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      Developmental toxicity of cyclohexanediaminetetraacetic acid (CDTA) in mice.

      Research communications in chemical pathology and pharmacology
      Abnormalities, Drug-Induced, etiology, Animals, Body Weight, drug effects, Cations, metabolism, Chelating Agents, toxicity, Edetic Acid, analogs & derivatives, Embryonic and Fetal Development, Female, Fetal Death, chemically induced, Fetus, Gestational Age, Injections, Intraperitoneal, Male, Maternal-Fetal Exchange, Mice, Organ Size, Pregnancy

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          Abstract

          Cyclohexanediaminetetraacetic acid (CDTA), an effective antagonist for the treatment of zinc, lead, and manganese poisoning was evaluated for maternal and developmental toxicity in pregnant Swiss mice. CDTA was given intraperitoneally on gestation days 6-15 at doses of 0, 270, 540, and 1080 mg/kg/day. On gestational day 18, the fetuses were examined for external, visceral, and skeletal malformations and variations. Treatment with CDTA at 1080 mg/kg/day resulted in a high level of maternal deaths, as well as less severe clinical signs (significant reduction in weight gain and food consumption). Increased resorptions, fetal deaths, and decreased number of live fetuses per litter were observed at 1080 mg/kg/day. Mean fetal body weights were also significantly decreased in this group. At 1080 mg/kg/day, CDTA caused external malformations, while the development of skeletal tissues was less affected. The no observable adverse effect level (NOAEL) for maternal and developmental toxicity of CDTA in mice was 540 mg/kg/day. Analyses of maternal and fetal tissues revealed only slight effects of CDTA on concentrations of calcium, magnesium, zinc, copper and iron. According to these results, the alterations in mineral metabolism should not be the major reason for CDTA-induced developmental toxicity.

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