Pagano G, Cipollaro M, Corsale G, Esposito A, Mineo A, Ragucci E, Giordano G G, Kobayashi N, Trieff N M
National Cancer Institute, Fondazione G. Pascale, Naples, Italy.
Teratog Carcinog Mutagen. 1988;8(6):363-76. doi: 10.1002/tcm.1770080606.
Sodium azide (SA) was tested on sea urchin embryos and gametes (Paracentrotus lividus). Developing embryos were exposed to SA (10(-6) to 10(-3) M) up to pluteus larval stage, or for shorter intervals before or after hatching. Developmental defects in SA-exposed embryos consisted mainly of gut abnormalities, without any detectable differences between pre- or post-hatch-exposed embryos. SA-induced damage to gut was exerted during gastrulation, as evident by lectin binding of extracellular matrix. No mitotic damage was observed in SA-exposed embryos, nor could pH-related variations be detected in SA-induced embryotoxicity at pH's ranging from 8 to 6. Concurrently, no effect ensued in the exposure of unfertilized eggs to SA (10(-5) to 10(-2) M) both in terms of fertilization success and of offspring quality. When sperm were suspended in filtered seawater at pH's ranging from 8 to 6, and SA levels ranging from 10(-5) to 10(-2) M, fertilization success of SA-exposed sperm appeared to be modulated by pH, by displaying three distinct dose-response trends at pH 8, 7, or 6. The consequences of sperm pretreatment on offspring quality failed to show any significant SA-induced changes on larval malformations or mortality, while confirming the previously reported pH-induced increase of developmental defects in the offspring of acid-exposed sperm (Pagano et al.: Teratogenesis Carcinogen Mutagen 5:113-121, 1985).
叠氮化钠(SA)在海胆胚胎和配子(地中海海胆)上进行了测试。发育中的胚胎暴露于SA(10⁻⁶至10⁻³ M)直至长腕幼虫阶段,或在孵化前或孵化后较短时间内暴露。暴露于SA的胚胎发育缺陷主要包括肠道异常,孵化前或孵化后暴露的胚胎之间没有任何可检测到的差异。SA对肠道的损伤在原肠胚形成期间发生,这通过细胞外基质的凝集素结合得以证明。在暴露于SA的胚胎中未观察到有丝分裂损伤,在pH值为8至6的范围内,SA诱导的胚胎毒性中也未检测到与pH相关的变化。同时,未受精卵暴露于SA(10⁻⁵至10⁻² M)在受精成功率和后代质量方面均未产生影响。当精子悬浮在pH值为8至6、SA水平为10⁻⁵至10⁻² M的过滤海水中时,暴露于SA的精子的受精成功率似乎受到pH的调节,在pH 8、7或6时呈现出三种不同的剂量反应趋势。精子预处理对后代质量的影响未能显示出SA对幼虫畸形或死亡率有任何显著的诱导变化,同时证实了先前报道的酸性暴露精子后代中pH诱导的发育缺陷增加(Pagano等人:《致畸致癌致突变》5:113 - 121,1985年)。