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No embryotoxicity of exogenous alpha-elastin evidenced through interference with the chick embryonic morphogenetic
K Kosar1, J Wimmerová, F Bartos
1Department of Pharmacological Propaedeutics, Faculty of Pharmacy, Charles University, Hradec Králové, Czechoslovakia.
Insights
Alpha-elastin (1) shows potential as a safe drug carrier. Low doses did not harm chick embryos, with rare toxicity observed only at very high doses.
Area of Science:
- Developmental biology
- Toxicology
- Pharmacology
Background:
- Alpha-elastin is a naturally occurring protein with potential applications.
- Understanding its effects on embryonic development is crucial for safety assessment.
Purpose of the Study:
- To evaluate the embryotoxic effects of alpha-elastin in chick embryos.
- To determine safe dosage limits for potential clinical use as a drug carrier.
Main Methods:
- Chick Embryotoxicity Screening Test (CHEST) was employed.
- Subgerminal and intraamniotic administration of alpha-elastin at various doses and developmental stages.
- Observation of morphogenetic systems, growth, and survival.
Main Results:
- Doses of 0.3 mg and higher induced caudal morphogenetic system (CMS) growth retardation.
- Embryotoxicity, including body wall defects and growth retardation, occurred rarely and predominantly at very high doses on day 2.
- The direct embryotoxicity range was identified between 0.3 and 1 mg per embryo.
Conclusions:
- Alpha-elastin demonstrates a low risk of embryotoxicity in chick models.
- Theoretical extrapolation suggests safe limits between 1-10 g.kg-1 maternal weight in mammals.
- Alpha-elastin is a potential safe natural drug carrier for clinical applications.
Abstract:
The effects of alpha-elastin (1) on the morphogenetic systems of the chick embryo were studied by means of the CHEST (chick embryotoxicity screening test). The subgerminal administration of doses of 0.3 mg and larger induced a growth retardation of the caudal morphogenetic systems (CMS). The administration of single effective doses of 1 subgerminally on the second day and intraamniotically on the third and fourth d of embryogenesis verified the beginning of the direct embryotoxicity range between the doses of 0.3 and 1 mg per embryo. It presents in the theoretical extrapolation for mammals the dose limits between 1 and 10 g.kg-1 of maternal weight. Embryotoxic manifestations (body wall defects, growth retardation and embryolethality) were induced predominantly in the embryos treated on d 2 with the very high doses only. Their frequency was rare. It has been concluded that 1 could be a safe potential natural drug carrier in clinical practice.