Cohen M M, Shiloh Y
Mutat Res. 1977;47(3-4):183-209. doi: 10.1016/0165-1110(77)90003-3.
The acute and the chronic psychotomimetic potentials of the hallucinogen lysergic acid diethylamide (LSD-25) have been recognized for almost 40 years. That additional types of the biological effects should have come under scrutiny was directly attributable to widespread use and abuse of this drug on a world-wide basis. Although "genetic toxicology" encompasses a broad spectrum of disciplines, including many areas of highly specialized research, perhaps the most germane, and those on which this review has concentrated, are Clastogenicity, Mutagenicity, Teratogenicity and Oncogenicity. Based on our current understanding and interpretation of the available data, the genetic toxicology of LSD provides an excellent example of Newton's "third law of motion", e.g., to every force there is an equal and opposite reaction force. From the published material it is impossible to draw clear cut conclusions regarding any of the above "problem areas" in spite of the considerable scientific effort invested. Most of the in vitro studies performed on the clastogenicity of LSD indicate either suppression of mitosis or enhanced chromosome damage. However, extrapolation of such results to the in vivo situation is very difficult. With regard to in vivo human use of the drug, no concensus is attainable as to chromosome breakage and the inconsistencies within and between studies remain inexplicable. However, several of the "controlled" investigations assessing the in vivo effect of chemically pure LSD suggest a transient increase in lymphocyte chromosome breakage. On the other hand, the results of cytogenetic studies on experimental animals are contradictory. Although human studies are nonexistent, in those experimental organisms tested, using accepted techniques, LSD proved to be, at best, a weak mutagen, if mutagenic at all. Teratogenicity studies in animals are confusing due to the multitude of organisms and plethora of discriminant parameters studied. However, with regard to man there has been ample opportunity and one can conclude that LSD is not teratogenic. As to the drug's oncogenic potential, the 3 reported cases of leukemia in LSD users are most likely the result of coincidence.
致幻剂麦角酸二乙酰胺（LSD-25）的急性和慢性拟精神病潜能已被认识近40年。由于该药物在全球范围内的广泛使用和滥用，其他类型的生物学效应也受到了审视。尽管“遗传毒理学”涵盖了广泛的学科领域，包括许多高度专业化的研究领域，但也许最相关的，也是本综述所关注的，是染色体断裂效应、诱变性、致畸性和致癌性。基于我们目前对现有数据的理解和解释，LSD的遗传毒理学为牛顿的“第三运动定律”提供了一个很好的例子，即每一个力都有一个大小相等、方向相反的反作用力。尽管投入了大量的科学努力，但从已发表的材料中，不可能就上述任何一个“问题领域”得出明确的结论。大多数关于LSD染色体断裂效应的体外研究表明，要么是有丝分裂受到抑制，要么是染色体损伤增强。然而，将这些结果外推到体内情况非常困难。关于该药物在人体的体内使用，对于染色体断裂无法达成共识，研究内部和研究之间的不一致仍然无法解释。然而，一些评估化学纯LSD体内效应的“对照”研究表明，淋巴细胞染色体断裂有短暂增加。另一方面，对实验动物的细胞遗传学研究结果相互矛盾。虽然没有人体研究，但在使用公认技术测试的那些实验生物中，LSD充其量被证明是一种弱诱变剂，如果它真的具有诱变性的话。由于研究的生物种类繁多和判别参数过多，动物致畸性研究令人困惑。然而，就人类而言，有足够的机会，可以得出结论，LSD不会致畸。至于该药物的致癌潜能，报告的3例LSD使用者患白血病的病例很可能是巧合。
