Developmental toxicity of acephate by gavage in mice

Farag, Ahmed A.; Eweidah, M.H; Tayel, Shawky; El‐Sebae, A. H.

doi:10.1016/s0890-6238(00)00074-5

Cited by 37 publications

(21 citation statements)

References 13 publications

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“…15 mg/kg/d. The study supports the finding of several authors (Lachner and Abdel-Rehman, 1984;Clemens et al, 1990;Leborde et al, 1996 andFarag et al, 2000). These studies suggest that doses which are not maternally toxic (symptoms appeared but no death occurred) were unable to produce fetotoxicity or teratogenicity.…”

Section: Discussionsupporting

confidence: 91%

Transplacental Disposition and Teratogenic Effects of Chlorpyrifos in Rats

2006

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-Rats were orally fed with different doses viz. 9.6, 12 and 15mg/kg/d from GD 0-20 and examined for evidence of fetotoxicity and teratogenecity to evaluate the potential effects of technical chlorpyrifos (97%). Fetotoxic effects were not observed at tested dose levels as evidenced by number of implantations, number of corpora lutea and live fetuses/dam, but significant alterations were noted in percent δ resorption and fetal weight. There were no major malformations, but some minor anomalies such as reduced parietal ossification and absence of phalanges found significant in high dose were not considered as compound-related effects. On the other hand the accumulation of chlorpyrifos residue in dams was more in brain (0.0328 μg/g) than in liver (0.0071 μg/g).The level of residue in fetuses was in the following order : liver (0.0531 μg/g) > brain (0.0364 μg/g) >placenta (0.040 μg/g) > amniotic fluid (0.0010 μg/g). Although, the total residue was higher in fetuses (0.0447 μg/g) than in dams (0.0120 μg/g), the absence of abnormalities in fetal gross morphology, visceral and skeleton suggest that technical chlorpyrifos at tested dose levels is non-teratogenic in rats.

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Section: Discussionsupporting

confidence: 91%

Transplacental Disposition and Teratogenic Effects of Chlorpyrifos in Rats

2006

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“…Conversely, dipterex and oxydemeton-methyl were shown to be teratogenic at higher exposure levels in rats and chickens, respectively (Staples et al, 1976;Lenselink et al, 1993). Recently, acephate, fenitrothion and flupyrazofos were found to reveal developmental toxicity at maternally toxic doses in rodents (Farag et al, 2000;Chung et al, 2002;Turner et al, 2002). OP compounds may cause alkylation of cellular DNA.…”

Section: Discussionmentioning

confidence: 99%

“…Parathion, diazinon, malathion and dichlorvos induced maternal toxicity but no teratogenicity in rats and rabbits (Vogin et al, 1971;Talens and Wooley, 1973;Baksi, 1978). However, acephate and flupyrizafos were found to induce developmental toxicity at maternally toxic doses in mice and rats, respectively (Farag et al, 2000;Chung et al, 2002). Anilofos (S-4-chloro-N-isopropylcarbaniloylmethyl-O,O-dimethylphosphorodithioate), a recently introduced OP herbicide, is selectively used to control annual grassy weeds and sedges in transplanted rice.…”

Section: Introductionmentioning

confidence: 99%

Effects of low‐level arsenic exposure on the developmental toxicity of anilofos in rats

Aggarwal

Wangikar

Sarkar

et al. 2007

J of Applied Toxicology

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In view of the increased use of anilofos for crop protection and ever increasing arsenic levels in drinking water in many countries, the coexistence of arsenic and anilofos in the environment is a reality and simultaneous exposure of humans and animals to these contaminants could be potentially hazardous. The aim of the present study was to examine whether coexposure to arsenic at the groundwater contamination level could alter the embryofetal toxicity of anilofos in rat model. Anilofos (100 mg kg(-1) day(-1)) and sodium arsenite (1 mg arsenic kg(-1) day(-1)) were administered by gavage either individually or in combination to the pregnant rats from day 6 to day 15 of gestation. Arsenic did not produce any significant effects either on maternal or fetal parameters at the given dose. Anilofos alone significantly decreased maternal weight gain, feed and water intakes, gravid uterine weights, number of live fetuses and fetal body weights and increased resorptions. There were increased incidences of gross, skeletal and visceral anomalies in the fetuses of anilofos-treated group. The main skeletal abnormality was increased intercostal space, while the visceral anomaly was an interventricular septal defect. Treatment with the combination of arsenic and anilofos significantly enhanced the fetal changes with much greater magnitude compared with the effects produced by anilofos alone. Anomalies such as midfacial cleft, exencephaly and anophthalmia were seen only in the fetuses of the combination group. The results show that anilofos interferes with embryofetal development and coexposure with arsenic at environmentally realistic concentrations produces additive or synergistic effects on the developmental toxicity of anilofos in rats.

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“…Developmental Toxicity --We evaluated developmental toxicity of surfactin C for the maternal animals and fetuses, as previously described. 17) Two adult virgin female mice after 3-week acclimation were placed overnight with a male of the same strain for mating. The female mice were checked for vaginal plugs in the next morning, and the presence of a vaginal plug was designated as the gestation day (GD) 0.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of Genetic and Developmental Toxicity of Surfactin C from Bacillus subtilis BC1212

Hwang

Park²,

Lim³

et al. 2008

JOURNAL OF HEALTH SCIENCE

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Surfactin C is a biosurfactant produced by Bacillus subtilis from Korean soybean paste. Surfactin C is known to have several therapeutic effects including anti-inflammatory, fibrinolytic, and thrombolytic activities. However, there is little information concerning its safety. In this study, we evaluated the genetic and developmental toxicity of surfactin C. Bacterial reverse mutation and rodent micronucleus assays were performed to determine its genotoxic potentials. Surfactin C at 0, 125, 250, and 500 mg/kg of body weight/day was administered orally to pregnant ICR mice during the period of major organogenesis. There was no genetic toxicity related to surfactin C treatment in in vitro and in vivo systems. In the developmental study, surfactin C did not demonstrate maternal toxicity, fetotoxicity, and teratogenicity, and hence the no observed effect level was concluded 500 mg/kg per day in ICR mice.

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Developmental toxicity of acephate by gavage in mice

Cited by 37 publications

References 13 publications

Transplacental Disposition and Teratogenic Effects of Chlorpyrifos in Rats

Transplacental Disposition and Teratogenic Effects of Chlorpyrifos in Rats

Effects of low‐level arsenic exposure on the developmental toxicity of anilofos in rats

Evaluation of Genetic and Developmental Toxicity of Surfactin C from Bacillus subtilis BC1212

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