Teratogenic effects of nickel chloride on embryonic mice and its transfer to embryonic mice.
Administration of nickel chloride to the pregnant mice on the seventh to eleventh day of their gestational period, resulted in significant embryotoxic effects in terms of an increased resorption rate, a decreased fetal weight, delay in skeletal ossification and high incidence of malformation. Among the cases of fetal malformation, the following malformations were observed to occur at a higher rate of incidence: acephalia, exencephaly, cerebral hernia, open eyelid, cleft palate, micromelia, ankylosis of the extremity, club foot and skeletal anomalies. Most skeletal anomalies were in the form of vertebral and/or rib fusions and were found mostly at thoracic and lumbar levels. The concentration of nickel retained in embryonic tissues was 800 times higher in the exposed compared to control groups and indicated that increased tissue levels of nickel chloride had a toxic influence on the developing embryo.
D000014:Abnormalities, Drug-Induced / Q000196:embryology*; D000818:Animals; D002972:Cleft Palate / Q000139:chemically induced; D004305:Dose-Response Relationship, Drug; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced; D005327:Fetal Resorption / Q000139:chemically induced; D005865:Gestational Age; D008431:Maternal-Fetal Exchange; D051379:Mice; D008813:Mice, Inbred ICR; D009532:Nickel / Q000008:administration & dosage / Q000633:toxicity*; D011247:Pregnancy; D013131:Spine / Q000002:abnormalities*
D009532:Nickel