Electroporation of thalidomide to medaka (&lt;i&gt;Oryzias latipes&lt;/i&gt;) embryo for evaluation of developmental toxicity

Nishiyama, Yuki; Uchida, Masaya; Terada, Aki; Kôno, Susumu; Ishibashi, Hiroshi; Arizono, Koji; Tominaga, Nobuaki

doi:10.2131/fts.8.189

Cited by 3 publications

(2 citation statements)

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“…On the other hand, however, it was also reported that effects of thalidomide by simple soaking in a thalidomide solution were very weak [ 30 ], as was confirmed in the present study. Thalidomide also had minor effects on the development of embryos/larvae by usual immersion but caused malformations including pectoral fin defects and curvature of the spine by electroporation in medaka ( Oryzias latipes ) [ 39 ]. In this study, thalidomide exposure (200 and 400 µM) did not cause any malformation in wild-type zebrafish when exposure was started from 17 hpf or 24 hpf.…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to a high concentration of thalidomide of more than 200 µM resulted in pectoral fin defects and other malformations even in hCYP3A7-expressing zebrafish. A high concentration of thalidomide was also required to cause developmental toxicity possibly due to lower absorption of thalidomide by embryos/larvae of medaka [ 39 ]. It was also suggested that zebrafish might be relatively insensitive to thalidomide compared to humans due to mutations of SALL4, a possible key gene in pectoral fin growth [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

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Augmentation of Pectoral Fin Teratogenicity by Thalidomide in Human Cytochrome P450 3A-Expressing Zebrafish

et al. 2023

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The pharmacological and toxicological effects of active metabolites of enzymes including cytochrome P450 (CYP) are important. While it has been believed for a long time that thalidomide causes characteristic limb malformation only in rabbits and primates including humans, the involvement of their CYP3A subtypes (CYP3As) has been suggested. Recently, however, it was reported that zebrafish were sensitive to thalidomide, showing defects of pectoral fins, homologous organs of forelimbs in mammals, as well as other deformities. In this study, we prepared human CYP3A7 (hCYP3A7)-expressing zebrafish (F0) using a transposon system. Thalidomide caused pectoral fin defects and other malformations including pericardial edema in hCYP3A7-expressing embryos/larvae but not in wild-type and hCYP1A1-expressing embryos/larvae. Thalidomide also reduced the expression of fibroblast growth factor 8 in pectoral fin buds in only hCYP3A7-expressing embryos/larvae. The results suggest the involvement of human-type CYP3A in thalidomide teratogenicity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%