Pagano G, His E, Beiras R, De Biase A, Korkina L G, Iaccarino M, Oral R, Quiniou F, Warnau M, Trieff N M
Istituto Nazionale Tumori, Fondazione G. Pascale, Naples, Italy.
Arch Environ Contam Toxicol. 1996 Nov;31(4):466-74. doi: 10.1007/BF00212429.
The present study was undertaken to evaluate the toxicity of aluminum sulfate, ferric chloride and their 1:1 mixture (Mix) on early development, fertilization and offspring quality in three sea urchins species (Sphaerechinus granularis, Paracentrotus lividus, Psammechinus microtuberculatus) and in mussels (Mytilus galloprovincialis). The endpoints were the following: a) larval malformations; b) developmental arrest; c) embryonic mortality; d) fertilization success; e) cytogenetic effects, and f) luminol-dependent chemiluminescence (LDCL). Overall data point to the induction of developmental defects in both sea urchin and mussel embryos following exposure of embryos to Al(III) or Fe(III) (10(-7) to 10(-6) M), whereas Mix caused varied effects vs. Al(III) or Fe(III) alone, from scarce or no additive effects (M. galloprovincialis and P. lividus) to a dramatic rise in embryolethality even at nominal levels of 10(-8) M (Ps. microtuberculatus).S. granularis sperm underwent a dose-dependent decrease in fertilization success following exposure to Al(III), or Fe(III), or Mix at levels ranging from 10(-8) to 10(-5) M. A significant increase of developmental defects was observed in the offspring of S. granularis sperm exposed to micromolar levels of the agents, suggesting an Al(III)- and Fe(III)-related transmissible damage to sperm. The cytogenetic analysis of Al(III)-, Fe(III)-, or Mix-exposed S. granularis embryos showed a significant increase in mitotic aberrations. A relevant feature of the observed cytogenetic damage included scattered chromosomes, suggesting cytoskeleton damage. The LDCL emission in S. granularis embryos showed a dose-related inhibition by agent levels ranging from 10(-7) to 10(-5) M; this held true for both spontaneous and, to a larger extent, for horseradish peroxidase (HRP)-activated LDCL. LDCL associated with fertilization was affected by Al(III), Fe(III) and Mix, with a time- and dose-related shift from stimulation to inhibition. The changes observed in LDCL emission suggested that the observed damage to embryogenesis, fertilization and mitotic activity may be related, at least partly, to alterations of the embryo prooxidant state. The present data point to developmental, cytogenetic and biochemical changes related to realistic levels of Al(III), Fe(III) and their mixtures, raising concern as to their environmental, occupational and iatrogenic exposures.
本研究旨在评估硫酸铝、氯化铁及其1:1混合物（混合物）对三种海胆物种（粒刺海胆、紫球海胆、微疣海胆）和贻贝（地中海贻贝）早期发育、受精及后代质量的毒性。研究终点如下：a）幼虫畸形；b）发育停滞；c）胚胎死亡率；d）受精成功率；e）细胞遗传学效应；f）鲁米诺依赖性化学发光（LDCL）。总体数据表明，胚胎暴露于Al(III)或Fe(III)（10⁻⁷至10⁻⁶ M）后，海胆和贻贝胚胎均出现发育缺陷，而混合物与单独的Al(III)或Fe(III)相比产生了不同影响，从几乎没有或没有相加效应（地中海贻贝和紫球海胆）到即使在10⁻⁸ M的标称水平下胚胎致死率也急剧上升（微疣海胆）。粒刺海胆精子在暴露于10⁻⁸至10⁻⁵ M的Al(III)、Fe(III)或混合物后，受精成功率呈剂量依赖性下降。在暴露于微摩尔水平这些物质的粒刺海胆精子的后代中，观察到发育缺陷显著增加，这表明Al(III)和Fe(III)相关的对精子的可传播损伤。对暴露于Al(III)、Fe(III)或混合物的粒刺海胆胚胎进行细胞遗传学分析，结果显示有丝分裂畸变显著增加。观察到的细胞遗传学损伤的一个相关特征包括染色体分散，提示细胞骨架损伤。粒刺海胆胚胎中的LDCL发射在10⁻⁷至1️⁻⁵ M的物质水平下呈现剂量相关的抑制；自发LDCL以及在更大程度上辣根过氧化物酶（HRP）激活的LDCL均如此。与受精相关的LDCL受到Al(III)、Fe(III)和混合物的影响，出现了从刺激到抑制的时间和剂量相关的转变。在LDCL发射中观察到的变化表明，观察到的对胚胎发生、受精和有丝分裂活性的损伤可能至少部分与胚胎促氧化状态的改变有关。目前的数据表明，与Al(III)、Fe(III)及其混合物的实际水平相关的发育、细胞遗传学和生化变化，引发了对其环境、职业和医源性暴露的担忧。
