Burk D, Beaudoin A R
Teratology. 1977 Dec;16(3):247-59. doi: 10.1002/tera.1420160303.
The developmental origin of arsenate-induced renal agenesis was investigated. Pregnant Wistar rats were each injected once ip with 45 mg/kg sodium arsenate at day 10 (sperm day = day 0). Pregnancy was terminated at various times following injection and the embryos recovered and serially sectioned. Renal agenesis resulted when the mesonephric duct failded to give rise to a ureteric bud with subsequent failure of induction of the metanephric blastema. The underlying defect was retardation in growth of the mesonephric duct, first observed 48 hours after arsenate injection. A shortened mesonephric duct also resulted in a failure of the mesonephros to attain normal size and in the male resulted in absence of the ductus deferens, seminal vesicle a variable portion of the epididymis. Due to the intimate association of the mesonephric and growing paramesonephric ducts, a shortened mesonephric duct resulted in a shortened paramesonephric duct with resultant lack of a uterine horn.
研究了砷酸盐诱导肾缺如的发育起源。将怀孕的Wistar大鼠在第10天(精子日 = 第0天)经腹腔注射一次45 mg/kg砷酸钠。在注射后的不同时间终止妊娠,取出胚胎并进行连续切片。当中肾管未能产生输尿管芽且随后诱导后肾胚基失败时,就会导致肾缺如。潜在缺陷是中肾管生长迟缓,在砷酸盐注射后48小时首次观察到。缩短的中肾管还导致中肾未能达到正常大小,在雄性中导致输精管、精囊以及附睾可变部分缺失。由于中肾管与正在生长的副中肾管密切相关,缩短的中肾管导致副中肾管缩短,从而导致子宫角缺失。