遗传毒性
钼酸钠
微核试验
钼酸铵
三氧化钼
体内
钼
碎屑成因
微核
染色体畸变
有丝分裂指数
化学
生物
体外
分子生物学
毒性
生物化学
钼酸盐
药理学
男科
细胞生物学
遗传学
有丝分裂
染色体
医学
无机化学
原材料
有机化学
基因
作者
Nina Titenko‐Holland,Jianhua Shao,L. Zhang,Liqiang Xi,Hailong Ngo,Nong Shang,Martyn T. Smith
标识
DOI:10.1002/(sici)1098-2280(1998)32:3<251::aid-em8>3.0.co;2-r
摘要
Molybdenum is an essential element in plants and animals as a cofactor for enzymes. Molybdenum trioxide is used in metallurgical processes, in cosmetics as a pigment, and in contact lens solution, yet limited information is available on molybdenum genotoxicity. In the present study the micronucleus (MN) assay in human lymphocytes and mouse bone marrow and the dominant lethal assay in mice were used to assess the genotoxic effects of molybdenum salts in vitro and in vivo. Two salts of molybdenum were tested in whole blood cultures. Ammonium molybdate was more potent than sodium molybdate in causing a dose-dependent decrease in viability and replicative index and an increase in MN formation in binucleated lymphocytes (P < 0.001). A dose–response in both kinetochore-positive MN (caused by chromosome lagging) and kinetochore-negative MN (associated with chromosome breakage) was observed. Based on the results of a toxicity study of sodium molybdate, two doses, 200 and 400 mg/kg, were assessed in the bone marrow MN assay in mice (two i.p. injections 24 and 48 hr prior to euthanasia). A modest but statistically significant increase in MN frequency in polychromatic erythrocytes was observed (P < 0.05). The same treatment protocol was used to analyze dominant lethality. A dose-dependent increase in postimplantation loss represented mostly by early resorptions was observed the first week after treatment (P = 0.003). These preliminary data suggest that sodium molybdate induces dominant lethality at the postmeiotic stage of spermatogenesis. Overall, molybdenum salts produced moderately positive results both in vitro in human cells and in vivo in mice. Environ. Mol. Mutagen. 32:251–259, 1998 © 1998 Wiley-Liss, Inc.
科研通智能强力驱动
Strongly Powered by AbleSci AI