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Biomedical subjects

S A Soliman

Publications and source records attributed to S A Soliman.

At least 37 records · Page 2Linked to original sources
PubMed1982

Species susceptibility to delayed toxic neuropathy in relation to in vivo inhibition of neurotoxic esterase by neurotoxic organophosphorus esters.

Tri-o-cresyl phosphate (TOCP) and O-ethyl O-(4-cyanophenyl) phenylphosphonothioate (cyanofenphos, Surecide) were found to be delayed neurotoxicants. They were administered to chickens by gavage at 100 and 30 mg/kg . d for 15 d, respectively. In CD-1 mice neither TOCP nor cyanophenphos induced any of the usually recognized clinical symptoms of neuropathy when administered daily by gavage at 262 or 31.25 mg/kg . d for 30 d, respectively. In the chickens, TOCP and cyanofenphos produced about 98 and 90% in vivo inhibition of brain neurotoxic esterase (NTE) activity. In the mice, 24 h after the last daily dose, TOCP and cyanofenphos produced only about 50 and 40% in vivo inhibition of the brain NTE activity. Parathion [O,O-diethyl O-(4-nitrophenyl) phosphorothioate], at 2 or 6.75 mg/kg . d for 15 or 30 d, did not induce neuropathy in either chicken or mice and produced no significant in vivo inhibition of brain NTE activity at the end of the dosing regimen. The specific activity of NTE in control chicken brain crude homogenate was much higher than that in mouse brain homogenate. These results suggest that the differences between chickens and mice in susceptibility to neurotoxic organophosphates may be attributed to (1) inhibitor specificity of NTE forms in the brain in these two different animal species and/or (2) inability of the active metabolites of these neurotoxic compounds to reach the site of action.

Animals↗
PubMed1982

Delayed neuropathy in hen by the insecticide synergist O-n-propyl O-(2-propynyl) phenylphosphonate (NIA-16388) and other phenylphosphonate esters.

O-n-Propyl O-(2-propynyl) phenylphosphonate (NIA-16388), which has been recommended for use as insecticide synergist, was synthesized and tested for acute and neurotoxicities in hens. The 24-h LD50 value of this compound in the hen was found to be about 340 mg/kg. Hens treated with this compound at 400 mg/kg with atropine sulfate as an antidote developed clear clinical signs of delayed neurotoxicity 12-17 d after single oral treatment. The signs of neurotoxicity gradually progressed from ataxia through paralysis. Biochemical tests indicated that at the tested dose level of this compound, the level of hen-brain neurotoxic esterase (NTE) was inhibited in vivo to less than 10% of the normal level 1 d after treatment. These clinical and biochemical signs of neurotoxicity are supported by histopathological findings. Degenerative lesions of axons were observed in the NIA-treated group of hens. The lesions in the spinal cord were seen most frequently and most prominently in the lateral columns, although they sometimes were observed in other areas, e.g., in the anterior columns (especially in thoracic and lumbar sections). Generally, the lesions were more apparent in the longitudinal sections than in the cross-sections. Two other phenylphosphonate derivatives, O-ethyl S-benzyl phenylphosphonothioate (ESBP) and O-methyl O-(4-benzylidenylphenylhydrazone) phenylphosphonothioate, were also synthesized and tested for neurotoxicity to hens. The LD50 values for these two compounds in the hen were more than 1000 mg/kg. No signs of delayed neuropathy were detected in hens given either ESBP or the hydrazone compound at single oral doses of 1000 mg/kg.

Animals↗
PubMed1981

A direct method to assay neurotoxic esterase activity.

A direct photometric method for assaying neurotoxic esterase (NTE) activity of chicken brain microsomal preparation has been developed using 4-nitrophenyl esters as substrates. Paired samples of the microsomal preparation were preincubated for 20 min with paraoxon plus either (a) buffer or (b) mipafox before addition of substrate. The initial rate of NTE activity was directly recorded at 410 nm by matching the content of tube (a) against tube (b) after addition of the substrate to both of them. The 4-nitrophenyl esters of propionic, butyric, valeric, lauric, capric and caproic acids were tested as substrates. Results indicated that 4-nitrophenyl valerate and caproate, respectively, are the most hydrolyzable substrates for NTE with this method; its also enables detailed kinetic studies of NTE to be made. The Michaelis constant (Km) for the hydrolysis of 4-nitrophenyl valerate by NTe was found to be 5.55 . 10(-5) M.

Animals↗
PubMed1981

Biochemical interaction of six OP delayed neurotoxicants with several neurotargets.

Five organophosphorous insecticides: Leptophos, EPN, Cyanofenphos, trichloronate and salithion proved to cause irreversible ataxia not only to chicken but also to mice and sheep. TOCP was included as a reference. Cyanofenphos blocked the catecholamine B-receptor binding activity with 3H-norepinephrine at a level similar to that of the specific inhibitor propranolol in the mouse heart preparation. In the lamb heart preparation, the B-receptor was more sensitive to Leptophos, salithion and TOCP than to propranolol. The six compounds and their oxons were screened for their in-vitro inhibition to monamine oxidase (MAO), acetyl cholinesterase (AChE) and neurotoxic esterase (NTE) in the brain of either mouse, lamb or chicken. It is believed that their AChE inhibition stands for their acute toxicity, while NTE inhibition is responsible for their paralytic ataxia.

Animals↗
PubMed1981

Biochemical effects of some organophosphorus insecticide on new targets in white rats.

The three S-n-propyl phosphates and phosphothioates: RH 218, profenofos and prothiophos were compared with fenitrothion in their potential as inhibitors of rat liver and brain AChE. Fenitrothion was more potent as an inhibitor than the three S-n-propyl derivatives. Incubation of hepatic protein enhanced ChE inhibition in brain in the case of fenitrothion, while it reduced the inhibitory effect of the S-n-propyl derivatives. On the other hand, the four organophosphorus esters caused hypoglycemia in both male and female rats and also reduced their blood urea with different degrees.

Animals↗
PubMed1980

Subcellular distribution of neurotoxic esterase activity in lamb and mouse brain.

Brain tissue samples of mice (7.6 g from 25 mouse brains and lamb (25 g) were homogenized and subcellular fractions prepared in order to assay the distribution of neurotoxic esterase (NTE) activity. The specific inhibitor, N,N-diisopropylphosphorodiamidic fluoride (mipafox) was synthesized and purified. Maximum specific activity of NTE was reached in the microsomal fraction (110,000 g) while the enzyme activity in the soluble fraction (110,000 g) was extremely low. This subcellular distribution of NTE activity in mammal brains is an original contribution. Brain microsomal fraction is suggested to be a more reliable source for the highest activity of NTE. The specific activity of NTE of lamb brain was much higher than that of mouse brain. This might help interpretation of the characteristic species variation in susceptibility to NTE inhibitors which are known to be potent delayed neurotoxic agents.

Animals↗
PubMed1980

Delayed neurotoxicity of Cyanofenphos in chickens.

Delayed neurotoxic ataxia, similar to that caused by neurotoxic organophosphorous compounds, has been shown to occur in hens after oral administration of Cyanofenphos (O-ethyl-O-Cyanophenyl phenyl phosphonothionate) following either single or repeated oral doses. Axonal and myelin degeneration affecting the long tracts in spinal cord, peripheral nerves and medulla was demonstrated. The distal fibers with large diameters were particularly affected. This finding is a new contribution which has not been previously recorded. It implies that a thorough study of the structure-activity relationships of phosphonothionates regarding their delayed neurotoxic effect is warranted.

Administration, Oral↗
PubMed1979

Occupational effect of phosfolan insecticide on spraymen during field exposure.

Phosfolan (Cyolane), 2-(diethoxy phosphinylimino)-1,3-dithiolane is one of the widely used insecticides in Egypt specially to protect cotton plants. The hazard of exposure of the spray workers team in the field was estimated in terms of the amount of Phosfolan insecticide retained on workmen body pads during field spraying. The health effect of such exposure was determined through recording of the AChE inhibition in the red blood cells at different intervals after exposure. The calculated percentage of the toxic dose received per every spraying day for each worker varied with the type of job in the range of 0.008 to 0.03 percent. The body of the mixer received the maximum exposure with 10 to 12 fold that of the assistants. The highly exposed group of workers suffered from 31 to 44 percent RBC's AChE inhibition. About half of the inhibited enzyme activity recovered after 48 hours. Then it took more than 3-4 weeks to reach complete recovery. Thus the RBC's AChE activity can be recommended as a criterion for the level of exposure to organophosphorous insecticides.

Acetylcholinesterase↗
PubMed1979

Delayed neuropathy in sheep by the phosphonothioate insecticide cyanofenphos.

Cyanofenphos (surecide)(R), 25% E.C., O-ethyl O-(4-cyanophenyl) phenylphosphonothioate, was orally administered to one year old lambs at sublethal doses of 1 mg, 2 mg and 4 mg active ingredient kg-1 day-1 for time intervals 60, 45 and 30 days respectively. Irreversible paralytic ataxia symptoms of delayed neuropathy appeared at about 80, 50 and 30 days respectively. In weekly blood samples, AChE (acetylcholine-sterase) and MAO (monoamine oxidase) activities were inhibited depending upon level of dosing and time interval. However no significant correlation was found between the extent of plasma AChE and MAO inhibition and the onset of ataxia symptoms. In brain samples from ataxiated animals, AChE, MAO and NTE (neurotoxic esterase) activities were assayed simultaneously with untreated animal. Direct correlation was shown between in vivo NTE inhibition and the occurrence of delayed neuropathy. Cyanofenphos is the third compound of the phenyl phosphonothioate type on the market showing delayed neuropathy together with Leptophos and EPN.

Acetylcholinesterase↗
PubMed1978

Effect of pre-exposure on acute toxicity of organophosphorus insecticides to white mice.

LD50 and in vitro ChE I50 values of Chlorpyrifos, Leptophos, Phosfolan, and Stirophos against white mice showed that the formulated insecticides were higher in their mammalian toxicity than the corresponding technical materials. Pretreatment of mice with a sublethal dose of Phosfolan potentiated the toxicity of post-treatment with formulated Stirophos, Phosfolan, or Chlorpyrifos, but antagonized the toxicity of post-treatment with Leptophos. On the other hand, pretreatment with sublethal doses of Leptophos resulted in potentiation of Stirophos or Phosfolan, but decreased the toxicity of Chlorpyrifos or Leptophos. Pretreatment of mice by sublethal dose of Phosfolan synergized the in vivo inhibitory power of post-treatment by Phosfolan, Chlorpyrifos or Leptophos against brain and Plasma ChE. On the other hand pretreatment with sublethal doses of Leptophos antagonized the inhibitory power of post-treatment with either Chlorpyrifos, Leptophos or Stirophos against mice brain-ChE.

Animals↗
PubMed1977

Neurotoxicity of organophosphorus insecticides Leptophos and EPN.

Phosfolan, chlorpyrifos, and stirophos when applied to white mice at sublethal doses did not induce any delayed neurotoxic effect. On the other hand, Leptophos and EPN when administered orally at sublethal or lethal levels clearly produced a delayed neurotoxic ataxia in treated mice. The five tested organophosphorus insecticides were compared for their ability to inhibit cholinesterase, neurotoxic esterases and monoamine oxidase. I50 values were estimated for each case. The results revealed that all five compounds were inhibitors of cholinesterase, but only Leptophos and EPN were shown to be potent inhibitors for both neurotoxic esterase and monoamine oxidase in the mouse brain. Additional particular properties of both Leptophos and EPN were found in their ability to cause delayed neurotoxic ataxia in chickens and sheep fed once on sublethal doses of these compounds. It is believed that the phosphonate ester configuration of EPN and Leptophos has a specific mode of toxic action which is mainly located at the central nervous system. It is also postulated that these delayed neurotoxic agents might inhibit postganglionic sympathetic neurons, thus resulting in chronic paralytic effects.

Administration, Oral↗
PubMed1977

Interference by acetylated aminoacetic acid in nonaqueous titration of nicotinic acid.

A nonaqueous titration procedure is described for determining aminoacetic acid and nicotinic acid in mixtures and elixirs. The effect of acetylated aminoacetic acid on the potentiometric titration of nicotinic acid is discussed. Above a 2:1 ration of aminoacetic acid to nicotinic acid, the former interferes with titration. The titration curve of nicotinic acid becomes progressively flatter with increasing amounts of the acetylated compound. Above this ratio, nicotinic acid had to be separated from the mixture by dissolving in ethanol for a successful titration.

Drug Combinations↗
PubMed1976

Nonaqueous titration of sulfates of quinine and quinidine using barium acetate.

A nonaqueous titrimetric method is proposed for determining the diastereomeric sulfates of quinine and quinidine. The sulfuric acid content of the alkaloid salts is precipitated, in the form of barium sulfate, with acetous barium acetate solution before the liberated alkaloid is titrated; the necessary calculations are provided. A favorable characteristic of the proposed procedure is the accuracy, speed, and ease of performance. The mean percent recoveries (p = 0.05) obtained with the proposed method for the sulfates of quinine and quinidine were 98.84 +/- 1.00 and 99.74 +/- 1.27, respectively, compared with 100.73 +/- 1.44 and 100.82 +/- 1.16, respectively, when the BP 1968 procedure was applied.

Acetates↗
PubMed1976

Rapid spectrophotometric determination of salicylamide in analgesic tablets.

An independent, simple, and rapid procedure is suggested for the routine analysis of salicylamide in analgesic tablets containing acetaminophen, phenobarbital, caffeine, codeine phosphate, prednisone, ascorbic acid, and chloroquine phosphate. The method does not require the preliminary separation of salicylamide from other constituents by the time-consuming solvent extraction technique or by chromatography prior to determination. The absorbance was linear for investigated concentrations of salicylamide from 0 to 4.0 mg/100 ml of solution at 308 nm.

Analgesics↗
PubMed1975

Chemistry of nonaqueous titration of chlopromazine.

The chemistry of the red color formed during perchloric acid titration of chlorpromazine hydrochloride in acetic acid in the presence of mercuric acetate is discussed. Addition of ascorbic acid prevents the color formation and allows titration using a crystal violet end-point. Ascorbic acid addition also sharpens the potentiometric end-point. Ascrobic acid and its oxidation product, dehydroascorbic acid, being neutral to perchloric acid, do not interfere with the titration.

Ascorbic Acid↗