Effects of cobalt sulfate on prenatal development of mice, rats, and rabbits, and on early postnatal development of rats

The effects of cobalt sulfate administered to pregnant C57Bl mice, OFA-SD r ats, and New Zealand rabbits was studied on fetal and postnatal offspring. Cobalt concentration in the maternal blood was increased in proportion to t he administered doses. Cobalt crossed the placenta and appeared in the feta l blood and amniotic fluid. Regardless of the administered dose of cobalt s ulfate, cobalt concentration in the blood peaked 2 h after administration. Cobalt produced dose-dependent maternal toxicity and was found to be embryo toxic in all three species, as evidenced by elevated frequency of fetuses w ith body weight or skeletal retardation and embryolethality. Cobalt increas ed the frequency of major anomalies significantly in mice and rats, with an omalies of the eyes, kidneys, skull, spine, and sternum in mice, and anomal ies of the urogenital system in rats. Cobalt sulfate was not teratogenic in rabbits. Intra-amnial administration of cobalt sulfate produced a dose-dep endent increase of the frequency of dead fetuses, and weight retardation of the live fetuses. The direct cytotoxic effect probably plays a role in the embryotoxic and teratogenic effects of cobalt. The postnatal examinations revealed a decrease of the perinatal index in the treated group. The body w eight of the pups in the treated group was lower during wk I of life, but n o difference was found between the control and treated by the end of wk 2. Eye opening was completed in the usual time period in both groups, while ti me of appearance of the teeth, descending of the testes, shaping of ears, a nd development of hearing was delayed in the treated group. The development of muscle strength and of the locomotor system was delayed. All the functi ons studied (forward movement, swimming, righting reflex) normalized by pos tnatal d 21, with the exception of muscle strength. It was concluded that c obalt sulfate exposure decreases the perinatal viability of the fetuses, bu t the functions of the surviving fetuses with perinatal retardation become compensated by postnatal wk 2-3. The development of fetuses is undisturbed thereafter.