This study investigated the developmental toxicity of carbendazim during the organogenesis period in mice. Mated CD-1 mice were administered carbendazim at dose levels 0, 150, 300, and 600 mg/kg/day by gavage. Body weights, weight gains, and feed consumption were significantly reduced in mice administered with 300 and 600 mg/kg/day. Carbendazim exposure increased maternal levels of cholesterol, triglyceride, glucose, protein, and creatinine; and reduced the levels of estradiol and progesterone in the 300- and 600-mg/kg/day groups. In addition, exposure to carbendazim significantly reduced the number of live fetuses and increased the number of dead and resorptions at the same dose levels. External, visceral, and skeleton malformations were observed in the 300- and 600-mg/kg/day. In conclusion, exposure of pregnant mice to carbendazim induced maternal and developmental toxicity at 300 and 600 mg/kg/day. 150 mg/kg/day carbendazim produced a very slight increase in postimplantation loss, which was within the range of historical controls, and no evidence of maternal toxicity.

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The uptake of biotin and biocytin was investigated in rat intestine using the everted sac technique. It has been shown that at biotin and biocytin concentrations less than 40 and 50 nM respectively, absorption proceeds by a saturable process, whereas at higher concentrations uptake by passive diffusion predominates. Fractionation of solubilized brush border preparations indicates that biotinidase is the only protein which binds biotin in this preparation.

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