubated with plant tubulin for 30 min at pH 6.9 and 25°C. The association constant for the oryzalin-tubulin complex is 2.08 ± 0.08 × 10⁵M^?1 at 25°C. The thermodynamic values for the formation of the oryzalin-tubulin complex at 25°C are ΔG^o = ?7.25 ± 0.02 kcal mol^?1, ΔH^o = 6.5 ± 0.2 kcal mol^?1, and ΔS^o = 46 ± 2 cal mol^?1 deg^?1 (mean ± standard error). Oryzalin has little or no affinity for intact microtubules, previously denatured plant tubulin, actin, bovine serum albumin, calmodulin, ferredoxin, trypsin, or urease, indicating oryzalin is specific for the biologically active conformation of plant tubulin. Oryzalin binds to plant tubulin to form a complex that may be incapable of polymerizing into microtubules.     

Pharmacokinetics of sulfluramid and its metabolite desethylsulfluramid after intravenous and intraruminal administration of sulfluramid to sheep

Pharmacokinetic properties and tissue residues of the insecticide sulfluramid (I) and its major metabolite desethylsulfluramid (II) were determined in healthy sheep after bolus intravenous (IV) administration (5 and 15 mg kg⁻¹; n = 10) and bolus intraruminal (IR) administration (100 and 400 mg kg⁻¹; n = 12) of I . Depression, lethargy, and dyspnea were noted for 4 h after the higher IV dose, but not after the other IV or IR doses. The time courses of the mean blood concentrations of I and II were best described by a two-compartment open model with rapid distribution and slow elimination phases. The blood-to-plasma concentration ratios for I and II were 1.43 (± 0.50) and 26.7 (± 9.41), respectively, suggesting binding of II to red blood cells. The T_1/2β values for I and II for the higher IV dose of I were 15.3 (± 4.68) h and 63.4 (± 4.75) h and for the higher IR dose of I , 31.5 (± 5.41) h and 74.9 (± 7.49) h, respectively. Bioavailability was 28.6 (± 2.96)% for the lower IR dose and 19.5 (± 0.99)% for the higher IR dose. C_max values for II were higher in female than male sheep after IR administration of I . Only II was found in tissue samples, with the highest concentration being in liver (9.4 (± 5.2) µg g⁻¹). © 1999 Society of Chemical Industry     

Metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide] inhibition of gibberellin precursor biosynthesis

[2-¹⁴C]Mevalonic acid incorporation into gibberellic acid precursors was measured in cell-free extracts from sorghum [Sorghum bicolor (L.) Moench var. G-522 DR] coleoptiles. ¹⁴C incorporation into ent-kaur-16-ene was inhibited ca. 90% by 10^?7 to 10^?4M metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide]. [¹⁴C]Geranylgeraniol (GG) content increased. [¹⁴C]Farnesol content was not altered and [¹⁴C]geraniol content decreased. Total ¹⁴C incorporation was decreased by metolachlor. In the safener [α-(cyanomethoximino)benacetonitrile]-treated sorghum seed coleoptile cell-free system, total ¹⁴C incorporation increased, [¹⁴C]kaurene and relative kaurence content increased 4× up to 10⁵M metolachlor, and [¹⁴C]farnesol, and [¹⁴C]GG contents increased while relative farnesol and relative GG contents were not influenced by metolachlor. Thus, the inhibition of kaurene synthesis by metolachlor was reversed by the safener. Since the biosynthetic processes are mevalonic acid → geraniol → farnesol → GG → copalylol → kaurene, these data corroborate a proposed gibberellic acid biosynthesis inhibition between GG and kaurene as well as a partial blockage between mevalonic acid and geraniol. Thus, a portion of metolachlor-induced growth inhibitions of sorghum could be explicable on the basis of gibberellic acid biosynthesis inhibitions.     

Acifluorfen metabolism in soybean: Diphenylether bond cleavage and the formation of homoglutathione, cysteine, and glucose conjugates

Metabolism of the substituted diphenylether herbicide, acifluorfen [sodium 5-(2-chloro-4-trifluoromethylphenoxy)-2-nitrobenzoate], was studied in excised leaf tissues of soybean [Glycine max (L.) Merr. ‘Evans’]. Studies with [chlorophenyl-¹⁴C]- and [nitrophenyl-¹⁴C]acifluorfen showed that the diphenylether bond was rapidly cleaved. From 85 to 95% of the absorbed [¹⁴C]acifluorfen was metabolized in less than 24 hr. Major polar metabolites were isolated and purified by solvent partitioning, adsorption, thin layer, and high-performance liquid chromatography. The major [chlorophenyl-¹⁴C]-labeled metabolite was identified as a malonyl-β- -glucoside (I) of 2-chloro-4-trifluoromethylphenol. Major [nitrophenyl-¹⁴C]-labeled metabolites were identified as a homoglutathione conjugate [S-(3-carboxy-4-nitrophenyl) γ-glutamyl-cysteinyl-β-alanine] (II), and a cysteine conjugate [S-(3-carboxy-4-nitrophenyl)cysteine] (III).     

Physiological response of rainbow trout (Salmo gairdneri) to acute fenvalerate intoxication

The physiological responses of rainbow trout (Salmo gairdneri) to fenvalerate intoxication during aqueous exposure were examined to provide information about the pyrethroid mode of action in fish. Trout (n = 4) were exposed to 412 ± 50 μg/liter fenvalerate and died in 10.9 ± 1.5 hr. Brain, liver, and carcass fenvalerate concentrations associated with mortality were 0.16 ± 0.05, 3.62 ± 0.57, and 0.25 ± 0.05 mg/kg, respectively. Visible signs of intoxication included elevated cough rate, tremors, and seizures. Histopathological examination of gill tissue showed damage consistent with irritation. An evaluation of respiratory-cardiovascular and blood chemistry responses indicated an elevated rate of metabolism associated with increasingly severe seizures. A cessation of ventilatory and cardiac activity, occurring with the seizures, was also observed. Finally, urine osmolality, Na⁺ and K⁺ concentrations, and Na⁺ and K⁺ excretion rates were elevated with intoxicated trout. The physiological responses of rainbow trout to fenvalerate intoxication suggest that besides effects on the nervous system, effects on respiratory surfaces and renal ion regulation may be associated with the mechanism of pyrethroid action in fish.     

Carotenogenic inhibition by norflurazon in wheat

Wheat (Triticum aestivum L. cv Holley) seedlings were exposed to [N-¹⁴CH₃]norflurazon in nutrient solution studies. The ¹⁴CH₃ group was incorporated into a compound eluting on GLC at a relative retention temperature R_f equivalent to n-C₂₁ H₃₆ and mass spectrometry validated a 295 MW. The concentration of [N-¹⁴CH₃]norflurazon and/or Rl[¹⁴C]norflurazon which resulted in carotenogenesis inhibition was 0.07 μM in the water contained in the leaves. The concentration of norflurazon required for phytoene accumulation as a mode-of-action was ca. 140 × the concentration of norflurazon required for geranylgeraniol accumulation. Geranylgeraniol accumulated at 1 ppbw (3.2 nM) norflurazon and phytofluene accumulated throughout the norflurazon concentration series (1 to 1000 ppbw). Carotene content was increased by 1 to 16 ppbw norflurazon but was decreased by 64 ppbw norflurazon. Thus, two modes-of-activity for norflurazon are documented that depend upon concentration of the toxicant in the tissue. Norflurazon demethylation in prephytoenepyrophosphate synthesis resulted in a C₂₁ conjugate and increased concentrations of GGPP and phytoene in the tissue. At approximately 31 ppbw norflurazon, an inhibition of phytoene dehydrogenation occurred and phytoene accumulated. At 62 ppbw norflurazon, phytofluene hydrogenation inhibition occurred and phytofluene accumulated while β-carotene synthesis was inhibited. These inhibitions may possibly be reversible when substrate concentrations are in excess.     

Alkylation of guanine in mice in vivo by organophosphorus insecticides. I. Trichlorphone and butonate

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.     

Degradation of the herbicide flamprop-isopropyl in soil under laboratory conditions

The degradation of the wild-oat herbicide flamprop-isopropyl, [isopropyl (±)-N-benzoyl-N-(3-chloro-4-fluorophenyl)alaninate], in four soils has been examined under laboratory conditions with sampling times of up to 45 weeks after treatment. The major degradation product of [¹⁴C]flamprop-isopropyl in all soils at up to 10 weeks after treatment was the carboxylic acid (±)-N-benzoyl-N-(3-chloro-4-fluorophenyl)alanine. This compound in turn underwent degradation by loss of the benzoyl group and the propionic acid moiety, with evolution of [¹⁴C]carbon dioxide to form 3-chloro-4-fluoroaniline (CFA). The CFA was formed slowly in soil and occurred mainly as a bound form. There was evidence to show that the CFA was subsequently converted into other polar products. The time for depletion of 50% of the applied herbicide was approximately 10 weeks in sandy loam and medium loam soils, 11 weeks in a clay loam soil and 23 weeks in a peat soil.     

Alachlor influence on sorghum growth and gibberellin precursor synthesis

Growth (14 days) of sorghum (Sorghum bicolor L. cv G522 DR) from seed planted in sand into which alachlor [2-chloro-2′,6′-diethyl-N-(methoxymethyl)acetanilide] was uniformly incorporated (0, 0.07, 0.14, 0.28, 0.56, 1.12, 2.24, or 4.48 kg/ha) was reduced by 0.14 kg/ha and severely inhibited (88%) by 0.56 kg/ha while cellular water cotent was not greatly influenced by 0.56 kg/ha. When added into the nutrient solution bathing the roots of 96-hr sorghum seedlings, alachlor (0, 0.0156, 0.0312, 0.0625, 0.125, 0.25, 0.5, 1, 2, 4, 8, 16, 32, 64, or 128 ppmw) was not lethal to 14-day-old sorghum at rates up to 32 ppmw (92% survival); however, shoot and root lengths were reduced 43 and 58%, respectively. Alachlor inhibition of sorghum growth appears to be closely associated with inhibition of cell enlargement; the coleoptile is the most susceptible stage of sorghum growth to alachlor. This situation closely resembles growth where gibberellic acid (GA) synthesis is inhibited. [2-¹⁴C]Mevalonic acid ([2-¹⁴C]MVA) incorporation into terpenoid GA precursors was evaluated using a cell-free enzyme system from etiolated sorghum coleoptiles. Alachlor did not inhibit total ¹⁴C incorporation but incorporation of ¹⁴C into kaurenol and sterols was decreased ca 80 and 75%, respectively, by 10^?6M alachlor. Analyses for [¹⁴C]geranylgeraniol (GG), [¹⁴C]farnesol, and [¹⁴C]geraniol contents showed accumulation of [¹⁴C]farnesol and [¹⁴C]GG, and decreased [¹⁴C]geraniol. When seeds to which CGA-43089 [α-(cyanomethoximino)-benzacetonitrile] was applied 8 weeks prior to planting were substituted for untreated seeds, incorporation of [2-¹⁴C]MVA into [¹⁴C]kaurenol was increased by alachlor while [¹⁴C]GG and [¹⁴C]farnesol accumulated and [¹⁴C]geraniol was absent at 10^?6M alachlor. Additionally, sterol content increased in “safened” systems but was still decreased by alachlor. These data demonstrate multiple sites of alachlor activity in the GA and terpenoid biosynthetic pathway.     

Cholinesterase inhibition by methamidophos and its subsequent reactivation

Methamidophos (O,S-dimethylphosphoramidothioate, Monitor) is an organophosphorus, cholinesterase-inhibiting insecticide. The rate constant (k_i) for inhibiting rat plasma cholinesterase (ChE) was 1.57 ± 0.03 × 10³M^?1 min^?1, for rat erythrocyte ChE was 8.86 ± 1.10 × 10³M^?1 min^?1, and for rat brain ChE was 6.58 ± 0.42 M^?1 min^?1. Brain and plasma cholinesterases spontaneously recovered from over 90% inhibition at 30 min to 50% inhibition in 4 and 14 hr, respectively. Pralidoxime increased the rate of reactivation in vitro. In vivo, rats poisoned with methamidophos exhibited signs of cholinergic stimulation. The LD₅₀ of ip methamidophos in male rats was 15 ± 0.7 mg/kg. Pralidoxime (60 mg/kg) and atropine (10 mg/kg) given with the methamidophos increased the LD₅₀ to 52 ± 4.9 mg/kg and 60 ± 0.4 mg/kg, respectively. In rats given 12.5 mg methamidophos (an LD₂₀), ChE activity was depressed 95 ± 12.5% in plasma, 92 ± 0.6% in stomach, and 88 ± 1% in brain at 1 hr after injection. At 48 hr after injection ChE activity had returned to 60% or more of control values in each of the tissues. Administration of a single dose of 60 mg/kg of pralidoxime along with methamidophos did not increase ChE activities at the times and places it was measured.     

Effects of the herbicide EPTC and the protectant DDCA on incorporation and distribution of [2-14C]acetate into major lipid fractions of maize cell suspension cultures

The rapid effects of the herbicide EPTC (S-ethyl dipropylthiocarbamate) and the protectant DDCA (N,N-diallyl-2,2-dichloroacetamide) on [2-¹⁴C]acetate incorporation into lipids of maize cell cultures were studied in order to determine whether they act at similar sites of lipid synthesis. DDCA, at 0.05 mM and 0.1 mM, increased the incorporation of [2-¹⁴C]acetate into neutral lipids of a total lipid extract within 2 h. It had very little effect on the major polar lipid constituents. DDCA altered neither the distribution of label within the major lipid classes, nor turnover of the major lipids within 2 h. EPTC (0.1 mM) inhibited overall uptake of [2-¹⁴C]acetate into both neutral and polar lipids by about 30% after a 2-h incubation. The major polar lipid affected was an unidentified glycolipid. In addition to reducing the quantity of lipids synthesized, EPTC changed the lipid profile, altering the distribution of label, mainly within the neutral lipid fraction. A crude membrane fraction from maize cells contained both polar lipids and some neutral lipids. DDCA stimulated [2-¹⁴C]acetate incorporation into different lipid species. EPTC inhibited incorporation of [2-¹⁴C]acetate into both neutral and polar membrane lipids but altered significantly only its distribution into neutral lipids. DDCA (0.1 mM) given together with EPTC (0.2 mM) partially counteracted the effect of EPTC within the neutral lipid fraction. It is suggested that DDCA has a rapid effect on lipid synthesis, but it is probably not sufficient to account for the entire mode of action of the protectant.     

The effect of impurities on the toxicokinetics of malathion in rats

The effect of the malathion impurities, isomalathion of O,S,S-trimethyl phosphorodithioate (OSS-Me), on the toxicokinetic behavior of [methoxy-¹⁴C]malathion in female rats was investigated. Malathion α- and β-monoacids and the diacid were the predominant metabolites in the blood of rats pretreated orally with corn oil followed 4 hr later with radiolabeled malathion. Pretreatment of rats with isomalathion or OSS-Me in corn oil followed by treatment with malathion resulted in a decrease of total radioactive metabolites in the blood. Moreover, a substantial reduction in the level of malathion β-monoacid and malathion diacid was observed in the blood of impurity pretreated animals. These results indicate that the impurities have a stronger effect in inhibiting carboxylesterases which preferentially hydrolyze the β-carboethoxy moiety of malathion. The major malathion metabolites excreted in the urine of pretreated and control rats generally matched those present in the blood. The potentiation of the acute toxicity of malathion by pretreatment with isomalathion or OSS-Me may be explained by the reduction in the rat's capacity to degrade malathion via carboxylesterase-catalyzed hydrolysis of the β-carboethoxy moiety.     

Differential tolerance of peas to prometryne and terbutryn

The phytotoxicity of 2,4-bis(isopropyl)-6-(methylthio)-s-triazine (prometryne) and 2-(tert-butylamino)-4-(ethylamino)-6-(methylthio)-s-triazine (terbutryn) to peas (Pisum sativum L. var. Perfection 3040) was studied. No differences were found when the herbicides were applied to the roots of intact plants in nutrient solution or directly to leaf discs. However, prometryne was much more toxic when uptake was from soil. Absorption and translocation of ¹⁴C-labeled prometryne and terbutryn showed that the majority of terbutryn accumulated in the roots, whereas prometryne was uniformly distributed between the roots and the shoot. Thin layer chromatography of extracts from prometryne-treated peas showed that only 20% of the absorbed compound was metabolized to produce one breakdown product. Extracts of terbutryn-treated plants contained three different metabolites. After 120 hr of exposure to terbutryn, about half of the absorbed herbicide was metabolized. The results show that the main factors responsible for the differential toxicity of the herbicides to peas were availability from the soil, translocation pattern and initial detoxication.     

Challenging the larvae of <Emphasis Type="Italic">Helicoverpa armigera</Emphasis> and assessing the immune responses to nematode-bacterium complex

Helicoverpa armigera is a strong insecticidal resistance developed insect pest. The understanding of its innate immune responses to emerging biocontrol agent entomopathogenic nematode-bacterial complex can provide an opportunity to control this insect in an environmentally benign manner. Study was focused on role of hemocytes changes and PO activity in Steinernema abbasi-Xenorhabdus indica challenged larvae of H. armigera over the time. Total cell count changed effectively from 10.2?±?1.81?×?10⁵ to 15.5?±?3.3?×?10⁵ cells/mm³ upto 9 h and reduced distinctly up to 8.0?±?2.49?×?10⁵ cells/ mm³ in 24 h. PO activity inclined significantly and was recorded highest at 9 h (24.67?±?1.08?×?10² units) and lowest at 24 h (14.34?±?0.74?×?10² units) in total hemolymph with a similar pattern in plasma and the cellular fraction. Phenoloxidase activity in total and cellular component of hemolymph was positively correlated with prohemocytes, granulocytes and oenocytoids. Study showed the hemocytes and PO accounted as active immune responses against nematode infection. The results provide the first insight to understand the hemolytic activity, quick immunosuppression responses of S. abbasi-X. indica and vulnerability of H. armigera.     

Metabolism of [14C]dieldrin in bluegill fish

The exposure of bluegill fish to 50 parts per billion [¹⁴C]dieldrin in a static system resulted in the absorption of 73.00% of the radioactivity in 48 hr. Following transfer of the fish to clean water, only 16.20% of the absorbed radiolabel was eliminated in 23 days. Out of the 93.65% of the absorbed radioactivity recovered, 9 radioactive spots were isolated which included unchanged dieldrin (74.39%), pentachloroketone (8.17%), and aldrin-trans-diol (8.04%) as major metabolites.