1-Methylnaphthalene is generally utilized in solvents, as an intermediate in organic synthesis, a dye carrier, in resins, and others. There are some toxicological studies of 1-methylnaphthalene; however, inhalation toxicity studies are rare. Each of 10 male and female F344 rats was exposed to vapors of 1-methylnaphthalene for 13 weeks (6 h a day, 5 days per week) at concentrations of 0, 0.5, 4, and 30 ppm in a whole-body inhalation chamber system. The exposure concentrations were 0.52 ± 0.05, 4.08 ± 0.25, and 30.83 ± 1.28 ppm for the low-, middle-, and high-dose group, respectively. Body weight changes were not affected by exposure to 1-methylnaphthalene. Blood prothrombin time was delayed at 30 ppm in male and female groups, and activated partial thromboplastin time was also delayed at 30 ppm in the male group. Values of alanine aminotransferase in the serum were decreased and those of albumin were increased at 30 ppm in the male group. Differential cell counts and levels of lactate dehydrogenase in the bronchoalveolar lavage fluid were not affected. However, mucous cell hyperplasia in the nasopharyngeal tissues was found and the severity was correlated to exposure concentrations. In conclusion, 1-methylnaphthalene mainly affects the upper respiratory system and the no-observed-adverse-effect level is suggested to be 4 ppm on the basis of histopathological findings.

We investigated the toxic effects of difenoconazole on the development in the African clawed frog, Xenopus laevis. To test the toxic effects, frog embryo teratogenesis assays using Xenopus were performed. Embryos were exposed to various concentrations of difenoconazole (0-30 μM). LC100 for difenoconazole was 30 μM, and the LC50 determined by probit analysis was 27.19 μM. Exposure to difenoconazole concentrations ≥5 μM resulted in 10 different types of severe external malformation. Histological examinations revealed dysplasia of the eye, heart, liver, somatic muscle, and swelling of the pronephric ducts. The tissue-specific toxic effects were investigated with an animal cap assay. Blood cells were normally induced at a high frequency by mSCF and activin A. However, the induction of blood cells was strongly inhibited by the addition of difenoconazole. Electron micrographs of tested embryos showed the degeneration of somatic muscle and the shrinkage of microvilli on pronephric duct. The gene expression of cultivated animal cap explants was investigated by reverse transcriptase-polymerase chain reaction (RT-PCR). It revealed that the expression of the blood-specific marker(β -globin Ⅱ) and muscle-specific marker (XMA) were more strongly inhibited than the neural-specific marker(XEn2) by the addition of difenoconazole.

We investigated the toxic effects of tebuconazole on development in the African clawed frog, Xenopus laevis. To test the toxic effects, frog embryo teratogenesis assays using Xenopus were performed. Embryos were exposed to various concentrations of tebuconazole(0-100 μM). LC100 for tebuconazole was 100 μM, and the LC50 determined by probit analysis was 82.35 μM. The exposure to tebuconazole concentrations ≥40 μM resulted in 11 different types of severe external malformations including gut dysplasia. Histological examinations revealed various dysplasia in the eye, heart, liver, intestine, somatic muscle, and in the pronephric ducts. The tissue-specific toxic effects were investigated with an animal cap assay. Blood cells are generally induced at a high frequency by the combination of mSCF and activin A, however, the induction of blood cells was strongly inhibited by the addition of tebuconazole. Electron micrographs of tested embryos showed many of multivesicular bodies and dysplasia of photo-receptive cell, however, the somatic muscle degeneration was not severe. The gene expression of cultivated animal cap explants was investigated by reverse transcriptase-polymerase chain reaction and revealed that expression of the blood-specific marker, β globin Ⅱ and muscle-specific marker, muscle actin were more strongly inhibited than the neural-specific marker, XEn2.