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Biomedical subjects

S A Soliman

Publications and source records attributed to S A Soliman.

At least 19 recordsLinked to original sources
PubMed1993

Mutagenic and carcinogenic pesticides used in the agricultural environment of Gaza Strip.

More than 100 metric tons of formulated pesticides (about 75 pesticides) are used annually in Gaza Strip. It was found that 19 of these pesticides, that have been used, are internationally suspended, cancelled and banned pesticides. About 1100 cases of cancer have been registered in Gaza Strip (1979-1983). The distribution of cancer types among those patients are lymphoma and hematological malignancy, breast, head and neck, gastrointestinal malignancy, reproductive system, urinary system, soft tissue tumors, brain tumors and others. Consequently, the introduction and heavy use of pesticides and other toxic substances in the Gaza Strip environment is suspected to correlate with the growing incidence of cancer and other abnormalities in the nation. Precise determination of the effects of chronic exposure is, therefore, urgently needed.

Agriculture↗
PubMed1991

Lindane may enhance nocturnal pineal N-acetyltransferase activity via beta-adrenergic receptors.

Lindane, a chlorinated hydrocarbon pesticide, was previously shown to enhance the nighttime rise in pineal N-acetyltransferase (NAT) activity and melatonin as well as serum melatonin levels. The purpose of the present study was to test whether lindane acts on the pineal gland by means of a beta-adrenergic receptor mechanism. Whereas lindane (total dose 17.8 mg/kg b.wt. over 6 days) by itself significantly augmented the nocturnal levels of pineal NAT activity in otherwise untreated rats, the pesticide was ineffective in reference to this enzyme when it was given in conjunction with the beta-adrenergic receptor antagonist propranolol (20 mg/kg b.wt., one hour before lights off). The augmentation of NAT activity by lindane also caused significant reductions in pineal serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA); again, both these responses were blocked by propranolol treatment. Neither pineal 5-hydroxytryptophan nor pineal or serum melatonin levels were significantly changed as a result of either lindane or propranolol treatment. The results are consistent with the idea that lindane influences pineal 5-HT metabolism either at the level of the beta-adrenergic receptor or via the sympathetic innervation to the pineal gland.

Animals↗
PubMed1991

Carbaryl-induced changes in indoleamine synthesis in the pineal gland and its effects on nighttime serum melatonin concentrations.

The effects of different doses of chronically administered carbaryl on rat pineal N-acetyltransferase (NAT) activity, hydroxyindole-O-methyltransferase (HIOMT) activity and pineal and serum melatonin levels during darkness (2300 h and 0100 h) when pineal melatonin synthesis is high were studied. Additionally, pineal levels of 5-hydroxytryptophan (5-HTP), serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) were estimated. Carbaryl was administered at total doses (over 6 days) of either 50, 125 or 250 mg/kg by gastric gavage. Control rats received vehicle (corn oil) only. During the study, the rats were exposed to light/dark cycles of 14:10 with lights off at 2100 h. Pineal NAT and HIOMT activities and pineal melatonin were increased at 0100 h following carbaryl administration at all three doses. Conversely, serum melatonin was increased at 2300 h after the 250 mg/kg dose of carbaryl while all three doses of the pesticide reduced serum melatonin levels at 0100 h. Pineal 5-HTP, 5-HT and 5-HIAA levels were usually increased at 2300 h but unaffected at 0100 h. The results indicate that carbaryl has significant effects on pineal melatonin synthesis and secretion.

5-Hydroxytryptophan↗
PubMed1991

Parathion (O,O-dimethyl-O-p-nitrophenyl phosphorothioate) induces pineal melatonin synthesis at night.

The effects of parathion on male rat pineal N-acetyltransferase (NAT) activity, hydroxyindole-O-methyltransferase (HIOMT) activity and pineal and serum melatonin levels at the end of light period (2000 h) and at night (2300 h and 0100 h) were studied. Additionally, pineal levels of 5-hydroxytryptophan (5-HTP), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were estimated. Parathion was administered intragastrically at total doses (over 6 days) of either 6.5 or 13 mg/kg. Control rats received vehicle (corn oil) only. During the study, the rats were exposed to light:dark cycles of 14:10 with light off at 2100 h. Pineal NAT activity was increased at 0100 h following parathion administration at both doses, but HIOMT activity was unaffected. Pineal and serum melatonin levels were increased at night (2300 h and 0100 h) after the 13 mg/kg dose of parathion while the lower dose increased pineal melatonin only at 0100 h. Also, both doses decreased 5-HTP at 2000 h while the lower dose increased it at 2300; 5-HT was significantly decreased at 2300 h and 5-HIAA levels were lower but only significantly so for the 13 mg/kg dose at 2000 h. The results indicate that parathion has significant effects on pineal melatonin synthesis by mechanisms which remain unknown.

Acetylserotonin O-Methyltransferase↗
PubMed1991

Chronic administration of sublethal doses of carbaryl increases pineal N-acetyltransferase and hydroxyindole-O-methyltransferase activities and serum melatonin levels.

The purpose of this study was to examine the effects of chronic administration of sublethal doses of carbaryl on pineal melatonin synthesis. N-methyl 1-naphthylcarbamate (carbaryl) (8.33 mg/kg B.W. daily) was administered orally to adult male albino rats for 6 successive days. Nocturnal (0100) N-acetyltransferase and hydroxyindole-O-methyltransferase activities were increased (roughly 75% and 60%, respectively) by carbaryl administration; likewise, carbaryl augmented serum melatonin levels at 2300. Pineal tryptophan. 5-hydroxytryptophan, serotonin, and 5-hydroxindole acetic acid levels were unaffected at all three time points. The results indicate that the carbamate pesticide, i.e., carbaryl, modifies pineal melatonin synthesis in vivo.

5-Hydroxytryptophan↗
PubMed1990

The organochlorine insecticide 1,2,3,4,5,6-hexachlorocyclohexane (lindane) but not 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) augments the nocturnal increase in pineal N-acetyltransferase activity and pineal and serum melatonin levels.

The effect of organochlorine insecticides lindane (1,2,3,4,5,6-hexachlorocyclohexane) and DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane) were studied in terms of their effects on the rat pineal N-acetyltransferase (NAT) activity, hydroxyindole-O-methyltransferase (HIOMT) activity and pineal and serum melatonin levels during the day (2000h) and at night (2300 and 0100h). Additionally, pineal levels of 5-hydroxytryptophan (5-HTP), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were estimated. Nocturnal NAT activity was increased after lindane administration; likewise, lindane augmented pineal and serum melatonin levels at 2300h. Conversely, DDT was without a statistically significant effect on either NAT activity or on pineal or serum melatonin levels. Neither lindane nor DDT significantly influenced pineal HIOMT values either during the day or at night. Likewise, neither insecticide consistently influenced pineal levels of either 5-HTP, 5-HT or 5-HIAA. The results indicate that the organochlorine insecticide, lindane, modifies pineal melatonin synthesis in vivo.

5-Hydroxytryptophan↗
PubMed1989

Studies on the mechanism of haloacetonitriles toxicity: inhibition of rat hepatic glutathione S-transferases in vitro.

Acetonitrile (AN) and seven of its halogenated derivatives known to be water disinfectant by-products were evaluated for their action on hepatic cytosolic glutathione S-transferase (GST) activity using 1-chloro-2,4-dinitrobenzene (CDNB) as substrate. Increasing concentrations of acetonitrile, monofluoroacetonitrile (MFAN), monochloroacetonitrile (MCAN), and monobromoacetonitrile (MBAN) up to 10 mM failed to produced 50% inhibition of the activity of GST enzyme. However, dichloroacetonitrile (DCAN), trichloroacetonitrile (TCAN), dibromoacetonitrile (DBAN), and monoiodoacetonitrile (MIAN) were potent inhibitors with 150 values of 2.49, 0.34, 0.82, and 4.44 mM, respectively. At concentrations equivalent to their 150, MIAN, DCAN, and DBAN decrease both apparent Km and Vmax of the enzyme activity toward glutathione (GSH) to 20-50% of control. TCAN significantly increases both apparent Km and Vmax for GSH to 650 and 120% of control values, respectively. The inhibitory effect of haloacetonitriles (HAN) on hepatic GST activity toward CDNB was found to be a mixed type. The inhibitory effect of DCAN, DBAN, and TCAN on the hepatic GST activity was found to be reversible and the activity was completely recovered after dialysis of the inhibited enzyme. MIAN, however, inhibited GST activity in an irreversible manner. Haloacetonitriles' induced inhibition of hepatic GST activity in vitro is consistent with that observed in vivo. The data presented in this study show that haloacetonitriles induced reversible inhibition of hepatic GST activities, and this effect may lead to decreased detoxification of other electrophilic chemicals.

Acetonitriles↗
PubMed1987

Application of transformation algorithm and nonparametric calculation in determining the reference intervals of some urine constituents and characteristics.

We have applied a multi-stage computer algorithm for normalization of distributions and calculation of reference intervals of some urine characteristics and constituents. The study analyzed 24-h urines, collected from adult male Saudis from different socioeconomic classes, for volume, pH, osmolality, specific gravity, creatine, creatinine, urea and uric acid. Frequency distributions, for each analyte, were found to be nongaussian as judged by the coefficients of skewness and kurtosis, chi 2 and Kolmogorov-Smirnov tests, and from probability plots. Data were transformed to gaussian distributions by multistage log-power transformation. Stepwise, this procedure removed skewness and residual kurtosis. Using the gaussian transformed data the reference intervals were estimated parametrically as the mean +/- 2 SD. In addition, the non-parametric percentile technique was applied to estimate these values. The former intervals were found to have narrower 0.90 confidence limits than the latter. When established limits were compared with those reported for Western subjects urine volume and uric acid showed the most marked variation.

Adult↗
PubMed1986

Delayed neurotoxicity in the wild mallard duckling caused by the organophosphorus insecticides cyanofenphos and leptophos.

The susceptibility of wild mallard ducklings to the delayed neurotoxic effect of the neurotoxic organophosphorus insecticides cyanofenphos and leptophos was evaluated following a daily dosing regimen. Ducklings were treated daily with either cyanofenphos or with leptophos at different dose levels for 90 days, or until they died, or became paralyzed. A control group of ducklings given corn oil at 1 ml/kg daily for 90 days was used for comparison. All treated birds were observed daily for any clinical signs of neurotoxicity during the course of this study. All of the surviving ducklings that were treated with cyanofenphos at 4 mg/kg/day or leptophos at 10 mg/kg/day developed clinical signs of delayed neurotoxicity after 7 to 11 weeks of intoxication. Symptoms included leg weakness, ataxia, severe ataxia and paralysis. The observed clinical signs were confirmed by histological changes found in the spinal cords of the treated birds. These changes were of the type associated with organophosphorus-induced delayed neuropathy (OPIDN). These results demonstrate that wild mallard ducklings are susceptible to OPIDN and this avian species can be used in screening organophosphorus compounds for such effect.

Animals↗
PubMed1984

Delayed neuropathy in adult Peking ducks induced by some organophosphorus esters.

Trio-o-cresyl phosphate (TOCP), leptophos [O-methyl O-(4-bromo-2,5,-dichlorophenyl) phenylphosphonothioate] and cyanofenphos [O-ethyl O-(4-cyanophenyl) phenyl-phosphonothioate] were used to determine whether adult peking ducks would exhibit neurotoxicity after exposure to such chemicals. Clinical, histopathological, and specific biochemical tests were used to detect the neurologic dysfunctions that were induced by these neurotoxic agents. Ducks were orally treated with TOCP or leptophos at 100 or 10 mg/kg X d for 30 d, respectively. Another group of ducks received cyanofenphos at 4 mg/kg X d for 10 d. All the TOCP- and leptophos-treated ducks developed clinical signs of delayed neuropathy, as manifested by ataxia and paralysis. Two of the cyanofenphos-treated ducks died from cholinergic effect during the course of dosing. Surviving ducks of this group completely recovered from the cholinergic effect 2 or 3 d after finishing the dosing regimen. However, they developed signs of delayed neurotoxicity 10-17 d later. Surviving ducks of all groups were sacrificed for biochemical and/or histopathologic tests 1 d after the last treatment or when they became paralyzed. Histopathologic examinations indicated that degenerative lesions of axons consistent with the type occurring in delayed neurotoxicity were seen in all TOCP-, leptophos-, or cyanofenphos-treated ducks and were specially evident in sections of spinal cord. Biochemically, it was found that duck brain neurotoxic esterase (NTE) activity was inhibited in vivo to less than 15% of control levels as measured 24 h after the last treatment with TOCP, leptophos, or cyanofenphos. These results indicate that adult peking ducks could be used to screen organophosphorus compounds for delayed toxic neuropathy.

Animals↗
PubMed1983

Six-month daily treatment of sheep with neurotoxic organophosphorus compounds.

The delayed neurotoxic effects of tri-o-cresyl-phosphate (TOCP), O-methyl-O-(4-bromo-2,5-dichlorophenyl) phenylphosphonothioate (leptophos), and O-ethyl O-(4-nitrophenyl) phenylphosphonothioate (EPN) at 5, 5, and 1 mg/kg/day, respectively, on male sheep were studied during 6 months of daily oral treatment under field conditions. A vehicle-control group of sheep given corn oil (0.1 ml/kg/day) only was used for comparison. All sheep were killed 24 h after the 180th daily treatment. Blood, brain, spinal cord, and sciatic nerve tissues were taken for histological and/or biochemical examinations. The results indicated that leptophos induced severe ataxia and paralysis in sheep following about 4 months of treatment. TOCP produced either mild ataxia or lameness in two of four sheep during the last week of experiment. On the other hand, none of the EPN-treated sheep showed clinical signs of neurotoxicity during the course of the experiment at the dosage tested. These clinical results were supported by histological findings and also by biochemical results with neurotoxic esterase (NTE) measurements. In the case of leptophos-treated sheep, numerous prominent degenerative lesions of axons were observed in spinal cords and brains. Similar but somewhat less numerous lesions were noted in sheep treated with TOCP. No histological changes were observed in similar tissues taken from EPN-treated sheep. The results also indicated that, for chronic exposure to these neurotoxic organophosphorus compounds in sheep, a threshold in excess of 60-70% prolonged inhibition of brain NTE, or 50-60% inhibition of spinal cord NTE must be exceeded to initiate clinical and/or histological neurotoxic effects.

Acetylcholinesterase↗
PubMed1982

Is delayed neurotoxicity a property of all organophosphorus compounds? A study with a model compound: parathion.

A recently reported hypothesis of other investigators that the induction of delayed neurotoxicity is a property of all organophosphorus compounds including parathion was evaluated in light of the inability of parathion to induce in our laboratory any clinical, histological, or biochemical signs of delayed neurotoxicity in hens following a very intensive dosing regimen. Parathion was administered orally or applied dermally as 1 mg/kg/day for 1 week and then the dose was increased by 1 mg/kg/day at weekly intervals up to 6 mg/kg/day which was given thereafter until a total of 90 doses. Results indicate that parathion either orally or dermally did not produce delayed neurotoxicity in hens comparable to that induced by tri-orthocresyl phosphate (TOCP) in this experiment. This finding is supported by clinical, histological, and biochemical evidences. No clinical signs or histopathological changes in spinal cords and sciatic nerves of the type associated with delayed neurotoxicity were observed in any of the surviving parathion-treated hens. Moreover, this extensive treatment with parathion resulted in no significant in vivo effect on neurotoxic esterase, an esterase believed to be the initial target in the genesis of delayed neurotoxicity. These results agree with the general hypothesis that delayed neurotoxicity is a special toxic effect of some but not all of the organophosphorus esters.

Acetylcholinesterase↗