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Teratogenicity causes

Administered to mouse embryo cultures in vitro, trimethylamine was teratogenic, causing neural mbe defects and inhibiting embryonic growth. Trimethylamine may exert these effects by reducing macromolecular synthesis. Repeated intraperitoneal injections of trimethylamine hydrochloride in pregnant mice caused fetotoxicity only at maternally toxic doses. ... [Pg.712]

Figure 6.26 The dose-response patterns for teratogenicity caused by the cytotoxic agent MNNG. Pregnant mice were treated on day 11 with MNNG. Abbreviation MNNG, /V-methyl-W-nitro-W-nitrosoguanidine. Source From Ref. 9. Figure 6.26 The dose-response patterns for teratogenicity caused by the cytotoxic agent MNNG. Pregnant mice were treated on day 11 with MNNG. Abbreviation MNNG, /V-methyl-W-nitro-W-nitrosoguanidine. Source From Ref. 9.
This is a sedative drug with low adult toxicity, which proved to be a very potent human teratogen, causing phocomelia (shortening of the limbs) and other defects when taken between the third and eighth week. In some cases, only a few doses were taken, but on the critical days (e.g., days 24-27 for phocomelia of arms). It is not readily reproducible in laboratory animals (e.g., rats). Mechanism is unknown, but a metabolite suspected, possibly produced by cytochrome P-450. A number of metabolites are produced and some chemical breakdown occurs. Phthalylglutamic acid metabolite is teratogenic in mice. Thalidomide may acylate nucleic acids and polyamines. The S-enantiomer is more embryotoxic than the R-enantiomer. [Pg.399]

Teratogenic. Causing deformities in the offspring of mothers dosed with a drug during pregnancy. [Pg.183]

More information is needed on teratogenicity of PCDEs as well as the role of thyrotoxicity in the developmental toxicity of PCDEs [104], Teratogenicity caused by nitro-PCDEs has been suggested to involve alterations in thyroid hormone status [87] and transient alterations in maternal thyroid status might affect development of the fetus [143], Effects of PCDEs after prenatal exposure have been similar to those of PCBs [104]. [Pg.197]

Toxicity, as with other antimetabolites, can be severe—even fatal. Oral lesions usually occur first, followed by gastrointestinal lesions, bone marrow depression, baldness, and hyperpigmentation. It is not surprising that these drugs are teratogenic, causing fetal abnormalities and death. [Pg.118]

TERATOGENIC Causing birth defects comes from the Greek word teratogenesis, meaning monster-making. ... [Pg.980]

Teratogens cause one-time birth defects in offspring resulting from maternal or paternal exposure to toxic materials. The word teratology is derived from the Latin meaning the study of monsters. It is actually the study of congenital malformations, which started with the study of the correlation of German measles to birth defects. [Pg.271]

Sodium cyanide is a teratogen, causing fetus damage and developmental abnormalities in the cardiovascular system in hamsters (NIOSH 1986). [Pg.323]

Hexachlorodibenzo- C12H2CI6O2 Teratogen causes specific developmental... [Pg.340]

Ethylene oxide is a teratogen, causing birth defects. Laboratory tests on animals indicated that exposure could cause fetal deaths, specific developmental abnormahties, and paternal effects related to testes and sperm ducts. [Pg.360]

Ethylene glycol C6H14O2 animals from high exposures were tremor, labored breathing, and hematuria eye irritant teratogen, causing stillbirth and developmental abnormalities in musculoskeletal system toxic effects in humans should be low LD50 oral (rats) 3,000 mg/kg Low toxicity via oral,... [Pg.419]

Bis(pentabromophenyl)ether [decabromodiphenyl ether decabromobiphenyl oxide l,l -oxybis(2,3,4,5,6-pentabromobenzene) Saytex 102] [1163-19-5] CiiBrioO 959.22 Br Br Br Br Br —0— Teratogenic caused postimplantation mortality in rats some evidence of carcinogenicity in test animals, oral feeding resulted in liver tumors in rats Noncombustible solid... [Pg.433]

Mutagenic carcinogenicity not reported teratogen, caused developmental abnormalities in eyes, ear, and central nervous system and showed harmful effects on embryo and fertility in rats... [Pg.1080]

Exhibited moderate toxicity in test animals from intraperi-toneal, subcutaneous, and oral intakes extent of toxicity varied with species target organs kidney and bladder LD50 oral (mice) 129 mg/kg teratogenic, causing fetotoxicity and developmental abnormalities in central nervous system in hamster exposure limit TLV-TWA 20 mg/m ... [Pg.1088]

Renal ectopy is the term for a kidney lying outside the renal fossa. As stated in Chapter 2 (Sect. 2.1.1), the kidney migrates cephalad early in gestation to arrive at its normal position. Abnormality of the ureteral bud or metanephric blastema, genetic abnormalities, teratogenic causes, or anomalous vasculature, acting as a barrier to ascent, are reasons for failure of the kidney to complete its ascent (Malek et al. 1971). The incidence of renal ectopy in postmortem studies varies from 1 in 500 (Campbell 1930) to 1 in 1,290 (Thompson and Pace 1937). There is a slight predilection for the left side, and 10% of cases are bilateral (Fig. 4.1). [Pg.82]

Reproductive Effects Reproductive damage in humans. Suspect human, teratogen causes birth defects fetal death in rats. Animal studies show damage to reproductive system in males females may be fetotoxic. Suspect human teratogen causes birth defects fetal ath in rats. Causes reproductive damage in men womert causes mutations in animals. [Pg.44]

Nontoxic. To the extent possible, consumables should not be toxic in the concentrations that organisms are likely to be exposed to them. In addition to their not being acutely toxic, consumables should not be mutagenic, carcinogenic, or teratogenic (cause birth defects). [Pg.599]

Teratogens cause birth defects. These usually arise from damage to embryonic or fetal cells. However, mutations in germ cells (egg or sperm cells) may cause birth defects such as Down s syndrome. The biochemical mechanisms by which teratogens act are varied. These include enz3mie inhibition by xenobiotics deprivation of the fetus of essential substrates, such as vitamins interference with energy supply or alteration of the permeabihty of the placental membrane. [Pg.741]


See other pages where Teratogenicity causes is mentioned: [Pg.550]    [Pg.1577]    [Pg.40]    [Pg.72]    [Pg.9]    [Pg.263]    [Pg.266]    [Pg.612]    [Pg.182]    [Pg.423]    [Pg.20]    [Pg.476]    [Pg.805]    [Pg.1693]    [Pg.848]    [Pg.175]    [Pg.627]    [Pg.624]    [Pg.775]    [Pg.426]    [Pg.71]    [Pg.199]    [Pg.7185]    [Pg.556]    [Pg.180]    [Pg.822]    [Pg.429]   
See also in sourсe #XX -- [ Pg.154 , Pg.167 ]




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