Takegawa K, Mitsumori K, Onodera H, Yasuhara K, Kitaura K, Shimo T, Takahashi M
Division of Pathology, National Institute of Health Sciences, Tokyo.
Jpn J Cancer Res. 1998 Feb;89(2):105-9. doi: 10.1111/j.1349-7006.1998.tb00536.x.
In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats, squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40 males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular proliferation with lobular atrophy was observed at high incidence in the submandibular glands of the high-dose animals, and squamous metaplasia was frequently evident within the proliferative ductules and the larger interlobular ducts. A transition from metaplasia to SCC was apparent. The results suggest that squamous metaplasia in proliferative ductules, occurring secondarily to lobular impairment induced by KI, may develop into SCCs via a non-genotoxic, proliferation-dependent mechanism.
在一项对F344/DuCrj大鼠进行的为期两年的碘化钾(KI)致癌性研究中,饮用水中含有1000 ppm KI的40只雄性大鼠中有4只、40只雌性大鼠中有3只的唾液腺出现了鳞状细胞癌(SCC)。在高剂量动物的下颌下腺中,导管增生伴小叶萎缩的发生率很高,并且在增生的小导管和较大的小叶间导管内经常可见鳞状化生。化生向SCC的转变很明显。结果表明,由KI诱导的小叶损伤继发于增生性小导管中的鳞状化生,可能通过非基因毒性、增殖依赖性机制发展为SCC。