Fetus, hamster

A heritable resistance in pine mice to endrin raises the LD50 from 3 mg/kg in sensitive voles to 40 mg/kg in resistant animals (Webb et al. 1973). This trait is correlated with the greater excretion of endrin as the anti-12-hydroxy metabolite in the resistant mice. Associations between lethality and concentration of 12-ketoendrin residues has been made for rats (Hutson et al. 1975), rat fetuses (Kavlock et al. 1981), and hamster fetuses (Chemoff et al. 1979a). Toxicity also occurs when endrin itself appears in the tissues. 

Figure 2. A. Lateral view of a 15-day-old hamster fetus from a dam given an intravenous injection of 20 mg/kg sodium arsenate on the 8th day of gestation. Note the exencephalia as characterized by everted, degenerative neural tissues with hemorrhagic necrosis. B. Ventral view of the fetus shown in A. Note the severe malformation of the craniofacial structures with bilateral anophthalmia. (About X 3.5).

Microwaves inhibit thymidine incorporation by DNA blockage in cultured cells of the Chinese hamster irradiated cells had a higher frequency of chromosome lesions (Garaj-Vrhovac et al. 1990). Microwaves induce teratogenic effects in mice when the intensity of exposure places a thermal burden on the dams and fetuses, resulting in a reduction in fetal body mass and an increased number of resorptions (O Connor 1990). 

Sparschu et al. reported the embryotoxicity of TCDD in rats (1970) (refs. 122a,b). Data are summarized for rats and mice in Table 5. The three major effects observed were intestinal hemorrhages (rat fetuses) and increased incidence of cleft palate and kidney abnormalities (mouse fetuses). TCDD in pg/kg doses has also been reported to cause embryotoxic effects in hamsters eye abnormalities, reduction of mean fetal weight GI hemorrhages, increased prenatal mortality- (ref. 123). 

Both V(IV) and V(V) have been found to have reproductive and developmental toxic effects in rodents. In addition to decreased fertility, lethal effects to embryos, toxicity to fetuses, and teratogenicity have been observed in mice, rats, and hamsters exposed to vanadium.3... 

Previous reproductive toxicology studies in laboratory animals examining the effects of prenatal exposure to fumonisin demonstrated a potential risk to the developing fetus. Studies using an aqueous extract of contaminated maize-culture material of F. verticillioides reported that fumonisin was developmentally toxic in hamsters (Floss et al., 1994 Penner et al., 1998). In addition, purified fumonisin Bi was shown experimentally to cause fetal toxicity in rats and mice (Collins et al., 1998 Reddy et al., 1996). In another study, pregnant CD1 mice treated with a semipurified extract... 

Three ocher papers were related to a special type of subchronic toxicity Induced by atropine alteration of cells, embryos, and fetuses exposed to the chemical. Ishldate e al. (44) exposed cultures of fibroblasts from Chinese hamsters to atropine sulfate at 250 ug/ml in saline for 48 h. At the end of the period of incubation,... 

Exposure of laboratory animals (rats, mice, and hamsters) to trichlorfon at higher doses during the gestation period caused adverse effects on reproduction. An increased number of embryonic deaths, a decreased number of live fetuses and an increased number of fetal abnormalities were observed in rats given a single oral dose of 80 mg kg body weight,... 

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